Subject Response in Biology - Research Paper Example

 Subject Response in Biology 304 Paper # I Among the laboratory methods used in diagnosing and identifying cancer includes the following: Anti-malignin Antibody Screen (AMAS), Biological Terraine Assessment (BTA), CBC blood test, DR-70, and Cancer Market Test (The Cancer Cure Foundation, 2010). For AMAS, the doctor takes a blood sample and takes it to laboratory to screen for anti-malignin antibody (AMA) (Abrams et al.., 1994). Normally, the level of AMA increases in the presence of a cancer cell. Since the serum level increases in patients with cancer, the use of this laboratory procedure is effective in detecting early signs of cancer. In BTA, patients’ blood, urine, and saliva specimens are analyzed using a computer to detect evidences of disease at cellular level such as the risk of malignant processes. In line with this, electron levels, pH balance, and minerals in blood, saliva, and urine are measured (Becchetti & Kessler, 1999). However, Barrett (2002) wrote an article claiming that this method is not effective in terms of diagnosing nor select inappropriate treatment for cancer. CBC blood test checks on the indicators of cancer cells in 44 substances that are commonly found in blood whereas darkfield microscopy enables doctors to view healthy and unhealthy blood cells. However, additional laboratory tests like DR-70 are required to verify the results of darkfield microscopy test. DR-70 is a simple blood test that screens for 13 different cancer cells in lungs, colon, breast, liver, rectum, ovary, stomach, cervix, esophagus, thyroid, pancreas, malignant lymphoma, and trophoblast (The Cancer Cure Foundation, 2010; CBC News, 2008). Cancer Marker Test is an immunological method used in detecting cancer cell markets. Specifically this method is use for early detection of cancer cells. Tumor markers used in detecting cancer cells includes: Alpha fetoprotein (AFP), CA 15.3, CA 19.9, CA 125, Carcinoembryonic antigen (CEA), and EVP (The Cancer Cure Foundation, 2010). Although the levels of alpha fetoprotein (AFP) among pregnant women, it is normal for cancer patients to have elevated levels of alpha fetoprotein (AFP) especially in case of liver, gastrointestinal, and testicular cancers (Yachida et al., 2003). It is also common for cancer patients to have an elevated CA 15.3 particularly among those individuals with breast cancer (Vizcarra et al., 1996). In case a person have a history of breast cancer, patients can be advice to have a regular breast mammogram. Cancer market test on CA 15.3 can be use in case doctors suspect that a patient has a breast cancer. For patients with gastric, pancreatic, and/or stomach cancer, it is best to make use of cancer marker test for CA 19.9 (Benamouzig et al., 1989). This can be done if the patient has severe symptoms of abdominal pain, gastritis, or gas. For women who are suspected to have cancer in their reproductive system like the uterus, fallopian tubes, and ovaries, cancer marker test for CA 125 can be use to verify signs of cancer in the uterus, fallopian tubes, and ovaries (Community Connect to Research, 2008). Even though the levels of CA 125 / CA 125-II can be high when a woman is pregnant or menstruating, doctors should take note that CA 125 level can also be high in case a woman has ovarian cysts, pericarditis, hepatitis, cirrhosis of the live, and infection in the abdominal lining. For this reason, measuring the levels of CA 125 can be use to verify whether or not the patient is positively responding to cancer treatment. Carcinoembryonic antigen (CEA) is a cancer marker test for colorectal and medullary thyroid cancer (Bojunga et al., 2001). It can also be use in detecting other malignant or non-malignant disorders related to diarrhea, frequent constipation, or bleeding of the piles. On the other hand, EVP is a cancer marker test that is commonly used for nasopharyngeal cancer (The Cancer Cure Foundation, 2010). Paper # 2 Alfred George Knudson is a geneticist that specializes in cancer genetics. In the study of cancer, Knudson formulated the Knudson hypothesis back in 1971. Basically, the knudson hypothesis explains the effects of mutation of carcinogenesis – the development of cancer (Lewis, 2003). His theory resulted in the accurate identification of cancer-related genes. Eventually, Knudson’s hypothesis behind the mutation of carcinogenesis has led other researchers like Carl Nordling to study how cancer cells mutate (Marte, 2006). Basically, the first ‘hit’ occurs in oncogene may not necessary lead to the development of cancer cells since tumor suppressor genes (TSGs) such as in the case of Rb1 gene in retinoblastoma would counteract such movement (Knudson, 1971). After performing Poisson statistical analysis on retinoblastoma cases – a tumor in retina, he found out that hereditary retinoblastoma occurs at a young age as compared to sporadic disease. With this, Knudson publicly introduced the idea that two hit model such that multiple ‘hits’ or two hits to DNA had to take place before tumor causing cancer can develop (Marte, 2006). Cancer cell mutation should be associated with a certain power of age since cancer cells takes place in successive hits. In line with this, Carl Nordling concludes that it takes seven mutations throughout the age distribution for a range of cancer cells to occur (Marte, 2006). This theory explains why not all individuals with