Cancer Essay, Research Paper Joseph Bonacci University of Pittsburgh Titusville Dr. Nancy Tress Non Majors Biology November 11, 2001 Cancer Fewer than ten percent of most cancers are thought to be due to strong hereditary factors. Many physicians believe that prevention is the best way to effectively tackle cancer.
Cancer Essay, Research Paper
University of Pittsburgh Titusville
Dr. Nancy Tress
Non Majors Biology
November 11, 2001
Fewer than ten percent of most cancers are thought to be due to strong hereditary factors. Many physicians believe that prevention is the best way to effectively tackle cancer. One of those factors in prevention is the individual knowing their family history so that they can develop an awareness of their families’ cancer lineage. Other factors are a balanced diet, not smoking, moderate alcohol consumption and exercise. Strong hereditary factors that increase cancer risk are more likely to be found in families that have:
• Individuals diagnosed with cancer at a younger than expected age (for example, breast cancer in the 40’s or prostate cancer in the 50’s)
• Three or more cancers on once side of the family
• Three or more generations affected with cancer
• Individuals diagnosed with two or more cancers (but not a metastasis or spread from a cancer to another part of the body).
The BRCA1 gene is on chromosome 17. BRCA2 is located on chromosome 13. A woman who inherits a mutation in either of these two genes has an increased risk of both breast and ovarian cancer. That is, the same genetic change results in an increased risk of these two cancers. In some families there is also an increased risk of pancreatic cancer, colon cancer, melanoma, and other cancers, but the risk of these cancers if far lower than the risk of breast and ovarian cancer.1-2
Another preventative step is to understand how cancer functions. If people can educate themselves about how cancer survives and works, they can take necessary steps to change their lifestyle to prevent cancer. Cancer is a loss of mitosis, or cell division. Cells begin to divide at an uncontrollable rate, which eventually spreads and eats away at different organs. This loss of mitosis can be attributed to five factors:
1) Oncogenes- normally activate cell division. If it activates at wrong time or place cancer will begin to develop.
2) Tumor Suppressor- gene fails to perform its normal function to suppress tumor formation.
a. Example Brca 1 Brca 2
3) Carcinogens- Direct carcinogens such as gasoline or direct exposure to ultraviolet light.
4) Procarcinogens- safe outside the body, but metabolized into carcinogens inside the body.
a. Example: cigarette tar
5) Promotor- Agents that make carcinogens more powerful.
a. Example: Alcohol, cigarette tar
There has been much debate as to how to prevent and predict different types of cancer including cervical cancer in women. Young age at first intercourse, high number of sexual partners, high parity, cigarette smoking, race, and low socioeconomic status have consistently emerged as significant risk factors for cervical cancer.3-5 These, however, are linked to sexual behavior and the acquisition of HPV, and, except for smoking, none have consistently been shown to be significant independent risk factors.
There has been considerable controversy regarding the association between oral contraceptives and cervical cancer.6,7,8 While E6 and E7 HPV oncogene expression can be potentiated by estrogen in laboratory experiments,6-9 few epidemiologic studies of oral contraceptive use and cervical cancer have been able to control for the fact that women using oral contraceptives tend not to use barrier contraceptives and may have more sexual contacts.
A common practice pattern among some clinicians has been to stop oral contraceptives when an abnormal Pap result is reported. This practice can result in unplanned pregnancy just as the patient presents for diagnostic evaluation and management. The instruction to discontinue oral contraceptives also ignores the current understanding of the epidemiology and natural history of the disease.
Cigarette smoking (even passive smoke) has been linked to an increased risk of cervical cancer.10-13 Interestingly, any observed effect appears to be linked to squamous carcinomas and not adenocarcinomas or adenosquamous carcinomas.14 The presence of cigarette carcinogens in cervical mucus has been described as a possible biological explanation for the epidemiologic association.17-19
Cancer is a very difficult disease to cure and it seems as if preventative medicine is the most effective way to stop cancer before it starts. Education can not only help people lead longer lives, but healthier lives. Education also starts with a person’s first teachers; their parents. If parents take time to condition their children to lead a healthy life, such as eating right, exercising and not smoking along with doing even easier things like using sunscreen, they will grown up with good habits, which will help reduce their risk.
