Essay on Cancer Treatment (For Medical Students) | Types | Diseases | Biology

Are you looking for an essay on ‘Cancer Treatment’? Find paragraphs, long and short essays on ‘Cancer Treatment’ especially written for college and medical students.  

1. Essay on Cancer Treatment: (Around 200 Words)

Success of Cancer Treatments:

The success rates for current cancer treatments are strongly influenced by the stage at which the disease is diagnosed. When cancer is detected early and tumor cells are still localized to their initial site of origin, cure rates tend to be very high, even for cancers that would other­wise have a poor prognosis (Figure 1).

Unfortunately, many cancers are difficult to detect in their early stages and by the time they are diagnosed, metastasis may have already occurred. If cancers were routinely detected at an earlier stage, many cancer deaths could be prevented.

Early detection is a feasible goal because despite the common perception that cancer arises rapidly and with little warning, most cancers develop slowly and only become aggressive and invasive after the gradual passage of time (usually measured in years rather than weeks or months). A prolonged window of opportunity therefore exists for detecting the disease in its earlier stages when treatments are more likely to be effective.

2. Essay on Cancer Treatment: (Around 350 Words)

Cancer has Few Symptoms that Arise Early or are Specific for the Disease:

The first thing to signal the presence of a disease is usually some type of physical symptom that prompts a visit to a doctor and helps guide the diagnosis. Few generalizations are possible about the symptoms of cancer because it can arise almost anywhere in the body.

When a cancer grows beyond a tiny localized clump of cells into a larger mass that invades surrounding tissues, symptoms may begin to be triggered as the tumor impinges on surrounding struc­tures and organs.

For example, if a tumor presses on a nerve it may cause pain, or it might disrupt blood vessels and cause bleeding. The location of symptoms varies widely, depending on the type of cancer involved. After a cancer has metastasized, symptoms may appear in other parts of the body and, in some cases, may represent the first signs of disease.

Tumors tend to produce few or no symptoms when they are small and localized, so it is difficult to come up with reliable guidelines to help people detect cancer early.

For many years, the American Cancer Society publicized a list of seven warning signs that are possible indicators of the presence of cancer:

1. Change in bowel or bladder habits.

2. A sore that does not heal.

3. Unusual bleeding or discharge.

4. Thickening or lump in the breast or elsewhere.

5. Indigestion or difficulty swallowing.

6. Obvious change in a wart or mole.

7. Nagging cough or hoarseness.

Any of the preceding symptoms might be a sign of cancer, but the list has two shortcomings that limit its usefulness. First, when one of these symptoms does arise because of cancer, it may not appear until the disease has advanced to a relatively late stage.

Second, none of the listed symptoms is specific for cancer, and in most cases a person exhibiting one or more of the symptoms will not actually have cancer. Yet despite these shortcomings, each warning sign in the list indicates a condition that should be assessed by a doctor because if it does signal the presence of cancer, the outcome will be much better if treatment is started early.

3. Essay on Cancer Treatment: (Around 480 Words)

Cancer Diagnosis Includes Information Regarding the Stage of the Disease:

The verdict that cancer is present is only the beginning of a complete cancer diagnosis. One of the next issues that needs to be addressed is the question of how far a person’s cancer has progressed.

Tumor staging uses three main criteria to establish a stage number that reflects how early a cancer has been detected:

(1) The size of the primary tumor and the extent of its spread into nearby tissues,

(2) The extent to which cancer cells have spread to regional lymph nodes, and

(3) The extent to which distant metastases are evident. A low stage number means that a cancer has been caught earlier and that treatment is more likely to be successful.

Sometimes a biopsy reveals tissue abnormalities that occur even earlier, prior to the formation of an actual tumor. For example, the development of cancer in some tissues is preceded by a distinct period of dysplasia (abnormal cell proliferation accompanied by the loss of normal tissue organization).

Areas of dysplasia may revert back to normal behavior, or the abnormalities can become more severe and gradually develop into cancer. Dysplasia is a common condition in the uterus, where it is often discovered when the uterine cervix is biopsied after an abnormal Pap smear.

The conversion of dysplasia into cancer typically requires several years, providing a signifi­cant “window of opportunity” during which the dysplastic region can be removed or destroyed to prevent cancer from arising. Even when the condition is not diagnosed until carcinoma in situ has developed, these pre-invasive tumors are relatively easy to treat because they have not yet begun to invade and spread.

A slightly different sequence of precancerous stages has been uncovered by screening tests for colon cancer. Colonoscopy sometimes reveals the presence of colon polyps that, upon microscopic examination, turn out to be adenomas (benign tumors of gland cells).

The cells in a polyp can acquire subsequent mutations, usually over a period of several years, that convert the polyp first into a localized, preinvasive adenocarcinoma (carcinoma in situ) and then into an invasive adenocarcinoma.

In other words, a benign tumor is often the first step on the road to malignancy in the colon. Removal of polyps while they are still benign is therefore an effective way of decreasing a person’s risk of developing colon cancer.

The preceding examples reinforce a point that cancer arises through a multistep process that begins with early cellular abnormalities, such as dysplasia or benign neo­plasia, followed by conversion into a preinvasive cancer that progresses into an invasive cancer that eventually metastasizes.

The initial stages of this process usually take a significant amount of time, providing ample opportu­nity for early diagnosis and treatment. When caught at any stage prior to the onset of invasion and metastasis, the disease can almost always be treated successfully.

4. Essay on Cancer Treatment: (Around 700 Words)

Cancer Diagnosis Includes Information Regarding the Microscopic Appearance and Molecular Properties of the Tumor Cells:

The diagnosis that a person has cancer is generally accom­panied by information concerning the cancer’s site of origin and the cell type involved. The site of origin may or may not be the site in which the cancer was initially detected.

For example, cancer discovered in the bones of the spinal column might turn out to be lung cancer that has metastasized to bone, or cancer discovered in the liver might turn out to be stomach cancer that has metastasized to the liver.

The type of cancer in such situations is always defined by the location of the primary tumor. In other words, lung cancer that has metastasized to bone is still lung cancer, not bone cancer, and stomach cancer that has metastasized to the liver is stomach cancer, not liver cancer. Knowing the site of origin is important because it determines the type of cancer and provides information as to how the cancer is likely to behave and how it should be treated.

After a tumor’s site of origin has been determined, additional information can be provided by microscopic examination of the biopsy specimen to determine the exact type of cells involved.

For example, there are different types of lung cancer, different types of stomach cancer, and different types of skin cancer, each determined by the identity of the cell type that has become malignant. Knowing the cell type, like knowing the site of origin, provides information regarding likely tumor behavior and guidance as to the most appropriate treatment.

For cancers arising in the same site and involving the same cell type, further distinctions can be made based on the severity of the abnormalities that are observed during microscopic examination of the biopsy specimen.

Patholo­gists have devised systems for tumor grading in which cancers of the same type assigned different numerical grades are based on the extent of the cellular and tissue disrup­tions that are seen with a microscope. Lower-grade cancers have a more normal appearance and often a better prog­nosis for long-term survival than do higher-grade cancers.

Biochemical tests for molecular components can further refine the picture regarding likely tumor behavior and appropriate treatment strategies. For example, breast cancer specimens are often tested for the presence of estrogen receptors, which are protein molecules involved in the mechanism by which estrogen stimulates the prolif­eration of breast cells. Breast cancers that possess estrogen receptors tend to have a better prognosis than cancers without estrogen receptors and are more likely to respond to hormone therapies.

Cancer cells also exhibit numerous changes in gene expression that can provide information about how tumors are likely to behave. One widely used approach for measuring gene expression is DNA microarray analysis, a technique which can monitor the activity of thousands of genes simultaneously.

Experiments involving DNA micro- arrays have led to the identification of differing patterns of gene expression among tumors of the same type that allow predictions to be made regarding tumor behavior. In the case of breast cancer, for example, the expression of 21 key genes turns out to be a good indicator of whether a given tumor is likely to metastasize.

Based on this discovery, a test called Oncotype DX has been devised that measures the activity of these 21 genes and converts the data into a single number called a recurrence score.

As shown in Figure 6, women with breast cancer whose tumors have a high recurrence score are more likely to develop metastases than are women whose tumors exhibit a low recurrence score. Such information is useful in guiding treatment strategies because patients with higher recurrence scores derive more benefit from subsequent chemotherapy.

 

People diagnosed with cancer have a variety of treatment options available that depend both on the type of cancer they have and how far it has spread. The ultimate goal of traditional cancer treatments is the complete removal or destruction of cancer cells accompanied by minimal damage to normal tissues.

This goal is usually pursued through a combination of surgery (when possible) to remove the primary tumor, followed (if necessary) by radiation, chemotherapy, or both to destroy any remaining cancer cells.

5. Essay on Cancer Treatment: (Around 650 Words)

Surgery can Cure Cancers when they have not yet Metasized:

Surgical techniques for removing tumors were first described more than three thousand years ago, making surgery the oldest approach for treating cancer. Its early use, however, was severely limited by the excruciating pain caused in the absence of anesthetics and by the extremely high death rate from infections.

The modern era of surgery was ushered in by the discovery of ether anesthesia in the 1840s and by the introduction of carbolic acid to inhibit bacterial infections in the 1860s. By 1890, these innovations had made it possible to perform the first mastectomy—that is, complete removal of the breast in women with breast cancer.

This milestone was followed in the early 1900s by the development of surgical techniques for removing tumors from virtually every organ of the body.

When people think of cancer surgery, they usually picture a doctor using a scalpel to cut out the tumor and perhaps surrounding tissues. Although that is certainly the most common surgical technique, a variety of newer procedures using different types of instruments have broadened the concept of what surgery is.

