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Etiology and Pathogenesis of the Pancreatic Cancer - Research Paper Example

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The paper 'Etiology and Pathogenesis of the Pancreatic Cancer' present cancer as the abnormal production of an organism's cells which are uncontrolled and sometimes spread. Cancer is commonly used for all types of malignant tumors, the swelling of any body tissue caused by inflammation…
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Etiology and Pathogenesis of the Pancreatic Cancer
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AR Pancreatic Cancer Pancreatic Cancer Introduction Cancer is the abnormal production of the cells of an organism which are proliferated in an uncontrolled way and sometimes spread. Cancer is commonly used for all types of malignant tumors, which is the swelling of any tissue of the body caused by inflammation, which are studied in Oncology. Neoplasm is defined by a British oncologist Willis as “Abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of the normal tissue and persists in the same excessive manner after cessation of the stimuli which evoked the change.”(Willis 5). Pancreatic cancer is known to be a lethal cancer which accounts for the fourth most renowned cancer which causes death in the United States of America. It starts with lesions in the epitheliums and may later on go to become invasive enough to cause death. This research essay would further revolve around the epidemiology, etiology and pathogenesis of the pancreatic cancer. Pancreas as an Organ Pancreas is a complex gland having both exocrine and endocrine functions. The organ has a very important role to play in the digestion of substances in the body but as the pancreas has a retroperitoneal location it does not show the progression of diseases in the initial stages. Thus it is very hard to detect diseases of pancreas in the initial stages. The exocrine part of the gland secretes digestive enzymes which help in digesting food particles whereas the endocrine portion secretes only a limited number of enzymes such as insulin and glucagon. The major abnormalities caused by the non-functioning of the endocrine portion of the pancreas are diabetes mellitus and neoplasms. And the major diseases caused by the exocrine portion are related to the inflammation of the pancreas itself (Catalano et al 2009). Probable causes of Pancreatic Cancer With latest researches being carried out much has become known about many cancers but the exact cause of pancreatic cancer is yet to be found. Most of the individuals suffering from pancreatic cancer are adults who are above 60 (Gold & Goldin 1998). Many factors have been studied in relation to the pancreatic cancer and it has been found that smoking is one of the foremost external influence which can trigger the cancer (Gold & Goldin 1998). Similarly inflammation of pancreas is also known to be an important factor that may cause the cancer (Lowenfels et al 1997). However some individuals do argue that it is because of the pancreatic cancer that the inflammation of pancreas occurs. As all cancers are related to genetics, pancreatic cancer is also known to be associated with the relative genetical disorders. Genetic Disorders Causing Pancreatic Cancer The genetic disorders may occur in an individual because of mutation in genes which may further go on to trigger carcinoma (Bardeesy & Depinho 2002). The genes which may cause pancreatic cancer are K-Ras, p16, SMAD4, p53, and other genes. Out of all these genes research has shown that K-Ras is the most frequent altered gene that might cause pancreatic cancer. This gene if altered may impair the function of several cells and because of it the process of transcription on the organ may increase. Thus this transcriptional process may cause more cells to be developed and hence would develop cancer. The gene p16 is a tumor supressor gene which if altered would give way to the cancer cells to develop excessively in the organ(Caldas et al 1994). Another similar tumor suppressor gene is SMAD4 which if inactivated would give a way to cells to proliferate rapidly and cause cancer (Hahn et al1996). The gene p53 is also a tumor suppressor gene which is also inactivated before pancreatic cancer