One 60-year old might develop cancer and another 60-year old with identical promoters might not develop cancer as a result of mutations that have occurred with the cancer-laden 60-year old. For example, while these two elderly adults may have started off with the same promoters, the person who eventually developed cancer did so as result mutations occurring in the noncoding region of the gene, such as the promoter sequences that regulate the gene (cancer.gov). A mutation which occurs in the promoter region can alter the rate of protein production. This can cause unregulated cell growth and amp up the progress of cancer (Cancer.gov). For example, the 60-year old with cancer might have originally had the same promoters as the non-cancerous 60-year old, but may have suffered from a wide variety of mutations in non-coding regions such as in his promoters causing the "…production of important checkpoint proteins to malfunction. Collectively, these mutations conspire to change a genome from normal to cancerous" (Cancer.gov).
Cellular Proliferation: Cancer
One-60-year-old might develop cancer and another 60-year-old with identical promoters might not develop cancer as a result of mutations that have occurred with the cancer-laden 60-year-old. For example, while these two elderly adults may have started off with the same promoters, the person who eventually developed cancer did so as result mutations occurring in the noncoding region of the gene, such as the promoter sequences that regulate the gene (cancer.gov). A mutation which occurs in the promoter region can alter the rate of protein production. This can cause unregulated cell growth and amp up the progress of cancer (Cancer.gov). For example, the 60-year-old with cancer might have originally had the same promoters as the non-cancerous 60-year-old, but may have suffered from a wide variety of mutations in non-coding regions such as in his promoters causing the "…production of important checkpoint proteins to malfunction. Collectively, these mutations conspire to change a genome from normal to cancerous" (Cancer.gov).
2. A perfect cell tumor marker refers to materials created by cancer cells or from cells in an organism's body which are responding to the presence of cancer or a harmless condition of the body (cancer.gov/topics). Normal cells and cancer cells can both create tumor markers, though cancer creates tumor markers in higher numbers. "These substances can be found in the blood, urine, stool, tumor tissue, or other tissues or bodily fluids of some patients with cancer. Most tumor markers are proteins. However, more recently, patterns of gene expression and changes to DNA have also begun to be used as tumor markers. Markers of the latter type are assessed in tumor tissue specifically" (cancer.gov/topics).
Tumor marker CA 19-9 is a common one used to screen conditions like colorectal cancer, bladder cancer and pancreatic cancer. Most people who have pancreatic cancer will demonstrate large amounts of CA 19-9 in their blood; the higher the levels of this tumor marker, the higher the likelihood that the cancer is spreading (cancer.org). CA 19-9 however is not a strong and entirely definitive tumor marker: "CA 19-9 is not sensitive or specific enough to use as a screening test for cancer and it is not diagnostic of a specific type of cancer" (labtestsonline.org). Rather, as a tumor marker, it helps to distinguish between things like cancer of the pancreas and other types, observance of treatment to types of cancer and as a means of screening the recurrence of types of cancer (labtestsonline.org). "CA 19-9 can only be used as a tumor marker if the cancer is producing elevated amounts of it. Since CA 19-9 is elevated in about 65% of those with bile duct (hepatobiliary) cancer, it may be ordered to help evaluate and monitor people with this type of cancer" (labtestsonline.org). Additional advantages of this tumor marker are that it can aid health care professionals by providing a means of following up with patients; patients who have low levels of this tumor marker generally have a better outlook than those who do not (cancer.org).
3. Angiogenesis and invasion both play a prominent role when it comes to the growth of tumors; in fact in order for invasive tumor growth and metastasis to even happen, angiogenesis is an absolute necessity (Folkman, 2002). Inhibiting angiogenesis is a valuable method to fighting and treating cancer: "Avascular tumors are severely restricted in their growth potential because of the lack of a blood supply. For tumors to develop in size and metastatic potential they must make an 'angiogenic switch' through perturbing the local balance of proangiogenic and antiangiogenic factors. Frequently, tumors overexpress proangiogenic factors, such as vascular endothelial growth factor, allowing them to make this angiogenic switch" (Folkman, 2002). Thus, being able to thwart or interrupt this process and its effectiveness is a means of cancer therapy, or at least one approach clinicians can suggest.
4. One of the biggest advantages of immunotherapy when fighting cancer is how specific it can be: it's friendly and natural to the patient and scientifically validated (cancerreasearch.org, 2009).Immunotherapists can provide sensitive and accurate cancer diagnostic tools for the successful treatment of the disease and to stop it well in its tracks (cancerresearch.org, 2009). The outward advantages of immunotherapy are as follows: certain drugs have fewer side effects and offer patients a higher quality of life, bolstered anti-cancer effectiveness and rates of survival, benefits are often reaped quickly for the patient (cisncancer.org). The disadvantages are as follows: some varieties of this treatment have serious side effects, are very expensive and occasionally offer just a short-term efficacy (cisncancer.org)
5. An overexpression of proto-oncogenes can cause cancer as mutated forms of these genes can promote unrestrained cell proliferation: "oncogenes actively promote proliferation (analogous to the gas pedal of the cell cycle). Mutations that convert proto-oncogenes to oncogenes typically increase the activity" (Hyland). An underexpression of tumor suppressor genes can also put an individual in a precarious situation. Tumor suppressor genes slam the brakes on cell proliferation: not enough of these genes could easily create a situation of unregulated cell growth (Hyland).
Lung Cancer: Case Study
1. Based on this limited history, the patient might have developed chronic bronchitis or chronic obstructive pulmonary disease.
2. I would ask the patient if her cough is wet or dry, if she's lost any weight or feels an increased sense of fatigue.
3. I would ask the patient if she's ever experience anxiety, if she's had pneumonia and if heart disease is in her family.
4. The pertinent positive on the exam are that her heartbeat is normal, her wheezes are scattered without crackle or rhonchi and she is experiencing no edema. These signs might indicate that the patient is just experiencing an aggravated form of emphysema but not the onset of pneumonia or heart disease. However, the fact that other muscles are helping her breathe indicates a progression of the emphysema.
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