For example, laser surgery utilizes a highly focused beam of laser light to cut through tissue or to vaporize certain cancers, such as those occurring in the cervix, larynx (voice box), liver, rectum, or skin. Electro surgery, which involves high- frequency electrical current, is sometimes used to destroy cancer cells in the skin and mouth. Cryosurgery involves the use of a liquid nitrogen spray or a very cold probe to freeze and kill cancer cells.

This technique is utilized for the treatment of certain prostate cancers and for precancerous conditions of the cervix such as dysplasia. Finally, high-intensity focused ultrasound (HIFU) is a technique that focuses acoustic energy at a selected location within the body, where the absorbed energy heats and destroys cancer cells with minimum damage to surrounding tissues.

When cancer is diagnosed before a primary tumor has spread to other sites, surgical removal of a tumor can usually cure the disease. In fact, most cancer cures are achieved in this way. But cancers arising in internal organs are difficult to detect in their early stages and have often metastasized by the time they are diagnosed.

Sometimes the metastatic tumors formed at distant sites are large enough to also be detected and surgically removed; in other cases, the body has simply been seeded with tiny clumps of cancer cells, known as micrometastases that are too small to be detected.

Because roughly half of all cancers (excluding skin cancers) have started to metasta­size by the time they are diagnosed, surgical removal of the primary tumor is frequently followed by radiation, chemotherapy, or both to attack any disseminated cells that were not removed during surgery.

The growing use of follow-up radiation and chemotherapy has allowed surgeons to decrease the amount of surgery they need to perform on the average cancer patient. For example, the standard treatment for breast cancer between 1900 and 1970 was the radical mastectomy, a drastic and disfiguring operation that involves complete surgical removal of the breast along with the underlying chest muscles and lymph nodes of the armpit.

However, radical mastectomies are rarely performed today because such extensive tissue removal has not been found to improve survival compared to less drastic procedures. From 1970 to 1990 the most common procedure was the modified radical mastectomy, which involves removal of the breast and lymph nodes but not the chest muscles.

Today more than half of all breast cancer patients are treated by partial mastectomy (lumpectomy), which removes just the tumor and a small amount of surrounding normal tissue. Surgery is usually followed by radiation therapy to the breast to destroy any cancer cells that may remain in the area.

6. Essay on Cancer Treatment: (Around 400 Words)

Radiation Therapy Kills Cancer Cells by Triggering Apoptosis or Mitotic Death:

If a tumor has invaded into surrounding tissues and pos­sibly metastasized to distant sites, surgery may not be able to remove all cancer cells from the body. In some cases, surgery is not even practical.

For example, the location of a brain tumor may make it impossible to remove the tumor without causing unacceptable brain damage, and leukemias cannot be treated surgically because the cancer cells reside mainly in the bloodstream. When surgery is insufficient by itself or impractical, other treatments are used (often after surgery) to destroy any cancer cells that may still reside in the body.

One type of treatment is radiation therapy, which uses high-energy X-rays or other forms of ionizing radiation to kill cancer cells. Ionizing radiation removes electrons from water and other intracellular molecules, thereby generating highly reactive free radicals that attack DNA. The resulting DNA damage can actually cause cancer to arise.

Ironically, the same type of radiation is used in higher doses to kill cancer cells in people who already have the disease. Radiation treat­ments do create a small risk that a second cancer will develop in the future, but the risk is far outweighed by the potential benefit of curing a cancer that already exists.

High doses of radiation kill cancer cells in two dif­ferent ways. First, DNA damage caused by the radiation treatment activates the p53 signaling pathway, which triggers cell death by apoptosis. Lymphomas and cancers arising in reproductive tissues are particularly sensitive to this type of radiation-induced apoptosis.

However, more than half of all human cancers have mutations that disable the p53 protein or other components of the p53 signaling pathway. As a consequence, p53-induced apoptosis plays only a modest role in the response of most cancers to radiation treatment.

Radiation also kills cells by causing chromosomal damage that is so severe that it prevents cells from progressing through mitosis, and the cells die while trying to divide. Because this process of mitotic death only occurs at the time of cell division, cells that divide more frequently are more susceptible to mitotic death than cells that divide less frequently (or are not dividing at all).

This difference in susceptibility makes rapidly growing cancers more sensitive to the Killing effects of radiation than slower-growing cancers and also helps protect non-dividing or slowly dividing normal cells in the surrounding tissue from being killed by the radiation.

7. Essay on Cancer Treatment: (Around 750 Words)

Radiation Treatments are Designed to Minimize Damage to Normal Tissues:

To minimize damage to normal tissues, radiation treat­ments must be accurately focused on those regions of the body that contain tumor cells. This goal, called radiation planning, is accomplished by taking X-ray pictures that define the three-dimensional boundaries of the tumor and then using that information to guide a moving beam of high-energy radiation that is directed toward the target region from a number of different angles. Such an approach allows maximum radiation to be directed at the tumor area with minimal exposure to surrounding tissues.

The effectiveness of radiation therapy is determined to a large extent by differences in the survival rates of normal versus cancer cells after irradiation. If the difference in survival rates is small and the entire radiation dose is administered as a single treatment, the survival curves will closely track one another and there will be little difference in the numbers of cancer cells and normal cells killed (Figure 7, left).

It might be possible to destroy a tumor this way, but it would be at the expense of a large amount of damage to normal tissue. If the same total amount of radiation is administered as a series of lower doses, however, small differences in the survival rates of normal and cancer cells after each treatment become magnified as the treatments are repeated multiple times (see Figure 7, right).

By the end of the series of treatments, all cancer cells could be destroyed while maintaining enough normal cells to avoid serious tissue damage. For this reason, radiation therapy is usually divided into multiple treatments admin­istered over several weeks or months.

An alternative approach for minimizing damage to normal tissues, called brachytherapy, uses a radiation source that can be inserted directly within (or close to) the tumor. For example, early stage prostate cancer is sometimes treated by implanting small radioactive pellets, about the size of a grain of rice, directly into the prostate gland.

The pellets emit low doses of radiation for weeks or months and are simply left in place after the radiation has all been emitted. The advantage of this approach is that most of the radiation is concentrated in the prostate gland itself, sparing surrounding tissues such as the bladder and rectum.

Another technique for improving the effectiveness of radiation therapy involves agents that sensitize tumor cells to the killing effects of radiation. One group of drugs, known as hypoxic radio sensitizers, mimic oxygen and are taken up by cancer cells, which frequently tend to be hypoxic (deficient in oxygen).

Radiation creates more cellular damage in the presence of adequate oxygen, so the uptake of these drugs by cancer cells increases the effectiveness of radiation therapy. Combining radiation treatments with certain anticancer drugs, such as fluorouracil and platinum compounds, can likewise enhance the effectiveness of radiation treatments. The properties of these and related anticancer drugs will be described shortly, when we discuss the topic of cancer chemotherapy.

Raising the temperature of tumor tissue by a few degrees—a technique known as hyperthermia—also sensitizes cells to the killing effects of radiation. Hyperthermia even works when it is administered after radiation treatment, suggesting that the heat may be interfering with cellular repair pathways.

The combination of radiation and hyperthermia is most effective for tumors that are located in relatively accessible regions of the body, where the applied heat can thoroughly penetrate the tumor tissue. The main difficulty with this approach is finding ways of applying heat to hard-to-reach tumors located deep inside the body.

Radiation therapy is associated with various side effects that limit the dose of radiation that can be safely administered. The most serious problems arise in tissues containing large numbers of normal dividing cells, which are also susceptible to radiation-induced killing. For example, radiation damage to the dividing cells that line the gastrointestinal tract causes nausea, vomiting, and diarrhea.

And damage to dividing cells in the bone marrow reduces the production of one or more types of blood cells, which can lead to anemia, defective blood clotting, and immune deficiencies that increase the sus­ceptibility to infections. The likelihood that such side effects will be severe depends to a great extent on the loca­tion of the tumor and its sensitivity to radiation-induced killing.

Some cancers are very sensitive to radiation and can be destroyed with modest doses that elicit minimal side effects, whereas other cancers require high radiation doses and are more difficult to control using radiation (Table 1).

8. Essay on Cancer Treatment: (Around 230 Words)

Chemotherapy Involves the Use of Drugs that Circulate in the Bloodstream to reach Cancer Cells Wherever they may Reside:

The third main approach for treating cancer (in addition to surgery and radiation) is chemotherapy, which involves the use of drugs that either kill cancer cells or interfere with the ability of cancer cells to proliferate.

Chemotherapy is especially well suited for treating cancers that have already metastasized because drugs circulate through the bloodstream to reach cancer cells wherever they may have spread, even if the metastasizing cells have not yet formed visible tumors. This also means, however, that the toxic side effects commonly associated with chemotherapy can occur anywhere in the body because most anticancer drugs, like radiation, are toxic to dividing cells in general.

Despite its various side effects, chemotherapy has been successfully applied to a wide range of cancers. In some cases, as with certain forms of leukemia, chemotherapy may cure cancer by itself. More com­monly, chemotherapy is employed in conjunction with surgery, radiation, or both.

Dozens of anticancer drugs are currently available and the best choice will vary, depending on the type and stage of the cancer being treated. Based on differences in the way they work, the various drugs can be grouped into several distinct categories (Table 2).

In the following sections, each cate­gory will be discussed in turn:

9. Essay on Cancer Treatment: (Around 600 Words)

Antimetabolites Disrupt DNA Synthesis by Substituting for Molecules Involved in Normal Metabolic Pathways:

Antimetabolites, the first group of chemotherapeutic drugs that we will consider, are molecules that resemble substances involved in normal cellular metabolism. This resemblance causes enzymes to bind to antimetabolites in place of the normal molecules, thereby disrupting essen­tial metabolic pathways and poisoning the cell. Most of the antimetabolites used in cancer chemotherapy disrupt pathways required for normal DNA synthesis and repair.

The use of this approach for treating cancer was pioneered in the 1940s by Sidney Farber, who had been studying the nutritional needs of children with leukemia. Farber initially believed that vitamin therapy might help children fight off the disease, so he provided them with supplements of various vitamins, including the B vitamin, folic acid.