occurs in some cases. This gene triggers cell death in the organ and stops the cells from invading the organ abnormally. However if the gene is inactivated cell death may not occur and many invading cells would take over the organ thus causing the carcinoma of pancreas. Not only do these genes trigger the pancreatic cancer but other genes have also been identified which may cause it. The examples of these genes are AKT2 gene, MYB gene, BRCA2 gene, MKK4 and RB1 gene. In some cases of pancreatic cancer it has also been noted that sulphur plays a role in lowering down the rate of the suppressor genes. If methylation of specific promoters occur then many tumor suppressor genes may not be able to develop thus again giving a way to the abnormal cells. All these genes mentioned above usually tend to lower down their function and cause pancreatic cancers while on the other hand it has been researched that there are other genes too which may hyper-express themselves during the onset of the pancreatic cancer. It has been noted that these genes can provide a scientific achievement if analyzed properly (Ryu et al 2002; Maitra et al 2002; Berman et al 2003). Cancers in Pancreas Most of the pancreatic cancers occur in the head of the pancreas but may also occur in other areas of the gland. The carcinomas that the pancreas may show would be huge blocks which would be poorly defined. Adenocarcinomas are believed to cause pancreatic cancer which may further invade the organ and cause the gland to secrete mucin. The pancreatic cancer is highly invasive and may invade all the portions of the organ in a short span of time. Furthermore, the migration of white blood cells to the affected area in a short span of time is also a characteristic feature of the pancreatic cancer. Research has shown that individuals who have carcinoma in the head of pancreas also have jaundice because the marked increase of cells in the pancreatic ductules cause the biliary duct to be obstructed too. Thus it is the carcinoma of the head of pancreas that is detected in the early stages because of the increased signs of jaundice in an individual. If the carcinoma is viewed in a microscope it is seen that dense clusters of cells are formed which form tubular structures and these cells then exhibit an invasive growth pattern. Similarly because of the carcinoma many white blood cells like lymphocytes migrate to the affected area so as to trigger an immune reaction in the body (Robbins et al 2003; Ghaneh et al 2008). Clinical Signs of Pancreatic Cancer Pancreatic cancer is a type of cancer which slowly invades whole of the organ without showing any such external advance. Thus it is very hard to detect pancreatic cancer in individuals who are suffering from it. However some clinical manifestations can still be studied in the patients suffering from pancreatic cancer. These may include pain and restlessness which usually is the most lethal sign of the advancement of the pancreatic cancer. If severe pain is manifested then it can be said that the cancer has advanced to its lethal stages. Jaundice can be a sign of clinical manifestation of the cancer but that is only in the case of the cancer which is associated with the head of pancreas. As the cells invade the organ it is seen that many of the procoagulants and platelet aggregating factors are released which may show a sign of the advancement of the cancer (Robbins et al 2003 & Ghaneh et al 2008). Treatment options for Pancreatic Cancer Nowadays different therapies are used for the treatment of cancer like chemotherapy, thermotherapy, tomotherapy, etc. Thermotherapy is the treatment of tumors with the help of microwave energy which heat up the tumor cells and notably can minimize and kill the tumor cells. Thermotherapy combined with chemotherapy can both significantly decrease and destroy much of the cancer cells. Tomotherapy is new form of radiation therapy which is the delivery of radiations to the cancer cells and is more accurate which leaves the nearby normal tissue unaffected. In radiation therapy, high energy photon particles are emitted which penetrate the body and tumor cells with more ease and create low energy secondary electrons which destroy tumor cells by destroying the genetic material DNA of the cancer cells. Researchers have shown that