1 Assess Your True Risk of Breast Cancer, Patricia T. Kelly, (Henry Holy & Co., NY) 2000
2. Richard A. McCartney M.D. Understanding and Dealing with Cancer
3. Herrero R, Brinton LA, Reeves WC, et al. Sexual behavior, venereal diseases, hygiene practices, and invasive cervical cancer in a high risk population. Cancer 1990;65:380-386.
4. Clarke EA, Morgan RW, Newman AM. Smoking as a risk factor in cancer of the cervix: Additional evidence from a case-control study. Am J Epidemiol 1982;115:59-66.
5. Brinton LA, Hamman RF, Huggins GR, et al. Sexual and reproductive risk factors for invasive squamous cell cervical cancer. J Natl Cancer Inst 1987;79:23-30.
6. Brinton LA, Reeves WC, Brenes MM, et al. Oral contraceptive use and risk of invasive cervical cancer. Int J Epidemiol 1990;19:4-11.
7. Hildesheim A, Reeves WC, Brinton LA, et al. Association of oral contraceptive use and human papillomaviruses in invasive cervical cancers. Int J Cancer 1990;45:860-864.
8. Beral V, Hannaford P, Kay C. Oral contraceptive use and malignancies of the genital tract. Results from the Royal College of General Practitioners’ Oral Contraception Study. Lancet 1988;2:1331-1335.
9. Chen Y, Huang LH, Chen TM. Differential effects of progestins and estrogens on long control regions of human papillomavirus types 16 and 18. Biochem Biophys Res Commun 1996; 224:651-659.
10. Arbeit JM, Howley PM, Hanahan D. Chronic estrogen-induced cervical and vaginal squamous carcinogenesis in human papillomavirus type 16 transgenic mice. Proc Natl Acad Sci USA 1996; 93:2930-2935.
11. Michelin D, Gissmann L, Street D, et al. Regulation of human papillomavirus type 18 in vivo: Effects of estrogen and progesterone in transgenic mice. Gynecol Oncol 1997; 66:202-208.
12. Schon H, Grgurin M, Szekeres T, et al. A new mode of treatment of human papilloma virus associated anogenital lesions using a nonsteroid estrogen analogue.Wien Klin Wochenschr 1996; 108:45-47.
13. Brinton LA, Schairer C, Haenszel W, et al. Cigarette smoking and invasive cervical cancer. JAMA 1986;255:3265-3269.
14. Clarke EA, Morgan RW, Newman AM. Smoking as a risk factor in cancer of the cervix: Additional evidence from a case-control study. Am J Epidemiol 1982;115:59-66.
15. La Vecchia C, Franceschi S, Decarli A, et al. Cigarette smoking and the risk of cervical neoplasia. Am J Epidemiol 1986; 123:22.
16. Slattery ML, Robinson LM, Schuman KL, et al. Cigarette smoking and exposure to passive smoke are risk factors for cervical cancer. JAMA 1989;261:1593.
17. Burger MM, Hollema H. Gouw AH, et al. Cigarette smoking and human papillomavirus in patients with reported cervical cytological abnormality. Br Med J 1993;306:749.
18. Schiffman MH, Haley NJ, Felton JS, et al. Biochemical epidemiology of cervical neoplasia: measuring cigarette smoke constituents in the cervix. Cancer Res 1987;47:3886.
19. Prokopczyk B, Cox JE, Hoffman D, et al. Identification of tobacco-specific carcinogens in the cervical mucus of smokers and nonsmokers. J Natl Cancer Inst 1997;89:868-873.
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