Unexpectedly, the added folic acid made the leukemias grow even faster. While that was certainly not the desired result, it raised an intriguing possibility: If cancer growth is stimulated by excess folic acid, blocking the action of folic acid might have the opposite effect and restrain the disease.

Farber therefore decided to treat some of his patients with folic acid analogs, which are chemical derivatives of folic acid that can substitute for the natural molecule and thereby disrupt any pathways in which folic acid is normally involved. When one analog, called aminopterin, was given to several children who were very sick with leukemia, the children quickly regained their health and returned to virtually normal lives.

Unfortunately, the improvement turned out to be only temporary, but these transient remissions caused a stir of excitement and stim­ulated the hunt for other antimetabolites whose effects might be more permanent than those of aminopterin.

The resulting search led to the discovery of methotrexate, a derivative of folic acid that efficiently binds to and inhibits the enzyme dihydrofolate reductase (Figure 8). Dihydrofolate reductase catalyzes the production of a reduced form of folic acid that is required for the synthesis of several bases found in DNA; inhibition of dihydrofolate reductase by methotrexate therefore dis­rupts pathways involved in DNA synthesis and repair.

Shortly after its discovery, methotrexate was shown to be an effective treatment for choriocarcinoma, a cancer arising from cells of the placental membranes that are sometimes left behind after childbirth. Choriocarcinoma was fatal for most women who developed the disease prior to the introduction of methotrexate chemotherapy in the mid-1950s.

After methotrexate began to be used, cure rates improved to almost 90%. Although its effects are not always this dramatic, methotrexate is currently used to treat a diverse spectrum of cancers, including acute leukemias and tumors of the breast, bladder, and bone.

In addition to analogs of folic acid such as methotrexate, analogs of the nitrogenous bases found in DNA are also useful for cancer chemotherapy.

DNA contains two types of bases: single-ring compounds called pyrimidines, which include the bases cytosine (C) and thymine (T); and double-ring compounds called purines, which include the bases adenine (A) and guanine (G).

Several analogs of pyrimidines and purines are routinely used as anticancer drugs. Examples include the pyrimidine analogs fluorouracil and cytarabine (also called cytosine arabinoside) and the purine analogs mercaptopurine and thioguanine.

As shown in Figure 9, the close resemblance of these substances to normal bases found in DNA causes the analogs to bind to and thereby disrupt the activity of enzymes involved in DNA synthesis and repair. Pyrimidine and purine analogs are used mainly for treating leukemias and lymphomas, although fluorouracil is effective against a broad spectrum of other cancers as well.

10. Essay on Cancer Treatment: (Around 650 Words)

Alkylating and Platinating Drugs Act by Crosslinking DNA:

Alkylating agents are highly reactive organic molecules that trigger DNA damage by linking themselves directly to DNA. This ability to attack DNA molecules makes alkylating agents mutagenic as well as carcinogenic.

However, alkylating agents are also employed as anti­cancer drugs because they kill cancer cells at higher doses, and the risk that they may cause cancer in such cases is outweighed by the potential benefit of curing a cancer that already exists.

The first alkylating agent to be employed for cancer chemotherapy has an interesting history. During World War I, the German military used an oily alkylating agent called sulfur mustard as a chemical weapon because it vaporizes easily and causes severe blistering injuries to the skin and lungs. A more toxic version, called nitrogen mustard, was produced and stockpiled by both Germany and the United States during World War II.

Nitrogen mustard was never employed on the battlefield, but German bombers attacked an Italian seaport in 1943 and sank a U.S. supply ship loaded with 100 tons of weapons containing the toxic chemical. Survivors pulled from the water, which had become heavily contaminated with nitrogen mustard, exhibited severe skin burns and quickly developed a variety of internal symptoms, including a dramatic drop in the number of blood lymphocytes.

Given this toxic effect on lymphocytes, scientists at Yale University decided to investigate whether nitrogen mustard would have a similar effect on cancers arising from lymphocytes. Shortly after the end of World War II, they reported that nitrogen mustard injections cause lymphocytic cancers to regress in animals and humans— the first demonstration of the potential usefulness of alkylating agents as anticancer drugs.

Better alkylating agents have subsequently been developed, but nitrogen mustard (now called mechlorethamine) is still occasionally used to treat Hodgkin’s lymphoma. Medical staffs who handle the drug take precautions to avoid inhaling the vapors of this one-time chemical weapon and must be certain that it is injected cleanly into a patient’s vein without contacting the skin.

Based on the initial promising results with nitrogen mustard, hundreds of other alkylating agents have been synthesized in the laboratory and tested in animals for anticancer activity. This effort has produced several drugs related to nitrogen mustard, including cyclophosphamide, chlorambucil, and melphalan that are routinely used to treat cancer patients.

In addition to substances related to nitrogen mustard, other alkylating agents have been developed for use as anticancer drugs, including thiotepa and nitrosourea compounds, such as BCNU (bischloroethyl nitrosourea). In general, the various alkylating agents disrupt normal DNA function by crosslinking the two strands of the DNA double helix (Figure 10, top). As a result, the two strands are unable to separate and DNA replication cannot take place, thereby preventing cell division.

Another group of DNA-crosslinking agents used in cancer chemotherapy contain the element platinum (see Figure 10, bottom). The ability of these substances, called platinating agents, to act as anticancer drugs was discov­ered in a roundabout manner. In some experiments performed during the 1960s that were totally unrelated to cancer biology, platinum electrodes were used to pass an electric current through a culture of bacterial cells to see how the cells react to electricity.

The bacteria stopped dividing, but it was soon discovered that this response was caused not by the electricity but by an unexpected reaction involving the platinum electrodes. In essence, ammonium chloride present in the culture medium had reacted with platinum in the electrodes to form a nitrogen-containing platinum compound called cisplatin, which in turn inhibited bacterial cell division.

The ability of cisplatin to block cell division led to successful tests on cancer cells, and the drug was approved for trials in human cancer patients in 1972. Cisplatin (trade name Platinol) is now one of the most effective agents in our arsenal of anticancer drugs, and efforts are being made to synthesize derivatives of cisplatin that might work even better.

11. Essay on Cancer Treatment: (Around 400 Words)

Antibiotics and Plant-Derived Drugs are Two Classes of Natural Substances Used in Cancer Chemotherapy:

Most of the antimetabolites and alkylating agents being used as anticancer drugs are synthetic molecules that were created in the laboratory for the purpose of treating cancer. Over the centuries, humans have also found ways of treating disease by drawing on natural substances produced by living organisms.

An especially dramatic twentieth-century example was the discovery of penicillin, a substance produced by a fungus that turned out to be one of the first effective drugs against bacterial infections.

Penicillin is an antibiotic, a term that refers to any substance produced by a microorganism, or a synthetic derivative, that kills or inhibits the growth of other microorganisms or cells. Antibiotics are generally thought of as being antibacterial drugs, but some of them exhibit anticancer properties as well.

One of the most fruitful sources of antibiotics for cancer chemotherapy has been a group of bacteria called Streptomyces. Besides producing streptomycin, which is an antibiotic used for treating tuberculosis and other serious bacterial infections, members of the Streptomyces group synthesize several antibiotics that have found their way into our arsenal of anticancer drugs, including doxorubicin, daunorubicin, mitomycin, and bleomycin.

All these antibiotics target the DNA molecule, although their mechanisms of action are somewhat different. Doxorubicin and daunorubicin insert themselves into the DNA double helix and inhibit the action of topoisomerase, an enzyme that normally breaks and rejoins DNA strands during DNA replication to prevent excessive twisting of the double helix. In contrast, mitomycin is a DNA crosslinking agent and bleomycin triggers DNA strand breaks.

Plants are another natural source of anticancer drugs. Several of the drugs obtained from plants act as topo­isomerase inhibitors; included in this category are etoposide and teniposide, derived from a substance present in the mayapple (mandrake) plant, and topotecan and irinotecan, derived from a substance present in the bark of the Chinese camptotheca tree.

Another group of plant- derived drugs attack the microtubules that make up the mitotic spindle. This class of drugs includes vinblastine and vincristine, obtained from the Madagascar periwinkle plant and Taxol (generic name paclitaxel), discovered in the bark of the Pacific yew tree.

Vinblastine and vincristine block the process of microtubule assembly, whereas Taxol stabilizes microtubules and promotes the formation of abnormal microtubule bundles. In either case, the mitotic spindle is disrupted and cells cannot divide.

12. Essay on Cancer Treatment: (Around 700 Words)

Hormones and Differentiating Agents are Relatively Nontoxic Tools for Halting the Growth of Certain Cancers:

One of the main problems with the drugs described thus far is that their toxic effects on DNA replication and cell division are harmful to normal cells as well as to cancer cells. When cancers arise in hormone-dependent tissues, an alternative and considerably less toxic approach can sometimes be used.

This approach, known as hormone therapy, was pioneered in the 1940s by Charles Huggins in studies involving prostate cancer patients. Based on earlier observations in animals, Huggins believed that the proliferation of prostate cells is dependent on steroid hor­mones known as androgens (testosterone is one example).

In an effort to eliminate the source of androgens in men with advanced prostate cancer, he surgically removed their testicles, which produce most of the testosterone, and also treated them with the female steroid hormone, estrogen. More than half of his prostate cancer patients improved and saw their tumor growth reduced.

These early observations eventually led to the develop­ment of drugs that block the production or the actions of androgens as an alternative to removing the testicles. Androgen production is normally controlled by peptide hormones called gonadotropins, which are synthesized in the pituitary gland.

One drug used to treat prostate cancer, named leuprolide, is an analog of the gonadotropin-releasing hormone that controls the release of these gonadotropins. By suppressing the release of gonadotropins, leuprolide inhibits androgen production by the testicles.