exposing the gold particles to radiations produces a large amount of cell killing low energy electrons which kills the cancer cells and not the normal cells (Dollinger 2007 & Trahan 2001). Among all the treatment options mentioned above, the best treatment for pancreatic cancer is thought to be chemotherapy. Surgeries are also considered to be important interventions to cure pancreatic cancer. The surgery depends upon the part of the organ that is affected by the cancer. The relevant parts of the organ are operated upon and removed if possible to relieve the person of the cancer (Robbins et al 2003). Conclusion Pancreatic cancer may be caused by smoking, irregularities in diet, chemical carcinogens or chronic pancreatitis. It has been known that all these factors cause an alteration in the gene functions of the pancreas and thus trigger a carcinoma in the organ. Research is being carried out to find out the exact cause of the cancer and further treatment options are being made available so that the cancer rate can be decreased all over the world. The important functions of pancreas are necessary for an individual to survive and thus to prevent the carcinoma early diagnosis of this disease is important (Robbins et al 2003). References Top of Form GHANEH, P., COSTELLO, E., & NEOPTOLEMOS, J. (2008). Biology and management of pancreatic cancer.Postgraduate Medical Journal. 84, 478-497. Bottom of Form GOLD EB, & GOLDIN SB. (1998). Epidemiology of and risk factors for pancreatic cancer. Surgical Oncology Clinics of North America. 7, 67-91. 50 Top of Form LOWENFELS, A. B., MAISONNEUVE, P., DIMAGNO, E. P., ELITSUR, Y., GATES JR, L. K., PERRAULT, J., & WHITCOMB, D. C. (1997). Hereditary Pancreatitis and the Risk of Pancreatic Cancer. Journal of the National Cancer Institute : JNCI. 89, 442. Top of Form BARDEESY N, & DEPINHO RA. (2002). Pancreatic cancer biology and genetics. Nature Reviews. Cancer. 2, 897-909. Bottom of Form CALDAS C, HAHN SA, DA COSTA LT, REDSTON MS, SCHUTTE M, SEYMOUR AB, WEINSTEIN CL, HRUBAN RH, YEO CJ, & KERN SE. (1994). Frequent somatic mutations and homozygous deletions of the p16 (MTS1) gene in pancreatic adenocarcinoma.Nature Genetics. 8, 27-32. Top of Form HAHN, S. A., SCHUTTE, M., SHAMSUL HOQUE, A. T. M., MOSKALUK, C. A., DA COSTA, L. T., ROZENBLUM, E., WEINSTEIN, C. L., FISCHER, A., YEO, C. J., & HRUBAN, R. H. (1996). DPC4, A Candidate Tumor Suppressor Gene at Human Chromosome 18q21.1. SCIENCE -NEW YORK THEN WASHINGTON-. 350-352. Bottom of Form Top of Form RYU B, JONES J, BLADES NJ, PARMIGIANI G, HOLLINGSWORTH MA, HRUBAN RH, & KERN SE. (2002). Relationships and differentially expressed genes among pancreatic cancers examined by large-scale serial analysis of gene expression. Cancer Research. 62, 819-26. Bottom of Form Top of Form IACOBUZIO-DONAHUE, C. A., MAITRA, A., SHEN-ONG, G. L., VAN HEEK, T., ASHFAQ, R., MEYER, R., WALTER, K., BERG, K., HOLLINGSWORTH, M. A., & CAMERON, J. L. (2002). Discovery of Novel Tumor Markers of Pancreatic Cancer using Global Gene Expression Technology. AMERICAN JOURNAL OF PATHOLOGY. 160, 1239-1250. Bottom of Form Top of Form BERMAN, D. M., KARHADKAR, S. S., MAITRA, A., DE OCA, R. M., GERSTENBLITH, M. R., BRIGGS, K., PARKER, A. R., SHIMADA, Y., ESHLEMAN, J. R., & WATKINS, D. N. (2003). Widespread requirement for Hedgehog ligand stimulation in growth of digestive tract tumours. NATURE -LONDON-. 846-850. Bottom of Form Catalano MF, A Sahai, M Levy, J Romagnuolo, M Wiersema, W Brugge, M Freeman, K Yamao, M Canto, and LV Hernandez. 2009. "EUS-based criteria for the diagnosis of chronic pancreatitis: the Rosemont classification". Gastrointestinal Endoscopy. 69 (7): 1251-61. Rieger, Paula Trahan. Biotherapy A Comprehensive Overview (Jones and Bartlett Series in Oncology). New York: Jones & Bartlett, 2001. Print. D., M., and Malin Dollinger. Everyones Guide to Cancer Therapy; Revised 5th Edition How Cancer Is Diagnosed, Treated, and Managed Day to Day (Everyones Guide to Cancer Therapy). Grand Rapids: Andrews McMeel, 2007. Print. Willis, Rupert Allan. The Spread of Tumors in the Human Body. London: Butterworths, 1952.Bottom of Form Kumar, Vinay, Ramzi S. Cotran, and Stanley L. Robbins.Robbins Basic Pathology. Philadelphia, PA: Saunders, 2003. Read More
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