tumor could experience the negative health effects of active cancer cells. Upon analyzing a total of 48 cancer cases of retinoblastoma particularly in the incidence of bilateral and/or unilateral tumors, Knudson suggests that carcinogenesis also known as the development of malignant cancer cells is highly dependent on the activation of proto-oncogenes – genes that can stimulate cell proliferation (Marte, 2006). It means that for malignant cancer cells to develop, the tumor suppressor genes which is responsible for keeping proliferation in check has to be deactivated in order for multiple hits to take place. Upon analyzing the study of Knudson, there is a higher risk in the development of retinoblastoma through hereditary as compared to sporadic path since hereditary retinoblastoma can result to multiple hits to DNA which is necessary in the development of cancer causing tumor to mutate (Marte, 2006). Paper # 3 Tumors can be either malignant or benign. Although malignant tumor uses the same schema used in benign tumors, it is a common knowledge that malignant cancer cells are caused by abnormalities in the genetic materials of a transformed cells due to the effects of carcinogens like tobacco smoking, radiation, chemicals, or other infectious agents (Pagano et al., 2004). Basically, cancer-promoting genetic abnormalities may occur either through hereditary of errors in the DNA replication. As a result of genetic abnormalities, cancer-promoting oncogenes are activated in the cancer cells. This causes the rapid growth and division of malignant cancer cells (Nelson et al., 2004). Although direct transplantation of tumor cells may occur via infected surgical instruments, the three common pathways wherein cancer cells may disseminate in the body includes: (1) direct seeding of body cavities or surface; (2) lymphatic spread; and (3) hematogenous spread. Seeding of body cavities or surface can take place when malignant neoplasm penetrates into an ‘open field’ such as open skin surface, joint spaces, and cavities related to peritoneal, pleural, pericardial, and subarachnoid. Once seeding of malignant neoplasm takes place, malignant cancer cells may travel around the body through the lymphatic system. For example: Carcinomas in breast which can be found in the upper outer quadrant can disseminate through the axillary lymph nodes going to the chest along the internal mammary arteries. This may cause the infraclavicular and supraclavicular nodes to become infected by malignant cancer cells. As part of hematogenous spread, malignant cancer cells may also disseminate to other body parts through arteries and veins. References Abrams, M., Bednarek, K., Bogoch, S., et. al. (1994). Early detection and monitoring of cancer with the anti-malignin antibody test. Cancer Detection and Prevention , 18(1), 65-78. Barrett, S. (2002, April 9). Quack Watch. Retrieved June 2, 2010, from Biological Terrain Assessment Is Nonsense: http://www.quackwatch.org/01QuackeryRelatedTopics/Tests/bioter.html. Becchetti, S., & Kessler, M. (1999). Dynamic Chiropractic. Retrieved June 2, 2010, from Biological Terrain Assessment: an Invaluable Tool. Vol. 17, Issue 23.: http://chiroweb.com/mpacms/dc/article.php?t=6&id=36339. Benamouzig, R., Buffet, C., Fourre, C., Ink, O., Moati, F., & Etienne, J. (1989). Serum levels of carbohydrate antigenic determinant (CA 19.9) in obstructive jaundice. Digestive Diseases and Sciences , 34(10), 1989. Bojunga, J., Dragan, C., Schumm-Draeger, P., Usadel, K., & Kusterer, K. (2001). Circulating calcitonin and carcinoembryonic antigen m-RNA detected by RT-PCR as tumour markers in medullary thyroid carcinoma. Br J Cancer , 85(10), 1546–1550. CBC News. (2008, June 23). Retrieved June 2, 2010, from Ovarian symptoms check with blood test improves detection, study finds: http://www.cbc.ca/health/story/2008/06/23/ovarian-cancer.html. Community Connect to Research. (2008, April 10). Retrieved June 2, 2010, from Fallopian Tube Cancer: http://www.connecttoresearch.org/publications/66. Knudson, A. (1971). Mutation and cancer: statistical study of retinoblastoma. Proceedings of the National Academy of Sciences , 68 (4), 820–823. Lewis, E. (2003). A tribute to Alfred G. Knudson. Genes Chromosomes Cancer , 38 (4), 292-293. Marte, B. (2006, April 1). Nature. Retrieved June 2, 2010, from Milestone 9: (1953) Two-hit hypothesis - It takes (at least) two to tango: http://www.nature.com/milestones/milecancer/full/milecancer09.html. Nelson, D., Tan, T., Rabson, A., Anderson, D., et. al. (2004). Hypoxia and defective apoptosis drive genomic instability and tumorigenesis. Genes & Development , 18 (17), 2095–2107. Pagano, J., Blaser, M., Buendia, M., et. al. (2004). Infectious agents and cancer: criteria for a causal relation. Semin. Cancer Biology , 14 (6), 453–471. The Cancer Cure Foundation. (2010). Retrieved June 2, 2010, from Laboratory Tests that Detect Cancer: http://www.cancure.org/tests_to_detect_cancer.htm. Vizcarra, E., Lluch, A., Cibrian, R., Jarque, F., et. al. (1996). Value of CA 15.3 in breast cancer and comparison with CEA and TPA: a study of specificity in disease-free follow-up patients and sensitivity in patients at diagnosis of the first metastasis. Breast Cancer Research and Treatment , 37(3), 209-216. Yachida, S., Fukushima, N., Nakanishi, Y., Akasu, T., et. al. (2003). Alpha-Fetoprotein-Producing Carcinoma of the Colon. Diseases of the Colon & Rectum , 46(6), 826-831. Read More