Another group of drugs inhibit the activity of androgen receptors, which are receptor proteins located in prostate epithelial cells that bind incoming androgens and transmit the signal that stimulates cell division. Flutamide and bicalutamide are examples of anticancer drugs that act by blocking androgen receptors.

Similar considerations apply to breast cancers, which arise from cells whose normal proliferation is driven by steroid hormones of the estrogen family. For breast cancers that retain this estrogen requirement, drugs that block estrogen action may be effective cancer treatments. One widely used drug that works in this way is tamoxifen, a molecule that exhibits some similarities to estrogen in chemical structure (Figure 11).

Estrogens normally exert their effects on target cells by binding to intracellular pro­teins called estrogen receptors. When tamoxifen is administered to breast cancer patients whose tumors require estrogen, it binds to estrogen receptors in place of estrogen and prevents the receptors from being activated. Another group of drugs, called aromatase inhibitors, inhibit one of the enzymes required for estrogen synthesis.

Generally these drugs are only recommended for treating breast cancer in postmenopausal women, where they inhibit the synthesis of the small amounts of estrogen that are being produced.

A somewhat different rationale is used when applying the principle of hormone therapy to lymphocytic cancers. The adrenal cortex produces a family of steroid hormones called glucocorticoids, whose properties include the ability to inhibit lymphocyte proliferation. Consequently prednisone, a synthetic glucocorticoid that slows down the proliferation of lymphocytes, is sometimes used in treating lymphomas and lymphocytic leukemias.

One advantage of hormone therapies is that their side effects tend to be mild because they do not destroy normal cells and because they only affect a selected group of target cells whose proliferation is controlled by the hormone in question. On the other hand, this latter property also imparts a significant limitation: Hormone-based treatments are only useful for cancers that arise in hormone-dependent tissues.

And even in these tissues, cancers do not always exhibit the hormone-dependence seen in the corresponding normal cells. For example, some breast cancers lack the estrogen receptors found in normal breast cells, and some prostate cancers lack the androgen receptors found in normal prostate cells. In such cases, hormone therapies are of little value.

Another relatively nontoxic approach to cancer chemotherapy involves the use of substances called differentiating agents. Whereas hormone therapies are designed to restrain cell proliferation, differentiating agents promote the process by which cells acquire the spe­cialized structural and functional traits of differentiated cells.

When cells undergo differentiation, they also lose the capacity to divide. Agents that promote cell differentiation therefore tend to decrease the overall level of cell proliferation. An example of a differentiating agent used in cancer therapy is retinoic acid, a form of vitamin A employed in the treatment of acute promyelocytic leukemia.

13. Essay on Cancer Treatment: (Around 850 Words)

Toxic Side Effects and Drug Resistance Limits the Effectiveness of Chemotherapy:

The ultimate goal of chemotherapy is to destroy or restrain the proliferation of cancer cells without harming normal cells. However, with the exception of hormones and differentiating agents, which are useful for only a few selected types of cancer, most chemotherapeutic drugs act by inhibiting DNA replication, damaging DNA, or blocking cell division—actions that are detrimental to normal dividing cells as well as to cancer cells.

Moreover, because chemotherapeutic drugs circulate throughout the body, they encounter normal dividing cells no matter where the cells reside. For example, the hair loss that commonly accompanies chemotherapy is a toxic side effect that is triggered when circulating drugs encounter the dividing cells that line the hair follicles.

The most serious side effects of chemotherapy involve the gastrointestinal tract and the bone marrow. As with radiation therapy, damage to normal dividing cells in these tissues can lead to nausea, vomiting, diarrhea, anemia, defective blood clotting, and immune deficiency.

Such side effects usually tend to be more severe with chemotherapy than with radiation because drugs cannot be easily focused on a particular region of the body to minimize toxicity to the gastrointestinal tract and bone marrow.

Fortunately, some cancer cells are particularly sensitive to chemotherapy and can be destroyed without excessive toxicity to normal cells; for many cancers, however, chemotherapy may fail because the drug dosage required to kill all cancer cells would trigger overwhelm­ingly toxic side effects.

Another problem that can reduce the effectiveness of chemotherapy is the tendency for tumors to become resis­tant to the killing effects of anticancer drugs, especially after a prolonged series of treatments. Even if most of the cancer cells in a person’s body are destroyed by a partic­ular drug, a few drug-resistant cells present in the initial population could proliferate and form a new tumor that would then be completely resistant to the drug.

And if drug-resistant cells are initially absent, cancers tend to be genetically unstable and may acquire mutations that impart drug resistance during the course of treatment. An illustration of this problem is provided by methotrexate, an anticancer drug that inhibits the enzyme dihydrofolate reductase (see Figure 8).

In cancers that are being treated with methotrexate, the gene for dihydrofolate reductase sometimes undergoes mutation or amplification. The mutations create altered forms of dihydrofolate reductase that are no longer inhibited by methotrexate, and gene amplification leads to increased production of dihydrofo­late reductase, thereby diminishing the effectiveness of methotrexate treatment. Such genetic changes, which alter the target of a drug to make it less susceptible to the drug’s effects, are commonly observed in individuals receiving chemotherapy.

Given the large number of anticancer drugs available, it might seem that a simple solution would be to just switch drugs when resistance arises. Unfortunately, the situation is complicated by the fact that tumors often develop resistance to several drugs at the same time, even though only a single drug is administered.

One way in which cancer cells become resistant to multiple drugs is by producing plasma membrane proteins that actively pump drugs out of the cells. These drug-pumping proteins, called multidrug resistance transport proteins, have a remarkably broad specificity. They export a wide range of chemically dissimilar molecules, thereby imparting resistance to a broad spectrum of drugs.

Another factor that can contribute to multidrug resistance is related to the mechanism by which anticancer drugs kill cells. Although multiple killing mechanisms appear to be involved, chemotherapeutic drugs sometime act by damaging DNA to such an extent that apoptosis is invoked to destroy the damaged cell.

In such cases, the effectiveness of chemotherapy may be reduced by mutations that disable apoptosis. Mutations of this type are often present at the time of initial diagnosis, or they may arise during chemotherapy. In either case, mutations that disable apoptosis would be expected to decrease the effectiveness of any drug that kills a particular type of cancer cell primarily by triggering apoptosis.

Another possible source of drug resistance is related to the heterogeneity of tumor cell populations. A growing body of evidence suggests that in any given tumor, only a small population of cells, called cancer stem cells, are able to proliferate indefinitely.

The existence of these cancer stem cells, which have been postulated to give rise to all the other cells found in a tumor, could help explain why treatments that cause tumors to shrink until they are undetectable may still not cure the disease.

While the treatment may eliminate the bulk of the cancer cells, a few remaining cancer stem cells may be all that is needed to replenish the tumor cell population. According to this theory, existing anticancer drugs may be more effective at killing the majority of a person’s tumor cells than they are at killing the rare cancer stem cells, which then regenerate the tumor after treatment is stopped.

Researchers are currently exploring this idea by searching for cancer stem cells in various tumor types and testing to see whether they exhibit any unique properties that could be targeted by future anticancer drugs.

14. Essay on Cancer Treatment: (Around 700 Words)

Combination Chemotherapy and Stem Cell Transplants are Two Strategies for Improving the Effectiveness of Chemotherapy:

For certain kinds of cancer, chemotherapy is successful in restoring normal life expectancies to many patients. Sometimes the chemotherapy by itself is responsible for the improved prognosis, but it is more common for chemotherapy to be used in conjunction with surgery or radiation.

Despite these successes, the effectiveness of chemotherapy is often hindered by the emergence of drug resistance and by the toxic side effects that restrict the dose that can be safely administered.

Additional chal­lenges are raised by the need for delivery techniques that convey drugs to tumor sites at the proper concentration for an appropriate period of time and by the existence of heterogeneous tumor populations containing mixtures of cells that respond differently to the same drug.

One strategy for trying to improve the effectiveness of chemotherapy is to administer several drugs in combina­tion rather than a single agent alone. Drug combinations are often named using an acronym that is derived from the initials of the drugs being used. For example, BEP chemotherapy (bleomycin, etoposide, and Platinol) is the name of a treatment for testicular cancer, and CMF chemotherapy (cyclophosphamide, methotrexate, and fluorouracil) is the name of a treatment for breast cancer.

This general approach, known as combination chemotherapy, is most effective with drugs that differ in their mechanisms of action. For example, consider three drugs exhibiting different side effects that limit the dose of each that can be safely administered. Combining the three drugs at their maximum tolerated doses will increase the overall tumor-killing effectiveness compared with each drug by itself, and yet the overall toxicity may remain at an acceptable level because each drug works in a different way.

Another advantage of drug combinations is that cancer cells are less likely to become resistant to chemotherapy when several drugs are administered simultaneously, especially if the drugs differ in their chemical properties, cellular targets, and mechanisms of action. The enormous challenge of combination therapy is finding the most effective drug mixtures for each type of cancer, especially given the dozens of drugs that could in theory be administered in thousands of different combinations.

Another approach for improving the effectiveness of chemotherapy deals with the potential problem of bone marrow damage. Many anticancer drugs are capable of killing all cancer cells if the dose is raised high enough. The dose that can be realistically administered, however, is limited by toxicity to the bone marrow, which contains the hematopoietic stem cells whose proliferation gives rise to blood cells.

If too many of these stem cells are destroyed during high-dose chemotherapy, blood cells will not be produced and a person cannot survive. One approach for addressing this problem is to use high-dose chemotherapy to destroy all cancer cells and then follow the treatment with stem cell transplantation (also called bone marrow transplantation) to replenish the person’s hematopoietic stem cells. Under such conditions, higher drug doses can be used because the blood-forming stem cells destroyed by the chemotherapy are subsequently being replaced.

The stem cells used for transplantation can be obtained either from a cancer patient’s own bone marrow or blood prior to administration of high-dose chemotherapy, or from the bone marrow or blood of a genetically compatible individual who is willing to serve as a stem cell donor.

Unfortunately, each approach has its complications. Using a cancer patient’s own stem cells for subsequent transplantation creates the risk of either rein­troducing cancer cells or relying on stem cells that have been damaged during earlier cancer treatments. On the other hand, finding an appropriately matched donor can be difficult, and immune cells present in the donor’s blood or bone marrow sometimes attack the tissues of the cancer patient, thereby creating a potentially life-threatening condition known as graft-versus-host disease.

An alternative is to use umbilical cord blood rather than bone marrow or peripheral blood as a source of stem cells for transplantation. The umbilical cord, which is normally discarded at birth, contains blood with a large number of hematopoietic stem cells.

These cells elicit a lower incidence of graft-versus-host disease, do not require as close a genetic match as do adult stem cells, and are readily obtained from blood banks that store frozen umbilical cord blood taken from healthy newborns. The possible usefulness of cord blood as a source of stem cells for cancer patients is currently under investigation.

15. Essay on Cancer Treatment: (Around 600 Words)

Molecular and Genetic Testing is Beginning to Allow Cancer Treatments to be Tailored to Individual Patients:

A final approach for enhancing the effectiveness of chemotherapy involves the possibility of designing drug treatments that are personalized for each individual patient. It has been known for many years that cancer patients with tumors that are indistinguishable from one another by traditional criteria often exhibit different outcomes after receiving the same treatment.

Experiments using DNA microarray technology to analyze gene activity have provided a likely explanation: Cancers of the same type exhibit different patterns of gene expression that cause them to behave differently. The Oncotype DX gene expression test, which measures the activity of 21 key genes in breast cancer cells, is able to predict which patients are most likely to have their cancers recur after surgery.

In the absence of such information, doctors would usually recommend that most patients receive chemotherapy. The value of gene expres­sion testing is that it can help identify those patients who really need chemotherapy and are likely to benefit from it.

Taking this approach one step further, analyzing cancer specimens for gene expression patterns and the presence of specific mutations may provide information about the exact type of cancer treatment that is most appropriate for each person. A striking example is provided by Iressa.

Iressa, which acts by inhibiting the receptor for epidermal growth factor (EGF), has been approved for use in the treatment of lung cancer. Tumor shrinkage occurs in only about 10% of the patients treated with Iressa, but when the drug does work, it works extremely well.

The reason Iressa is more effective in some individ­uals than others has been traced to the presence of a mutant form of the EGF receptor gene in the cancers of those patients who respond well to the drug.

When lung cancer cells containing the mutant form of the EGF receptor are grown in laboratory culture, they are found to be much more sensitive to the growth-inhibiting effects of Iressa than are cancer cells that contain the normal form of the EGF receptor (Figure 12).

This discovery opens the door to a personalized type of cancer therapy in which genetic testing of cancer cells is used to identify those particular patients who are most likely to benefit from treatment with Iressa.

A patient’s hereditary background can also affect how he or she responds to different types of treatment. For example, inherited genes that influence steps in drug metabolism have been found to influence how well a person responds to different kinds of drugs. It is therefore hoped that a better understanding of patient-specific and tumor-specific differences in genetic makeup will eventu­ally allow treatments to be tailor-made for each individual cancer patient.

The use of surgery, radiation, or chemotherapy—either alone or in various combinations—can cure or signifi­cantly prolong survival times for many types of cancer, especially when the disease is diagnosed early. However, some of the more aggressive cancers, including those involving the lung, pancreas, or liver, are difficult to control in these ways, nor are current approaches very successful with cancers diagnosed in their advanced stages.

In trying to find more effective ways of treating such cancers, scientists have been working to develop “magic bullets” that will selectively seek out and destroy cancer cells without damaging normal cells in the process. Although this goal presents a formidable challenge, several approaches for achieving better selectivity in targeting cancer cells are beginning to show signs of success.

Essay # 16. Essay on Cancer Treatment: (Around 400 Words)

Immunotherapies Exploit the Ability of the Immune System to Recognize Cancer Cells:

One way of introducing better selectivity into cancer treatments is to exploit the ability of the immune system to recognize cancer cells. This general approach, called immunotherapy, was first proposed in the 1800s after doctors noticed that tumors occasionally regress in people who develop bacterial infections.

Since infections stimulate the immune system, it was postulated that the stimulated immune cells might be attacking cancer cells as well as the invading bacteria. Efforts were therefore made to build on this idea by using live or dead bacteria to provoke the immune system of cancer patients. Some success was eventually seen with Bacillus Calmette- Guerin (BCG), a bacterial strain that does not cause disease but elicits a strong immune response at the site where it is introduced into the body.

One use of BCG is in the treatment of early stage bladder cancers that are local­ized to the bladder wall. After the cancer is surgically removed, inserting BCG into the bladder elicits a pro­longed activation of immune cells that leads to lower rates of cancer recurrence.

Although this example demonstrates the potential value of stimulating the immune system, BCG must be administered directly into the bladder to provoke an immune response at the primary tumor site.

With other types of cancer, especially when they have metastasized to unknown locations, it becomes necessary to stimulate an immune response against cancer cells wherever they may have traveled. For this purpose scientists have turned to molecules called cytokines, which are proteins produced by the body to stimulate immune responses against infectious agents.

The first cytokine found to be helpful in treating cancer was interferon alpha, a protein produced in response to viral infections. Interferon alpha is used in the treatment of several kinds of cancer, including hairy cell leukemia and Kaposi’s sarcoma. Interleukin-2 (IL-2) and tumor necrosis factor (TNF) are two other cytokines that are being evaluated for possible use as immune stimulators in cancer patients.

IL-2 and TNF both elicit a strong antitumor response in laboratory animals, but they are extremely toxic when administered to humans. At present, TNF is still under active investigation and IL-2 is an approved treatment for advanced kidney cancer and melanoma.

As we will see shortly, IL-2 is also being used experimentally to stimulate antitumor lymphocytes that are isolated from a patient’s tumor site and grown in the laboratory prior to being injected back into the bloodstream.

17. Essay on Cancer Treatment: (Around 400 Words)

Large Quantities of Identical Antibody Molecules can be Produced Using the Monoclonal Antibody Technique:

BCG and cytokines are relatively nonspecific approaches to immunotherapy because they strengthen the overall activity of the immune system rather than preferentially directing an attack against cancer cells. Devising immunotherapies that act more selectively requires approaches for distinguishing cancer cells from normal cells.

The immune system sometimes recognizes cancer cells through the presence of specific antigens that cancer cells carry. One way in which the immune system responds to antigens is by producing antibodies, which are soluble proteins manufactured by immune cells known as B lym­phocytes. Antibodies circulate in the bloodstream and penetrate into extracellular fluids, where they specifically bind to the antigens that triggered the immune response.

Antibody molecules recognize and bind to their corre­sponding antigens with extraordinary precision, making antibodies ideally suited to serving as “magic bullets” that selectively target antigens that are unique to (or preferen­tially concentrated in) cancer cells.

For many years, the use of antibodies for treating cancer was hampered by the lack of a reproducible method for producing large quantities of pure antibody molecules directed against the same antigen. Then in 1975, Georges Kohler and Cesar Milstein solved the problem by devising the procedure illustrated in Figure 13.

In this technique, animals are injected with material containing an antigen of interest, and antibody-producing lymphocytes are isolated from the animal a few weeks later. Within such a heteroge­neous lymphocyte population, each lymphocyte produces a single type of antibody directed against one particular antigen.

To facilitate the selection and growth of individual lymphocytes, the lymphocytes are fused with cells that divide rapidly and have an unlimited lifespan in culture. The resulting hybrid cells are then individually selected and grown to form a series of clones called hybridomas.

The antibodies produced by hybridomas are referred to as monoclonal antibodies because each one is a pure anti­body produced by a cloned population of lymphocytes. Hybridomas can be maintained in culture indefinitely and represent inexhaustible sources of individual antibody molecules, each directed against a different antigen.

18. Essay on Cancer Treatment: (Around 600 Words)

Monoclonal Antibodies can be Used to Trigger Cancer Cell Destruction Either by themselves or Linked to Radioactive Substances:

The ability to obtain monoclonal antibodies in large quantities gave rise to high expectations regarding their usefulness for selectively targeting cancer cells. The basic strategy is to immunize animals with human cancer tissue and then select those monoclonal antibodies that bind to antigens on the cancer cell surface.

When they are injected into individuals with cancer, these antibody molecules would be expected to circulate throughout the body until they encounter cancer cells. The antibodies then bind to the cancer cell surface, where their presence triggers an immune attack that destroys only those cells to which the antibody is attached (Figure 14, top).

Antibodies can also be used as delivery vehicles for toxic molecules by linking them to radioactive substances, chemotherapeutic drugs, or other kinds of toxic substances that are too lethal to administer alone (Figure 14, bottom).

Attaching these sub­stances to monoclonal antibodies allows the toxins or radioactivity to be selectively concentrated at tumor sites by the antibody without accumulating to toxic levels else­where in the body.

Although this strategy sounds simple in theory, several obstacles have slowed its application to cancer patients. One problem is that monoclonal antibodies are usually produced in mice by injecting them with human cancer tissue.

The resulting antibodies are therefore recognized as foreign proteins when administered to cancer patients, who mount an immune response that inactivates the mouse antibody molecules, especially if the antibody is administered more than once.

For this reason, monoclonal antibodies cannot be used for repeated treatments unless they are first made more human-like by replacing large parts of the mouse antibody molecule with corresponding sequences derived from human antibodies.

A second complication encountered with monoclonal antibodies is that the cancer cell antigens they recognize may be present on certain normal cells as well. Each newly developed antibody must therefore be tested by linking it to a radioisotope and injecting it into patients to see whether the radioactivity becomes preferentially localized to sites where tumor cells are present.

The preceding issues have complicated the develop­ment of antibody-based therapies, but several successes have already been achieved. For example, the monoclonal antibodies Rituxan, Zevalin, and Bexxar are now among the approved treatments for non-Hodgkin’s B cell lymphoma.

All three antibodies target B lymphocytes for destruction by binding to the CD20 antigen, which is present on the surface of malignant as well as normal B lymphocytes. Although antibodies that target CD20 are toxic to normal B lymphocytes, CD20 is not present on the precursor cells whose proliferation gives rise to B lymphocytes.

These precursor cells therefore replenish the normal B lymphocyte population that is inadvertently destroyed along with malignant B lymphocytes during antibody treatment (Figure 15).

Besides being adminis­tered by themselves, monoclonal antibodies directed against CD20 have been linked to radioactive chemicals and used to direct high doses of radiation to tumor sites, which may be more effective in killing cancer cells than the use of antibodies alone. Radioactive antibodies are also useful for determining where cancer cells are localized and for monitoring changes in tumor cell numbers in response to treatment.

The value of monoclonal antibodies is not restricted to their ability to target cancer cells for destruction. Monoclonal antibodies have also been developed that target signaling pathway components required by cancer cells for their proliferation.

For example, some breast cancer patients are being treated with Herceptin, a mono­clonal antibody that binds to and blocks a growth factor receptor. Because monoclonal antibodies are not the only tools used for targeting signaling pathway components, we will delay a discussion of this type of cancer therapy until the section on molecular targeting.

19. Essay on Cancer Treatment: (Around 450 Words)

Several Types of Cancer Vaccines are Currently under Development:

Antibodies are one of two basic mechanisms used by the immune system for attacking foreign antigens. The second mechanism, known as cell-mediated immunity, utilizes cytotoxic T lymphocytes that bind to the surface of cells exhibiting foreign antigens and kill the targeted cells by causing them to burst. This tactic is normally used to destroy cells harboring infectious agents such as viruses, bacteria, and fungi, and it also plays a role in the destruc­tion of foreign tissue grafts and organ transplants.

The realization that cytotoxic T lymphocytes might be able to mount an attack against cancer cells first emerged in the 1940s from studies in which cancer was induced in mice by exposing them to carcinogenic chemicals or viruses. The resulting tumors were found to contain antigens whose administration to other mice immunized the animals against transplants of the same tumor.

When T lymphocytes were isolated from the immunized animals, these T lymphocytes could kill tumor cells in culture and transfer tumor immunity when injected into other animals. In contrast, antibodies produced by the tumor-bearing animals were relatively ineffective at killing cancer cells or transferring immunity.

These observations have stimulated interest in the idea of developing vaccines that will stimulate a cancer patient’s own T lymphocytes to attack cancer cells. The underlying rationale is that tumor antigens tend to be weak antigens that do not elicit a strong immune response, but an appro­priate vaccine might be able to present the antigens in a way that would stimulate the immune system to become more aware of their existence.

Among the candidates for vaccine antigens are the abnormal proteins that cancer cells produce as a result of genetic mutations. Since these proteins are not produced by normal cells, putting them into vaccines should stimulate an immune response that is selectively directed against cancer cells. Other proteins that are overproduced by tumors might also be useful candi­dates for incorporation into cancer vaccines.

It is possible to vaccinate cancer patients by simply injecting them with tumor antigens, but attempts are being made to improve vaccination efficiency by first introducing the antigens into dendritic cells for antigen processing. Triggering an efficient immune response requires that antigens be broken into fragments and pre­sented to the immune system by antigen-presenting cells such as dendritic cells.

When dendritic cells obtained from cancer patients are grown in the laboratory together with tumor antigens, the dendritic cells take up the anti­gens, chop them into pieces, and present the resulting fragments on their cell surface in a way that activates an immune response. Experiments are currently under way to determine whether the injection of such antigen-loaded dendritic cells into patients is a feasible tactic for treating cancer.

20. Essay on Cancer Treatment: (Around 500 Words)

Adoptive-Cell-Transfer Therapy Uses a Person’s own Antitumor Lymphocytes that have been Selected and Grown in the Laboratory:

Adoptive-cell-transfer (ACT) therapy is an alternative to vaccination in which a patient’s own lymphocytes are first isolated, selected, and grown in the laboratory to enhance their cancer-fighting properties prior to injecting the cells back into the body. The underlying reasoning is that individuals with cancer often possess lymphocytes that are capable of attacking tumor cells, but these lymphocytes are not produced in sufficient quantities to keep the tumor under control.

ACT therapy attempts to solve this problem by removing some of these lymphocytes from the body and increasing their numbers by growing them in culture prior to reintro­ducing the cells into the patient.

If a person with cancer has any lymphocytes that are capable of attacking tumor cells, the most likely place to find them would be within the tumor itself. Lymphocytes that are located at the tumor site, called tumor-infiltrating lymphocytes (TILs), have therefore been used as a source of cells for ACT therapy.

In one set of studies, illustrated in Figure 16, multiple samples of TILs were isolated from the tumors of advanced stage melanoma patients and tested for their ability to attack tumor cells. TIL samples exhibiting the greatest anti-tumor activity were then selected and grown in culture in the presence of interleukin-2 (IL-2), a cytokine that stimulates the proliferation and cancer-destroying properties of the lymphocytes.

Before introducing the tumor-killing lymphocytes back into the body, each cancer patient was treated with high-dose chemotherapy to destroy a large fraction of their existing lymphocytes.

The tumor-killing lymphocytes were then injected back into the bloodstream and the patients were treated with IL-2 to further stimu­late the proliferation of the injected cells. The net result was that tumor-killing lymphocytes became a large portion of each person’s immune system, and a significant number of patients experienced tumor regressions.

ACT therapy is still an experimental procedure and will be difficult to apply to large numbers of patients, but these results suggest that cancer therapies may eventually be able to exploit the ability of lymphocytes to recognize and kill cancer cells. Several problems remain to be solved, however.

First, the possibility exists that lymphocytes targeted against cancer cell antigens will mistakenly attack healthy cells possessing similar antigens. Another problem is that cancer cells can devise ways of evading immune attack. For example, sometimes cancer cells acquire muta­tions that cause them to stop making the antigens being targeted by the immune system.

In other cases, cancer cells become resistant to immune attack by producing mole­cules that either kill lymphocytes or disrupt their ability to function. Of course, the possibility that resistance will develop is not unique to immunotherapy; we have already seen that resistance arises with chemotherapy as well. For this reason, a combination of different therapeutic approaches may end up being the best approach for treating cancer.

21. Essay on Cancer Treatment: (Around 500 Words)

Herceptin and Gleevec are Anticancer Drugs that Illustrate the Concept of Molecular Targeting:

Until the early 1980s, research into new cancer treatments focused largely on the development of drugs that disrupt DNA synthesis and interfere with cell division. Although some of the resulting drugs have turned out to be useful in treating cancer, their effectiveness is often limited by toxic effects on normal dividing cells.

In the past two decades, the identification of specific genes whose mutation or altered expression can lead to cancer has opened up a new possibility—molecular targeting—in which drugs are designed to target those proteins that are critical to the cancerous state.

One way to pursue the goal of molecular targeting is to take advantage of the specificity of antibodies. Substantial efforts are currently being made to develop monoclonal antibodies that bind to and inactivate key proteins involved in the signaling pathways required for cancer cell proliferation.

The first such antibody to be approved for use in treating cancer patients, called Herceptin, binds to and inactivates a cell surface growth factor receptor called the ErbB2 receptor, which is produced by the ERBB2 gene (also called HER2).

About 25% of all breast and ovarian cancers have amplified ERBB2 genes, which produce excessive amounts of ErbB2 receptor that in turn causes hyperactive signaling. When individuals whose cancers overexpress the ErbB2 receptor are treated with Herceptin, the Herceptin antibody binds to the ErbB2 receptor and the ability of the receptor to stimulate cell proliferation is blocked, thereby slowing or stopping tumor growth.

Monoclonal antibodies are not the only way to target specific molecules for inactivation. Another approach, called rational drug design, involves the laboratory synthesis of small molecule inhibitors that are designed to bind to and inactivate specific target molecules. Unlike antibodies, these inhibitors are small enough to enter cells and affect intracellular proteins.

One of the first such drugs to be developed, called Gleevec (generic name – imatinib), is a small molecule that binds to and inhibits the abnormal tyrosine kinase produced by the BCR-ABL oncogene present in chronic myelogenous leukemias. BCR-ABL is a fusion gene generated during the chromo­somal translocation that creates the Philadelphia chromosome.

Because it arises from the fusion of DNA sequences derived from two different genes, BCR-ABL produces a structurally abnormal protein—the Bcr-Abl tyrosine kinase—that represents an ideal drug target because it is produced only by cancer cells.

Initial studies of the effectiveness of Gleevec as a treatment for chronic myelogenous leukemia were extremely encouraging, In patients with early stage disease, more than 50% had no signs of cancer six months after treatment (a response rate ten times better than had been seen before).

Unfortunately, patients with late stage disease frequently develop mutations that alter the structure of the Bcr-Abl tyrosine Kinase, thereby making it resistant to Gleevec. Additional small molecule inhibitors that overcome this resistance to Gleevec have been devel­oped, but it takes many years to take each new compound through the necessary testing before it can be approved for routine medical use.

22. Essay on Cancer Treatment: (Around 800 Words)

A Diverse Group of Potential Targets for Anticancer Drugs are Currently being Investigated:

The drugs Herceptin and Gleevec illustrate two different approaches—monoclonal antibodies and small mole­cule inhibitors—for targeting specific proteins found in cancer cells. These two drugs are relatively recent accomplishments in the long history of cancer drug research; Herceptin was introduced in 1998 and Gleevec in 2001.

As might be expected, their success has stimu­lated interest in developing other drugs that target molecules important to cancer cells. For example, the introduction of Gleevec in 2001 was followed in 2003 by another small molecule inhibitor called Iressa (generic name gefitinib).

Iressa targets the receptor for epidermal growth factor and is effective in a subset of lung cancer patients whose cancer cells possess a mutant form of the EGF receptor (see Figure 12).

Dozens of other drugs based on the principle of molecular targeting are currently under investigation. Tyrosine kinases and growth factor receptors (the targets for Gleevec and Herceptin, respectively) are just two of many potential targets. The uncontrolled proliferation of cancer cells can be traced to disruptions in a variety of growth signaling pathways, including the Ras-MAFK, JaK-STAT, Wnt, and PI3K-Akt pathways.

Any of the proteins involved in these pathways could represent a potential target for an anticancer drug. Other proteins whose activi­ties contribute to the six hallmark traits of cancer cells might likewise be good candidates. Table 3 lists some examples of proteins in these various categories that are now being investigated as potential targets for anticancer drugs.

Despite the attractiveness of molecular targeting, many of the drugs developed after the initial successes with Herceptin and Gleevec have failed to work well when tested in cancer patients. While such disappointments may simply mean that these particular drugs are ineffec­tive, several factors complicate the testing of anticancer drugs that could have contributed to the failures.

First, targeted therapies would only be expected to work in those individuals whose cancer cells exhibit the appro­priate molecular target. Since cancers of the same type often differ in their molecular properties from person to person, obtaining a molecular profile of each person’s tumor might assist in identifying patients most likely to benefit from a given type of treatment.

Second, testing of new drugs is generally done in patients who also receive standard chemotherapy, which might obscure the benefits of an experimental drug. For example, in the case of tamoxifen, which targets the estrogen receptor, inferior results are obtained when tamoxifen is combined with standard chemotherapy compared with giving tamoxifen either alone or after chemotherapy.

In theory, the most reliable results would be obtained by comparing a new drug given to one group of patients versus standard chemotherapy given to another group of patients. However, ethical considera­tions make it inappropriate to withhold standard treatment from the first group of patients if the standard treatment is known to be beneficial.

A third type of problem is related to the need for better drug delivery methods that reliably convey drugs to tumor sites at the proper concentration for an appropriate period of time. In many cases, drugs are simply degraded too quickly after entering the body and do not accumulate in tumor tissues.

One way to improve drug delivery is through the use of water-soluble polymers such as polyethylene glycol or N-(2-hydroxypropyl) methacrylamide. Binding drugs to these polymers prolongs a drug’s lifetime in the body and alters its pattern of distribution.

The reason for the altered behavior is that the large size of drug-polymer complexes prevents them from passing out of the bloodstream and into cells as rapidly as the free drug itself. In addition, tumor blood vessels tend to be “leaky,” causing drug-polymer complexes to leave the bloodstream and enter tumor tissues more readily than normal tissues.

A final problem that complicates drug testing is that clinical trials are usually carried out in late-stage cancer patients after all other treatments have failed. At this advanced stage, targeted molecular therapy may no longer be useful. For example, consider the behavior of drugs that inhibit matrix metalloproteinases (MMPs), which are attractive targets because they play important roles in angiogenesis, tissue invasion, and metastasis.

Animal studies have shown that MMP inhibitors are effective antitumor agents during the early stages of cancer progression, when tumor invasion and metastasis are just beginning. Human testing, however, has been performed mainly in patients with late stage disease, when MMP inhibitors appear to be largely ineffective.

This is just one of many examples of experimental anti­cancer drugs that have been tested in late stages of cancer progression rather than early in the disease, when they are more likely to work. Such problems are difficult to avoid for the simple reason that experimental new treat­ments are not likely to be tried on patients until other treatments have failed, at which point the disease may have reached an advanced stage that makes it unrespon­sive to targeted therapies.

23. Essay on Cancer Treatment: (Around 600 Words)

Anti-Angiogenic Therapy Illustrates the Difficulties Involved in Translating Laboratory Research into Human Cancer Treatments:

Tumor growth and metastasis depend on angiogenesis— that is, the growth of blood vessels that supply nutrients and oxygen to tumor cells and remove waste products. It is therefore logical to expect that angiogenesis inhibitors might be useful for treating cancer patients.

Initial support for this concept of anti-angiogenic therapy came from the studies of Judah Folkman, who reported that treating tumor-bearing mice with the angiogenesis- inhibiting proteins angiostatin and endostatin makes tumors shrink and disappear. When these experiments were first described in 1998 in a front page story appearing in the New York Times, a distinguished scientist was quoted as saying, “judah is going to cure cancer in two years.”

Needless to say, such sensational news coverage led to unrealistic expectations concerning the prospects for an immediate cancer cure. Applying the results of animal studies to human patients takes many years of testing, and humans do not always respond in the same way as animals.

Dozens of angiogenesis-inhibiting drugs are therefore being evaluated in cancer patients to see if the promising results observed in animals will apply to humans. On the positive side, the early human studies showed that anti-angiogenic therapy elicits few of the harsh side effects seen with chemotherapy, and in a few cancer patients, tumors seemed to stop growing. However, some disappointment was expressed with the early results because they failed to show the quick cure for cancer that people had been led to expect.

Of course, expectations for a quick cancer cure were unrealistic, and there are many reasons why it would be premature to come to any definitive conclusions at this point regarding the effectiveness of anti-angiogenic therapy. First, the early human trials were carried out mainly on cancer patients with late stage disease, and anti-angiogenic therapy may work better at earlier stages.

Second, the optimal dose for angiogenesis-inhibiting drugs may need to be tailored to each individual patient based on the concentration of angiogenesis-stimulating molecules their tumors produce. Third, angiogenesis inhibitors may work best when their concentration within the body is maintained at a relatively constant level, which is quite different from the way in which standard chemotherapy is typically, administered using large intermittent doses.

Finally, the effectiveness of anticancer drugs is usually measured by assessing their ability to make tumors shrink or disappear. This outcome might be an appropriate expectation for a drug that kills cancer cells, but inhibiting blood vessel growth may simply stop tumors from becoming any larger.

Such a state, called stable disease, could represent an acceptable outcome for an anti-angiogenic drug if it allowed patients to live with cancer as a chronic but manageable disease condition, especially in view of the minimal side effects associated with the use of angiogenesis inhibitors.

The complexities raised by the preceding issues mean that it will take many years to assess the effectiveness of angiogenesis-inhibiting drugs and determine how best to use them. Nonetheless, signs of progress are already evident. In 2004, Avastin became the first anti-angiogenic drug to be approved for routine medical use in cancer patients.

Avastin is a monoclonal antibody that binds to and inactivates the angiogenesis-stimulating growth factor, VEGF. In tumors that depend on VEGF to stimu­late angiogenesis, blocking VEGF with Avastin would be expected to inhibit angiogenesis and thereby inhibit tumor growth.

Human clinical trials have shown that patients with metastatic colon cancer who received stan­dard chemotherapy plus Avastin lived longer than patients who received standard chemotherapy without Avastin. These results were one of the first signs that anti-angiogenic therapy may one day become an integral component of human cancer treatment.

24. Essay on Cancer Treatment: (Around 900 Words)

Engineered Viruses are Potential Tools for Repairing or Killing Cancer Cells:

Over the past two decades, the roles played by oncogenes and tumor suppressor genes in the development of cancer have become increasingly apparent. This discovery raises the possibility of attacking the disease at its root cause- defective genes. In other words, rather than trying to kill or restrain the proliferation of cancer cells, it might be possible to repair the defective genes that are responsible for the cancerous state.

The process of replacing defective genes with normal versions is called gene therapy. Gene therapy was initially envisioned as a treatment for genetic diseases in which a person inherits a single defective gene, such as a gene responsible for cystic fibrosis, hemophilia, or certain immune deficiencies.

Curing illnesses of this type would simply require that a normal copy of the single defective gene be inserted into a person’s cells under conditions that allow the inserted gene to be actively expressed.

While the concept sounds simple in theory, it is difficult to transfer genes into cells efficiently under conditions that permit the transferred genes to become permanently incorpo­rated and expressed. As a result, gene therapy had been of limited usefulness in treating genetic diseases thus far.

Applying gene therapy to cancer is even more com­plicated than treating an inherited genetic disease because it may be necessary to repair the defect in all cancer cells, not just some of them. Moreover, cancer cells usually exhibit defects in several genes rather than just one, although it may not be necessary to repair them all. Human cancers often exhibit defects in the p53 pathway that prevent cells from undergoing apoptosis.

If this single pathway could be restored, the other abnormalities exhibited by cancer cells might trigger the p53 pathway and cause the cells to self-destruct by apoptosis. Attempts have therefore been made to repair the p53 gene in cancers in which this gene is defective (Figure 17).

Support for this approach has come from animal studies showing that tumor regression can be induced by injecting animals with a virus whose DNA contains a normal copy of the p53 gene. In early human testing, a similar virus injected into the tumors of lung cancer patients has been found to restore p53 production and induce disease stabilization in some patients.

An alternative to using viruses for gene therapy is to engineer them to kill cancer cells selectively. It has been known for many years that some viruses cause infected cells to rupture and die, a process called lysis. Attempts are therefore being made to create viruses that selectively infect and cause the lysis of cancer cells.

One of the first of these viruses to be tested in humans was ONYX-O15, an adenovirus containing a mutation designed to permit the virus to replicate only in cells with a defective p53 pathway.

Since the p53 pathway is defective in a majority of human cancers, it was predicted that ONYX-015 might be a broadly useful tool for killing cancer cells. Early investigations appeared to verify the ability of ONYX-015 to replicate preferentially in cancer cells, but follow-up studies failed to confirm the dependence of viral replica­tion on the presence of a defective p53 pathway and future development of this particular virus is uncertain.

ONYX-015, however, represents just one of many engineered viruses that are being developed to kill cancer cells without harming normal cells. Like ONYX-015, these viruses have been genetically altered to make their replica­tion dependent either on the absence of genes that are inactive only in cancer cells or on the presence of genes that are active only in cancer cells (Figure 18, left).

Another potential strategy is to modify viruses in ways that cause them to interact preferentially with cancer cells, perhaps by altering viral coat proteins so that they bind to receptors present on the surface of cancer cells (see Figure 18, right). Such approaches are currently under active investigation to see whether they might be of any use in the treatment of cancer.

Before any new treatment can be incorporated into standard medical practice, it must first undergo a lengthy and painstaking evaluation process. In the early days of cancer research, identifying and evaluating new treatments was especially time consuming because anticancer drugs were often discovered through a largely random approach.

For example, the National Cancer Institute established a massive screening program in the mid-1960s that system­atically tested thousands of chemical compounds for possible anticancer activity. Those substances that exhib­ited the most promise in killing cancer cells in laboratory culture or in animal studies were eventually tested in humans, and a number of drugs now used in cancer chemotherapy were discovered in this way.

In recent years, our growing understanding of the molecular abnormalities exhibited by cancer cells has permitted more selective approaches for developing drugs that target cancer cells. Nonetheless, such drugs still require extensive testing before they can be incorporated into standard medical practice.

The testing process, which is regulated in the United States by the Food and Drug Administration (FDA), requires that any drug proposed for human use first undergo preclinical testing in animals to demonstrate that the treatment is safe and effective.

If successful, animal testing is followed by an extensive series of human tests to determine whether the drug works in humans and whether it compares favorably to existing methods of treatment.

25. Essay on Cancer Treatment: (Around 650 Words)

Human Clinical Trials Involve Multiple Phases of Testing:

Evaluating a new drug in humans involves a series of tests called clinical trials. Patients who volunteer for a clinical trial are given information regarding the nature of their disease, the potential risks and benefits of the treatment being tested, and the availability of other treatment options.

Before participating, all patients must sign informed consent documents indicating their under­standing of these conditions and providing their voluntary consent. Each trial involves several phases of testing; often requiring five to ten years to complete at a cost of several hundred million dollars, before a drug can be approved for routine medical use (Figure 19).

In the first phase of testing, called a Phase I clinical trial, a new drug is administered to several dozen people to determine the safe dose. The first few individuals are given a very low dose of the drug and monitored closely for toxic side effects. If the drug is well tolerated, the dose is gradually increased in subsequent groups of patients until an appropriate dose is determined that is likely to be effective without severe side effects.

If the drug is found to be reasonably safe, the optimal dose determined during Phase I testing is then administered to a somewhat larger group of cancer patients—usually from 25 to 100—in a Phase II clinical trial to determine whether the drug exhibits any effectiveness in treating cancer. Evidence of effectiveness might be the complete dis­appearance of a tumor (complete response), a tumor that gets smaller (partial response), or a tumor that stops growing (stable disease). To justify further testing, a significant per­centage of the treated patients must exhibit one of these three responses.

The required percentage may vary, however, depending on the type of cancer being treated and the effec­tiveness of currently available drugs. For example, a 10% response rate might justify continued testing of a treatment for an aggressive tumor like pancreatic cancer that tends to be resistant to most current drugs, whereas a much higher response rate would be required for low-grade lymphomas, for which several effective drugs are already available.

If a drug exhibits sufficient signs of anticancer activity in Phase II testing, its effectiveness and safety are thor­oughly evaluated in a Phase III clinical trial. A Phase III trial is a randomized trial in which hundreds or thousands of patients are randomly assigned to two dif­ferent groups- an experimental group that receives the new treatment and a control group that does not.

To avoid possible bias in interpreting the results, randomized trials are generally double blind; that is, neither doctors nor patients know who is receiving the treatment and who is not. Patients in the control group may be given a placebo (inactive substance) that resembles the new drug in appearance so that no individual will know whether they are in the control group or the experimental group.

The purpose is to control for the placebo effect, which is any beneficial effect on a patient’s condition that may be caused by a person’s expectations concerning a drug rather than by the drug itself. Placebos, however, are not used to substitute for currently existing treatments that are known to be beneficial.

For example, the experimental group might receive the standard treatment along with the new drug, while the control group receives the standard treatment along with a placebo.

Based on the results of Phase III randomized trials, the FDA decides whether or not to approve a new drug as an acceptable treatment for standard medical use. After approval has been granted, further Phase IV clinical trials may be carried out to answer additional questions con­cerning the best ways to use the drug or to explore possible side effects that were not detected in earlier testing.

26. Essay on Cancer Treatment: (Around 640 Words)

Complementary and Alternative Cancer Treatments are Frequently Used by People who have Cancer:

Prior to obtaining FDA approval, new drugs undergoing laboratory and clinical testing are referred to as experimental treatments. It usually takes many years to obtain enough evidence to justify incorporating an experimental treatment into standard medical practice. In addition to experimental treatments, a diverse array of unproven and largely untested cancer treatments exists that are not part of standard medical practice.

These treatments can be subdivided into complementary treatments, which are used along with standard medical care, and alternative treatments, which are used as a substitute for standard medical care.

Complementary and alternative treatments include herbal remedies, vitamins, special diets, and a variety of physical and psychological practices such as massage and relaxation techniques. More than half of all individuals with cancer have been reported to use one of more of these practices, often without discussing it with their doctor.

Complementary treatments are usually used to control symptoms and improve a person’s quality of life while under standard medical care. In contrast, many alternative treatments are claimed to cure cancer. Individuals who rely solely on these alternative remedies may put themselves at considerable risk.

A striking example is provided by the history of laetrile (also called amygdalin or vitamin B17), a natural substance extracted from apricot pits that attracted considerable attention in the 1970s when medical clinics in Mexico claimed that it cured cancer. Research in laboratory animals failed to show any anticancer effects of laetrile, so it did not meet the normal standards for human testing in the United States.

However, the prominence of laetrile and its use by thousands of Americans (many of whom trav­eled to Mexico for treatment) led the National Cancer Institute to sponsor a human clinical trial despite the absence of supporting data from animal testing. After the trial showed laetrile to be ineffective against cancer, its popularity gradually declined.

In retrospect, the lack of anticancer properties was not the only problem with laetrile. The drug also has hidden dangers because it breaks down to form cyanide, and some people treated with laetrile may have died of cyanide poisoning rather than their cancers.

Another risk incurred by individuals who rely on unproven remedies such as laetrile is that they deny themselves the benefits of any proven methods that may be genuinely useful for their particular type of cancer.

Although the experience with laetrile highlights the need for caution, it does not mean that alternative reme­dies are always risky and without value. An intriguing example involves an herbal product called PC-SPES (“PC” for Prostate Cancer and “SPES” from the Latin word for “hope”).

PC-SPES, which consists of extracts from eight herbs, was introduced in 1996 as a remedy for prostate cancer. Because it was being sold as a dietary supplement consisting entirely of natural ingredients, PC-SPES did not require a doctor’s prescription or fall under governmental regulations for purity or effective­ness.

Shortly after it was introduced, several studies reported that PC-SPES slowed the growth of prostate cancer in humans (Figure 20). These encouraging results made PC-SPES one of the best prospects for an alternative cancer treatment that might stand up to the scrutiny of rigorous scientific testing.

However, chemical analyses of PC-SPES subsequently revealed that this supposedly “all natural” herbal mixture was contaminated with several synthetic drugs, and the manufacturer voluntarily stopped selling it.

When it was discovered that several other herbal products sold by the same company were also adulterated with synthetic drugs, the company went out of business and PC-SPES is no longer available today.

This cautionary tale illustrates the problems that arise when trying to eval­uate the possible effectiveness of herbal remedies, which are not subject to the kinds of strict governmental regula­tions for purity, composition, and effectiveness that apply to the drugs manufactured by pharmaceutical companies.

27. Essay on Cancer Treatment: (Around 400 Words)

Psychological Factors are not a Significant Cause of Cancer but may Influence the Course of the Disease:

Cancer patients who have been treated with placebos in clinical trials sometimes exhibit improvement in symptoms such as pain and poor appetite. Since placebos contain no active ingredients, this phenomenon raises the question of the relationship between psychological factors and cancer.

Numerous investigations into the role of psycholog­ical factors have been carried out over the years, with special attention paid to stress and depression because both can trigger changes in the immune system.

Early studies revealed that cancer patients are more likely than other individuals to be depressed and anxious, which was initially interpreted to mean that psychological stress can cause cancer. A more straightforward interpretation, however, is that depression and anxiety are triggered by the discovery that a person has cancer, occurring after the disease arises rather than being the underlying cause.

Large prospective studies in which psychological traits are measured in healthy individuals who are then followed into the future to see who develops cancer have generally failed to support the idea that psychological factors are a significant cause of cancer. Some studies have documented an increased rate of cancer deaths among people who have recently experienced a highly stressful or depressing event, such as the loss of a spouse or other close family member.

However, cancer typically takes ten or more years to develop, so these cancer deaths are likely to involve tumors that were already growing in the body at the time of the psychological disturbance (even if the disease had not yet been diagnosed). The overall body of evidence therefore suggests that psychological factors are not a significant cause of cancer, but they may influence the course of the disease after it has already begun.

If that is true, it raises the question of whether psy­chological interventions might be beneficial for cancer patients. In 1989, a widely publicized study reported that women with advanced breast cancer who participated in cancer support groups lived about 18 months longer than women who did not.

Although these findings were widely accepted at the time, subsequent studies have failed to confirm the conclusion that cancer patients participating in support groups live longer than nonparticipating patients.

Support group participation is, however, consistently associated with improvements in patients’ awareness about their illness and reductions in anxiety and distress. Whether support groups or other types of psychological intervention can extend survival for certain individuals remains an open question.