Pancreatic cancer is ranked as the fourth-leading cause of cancer-related death in the United States. Thus, researchers are carrying out studies to understand the biologic mechanism that explain the behavior of pancreatic cell and reasons it is growing at a rapid pace. The researchers' hope that with the information discovered there will be leads to the development of improved diagnostic mechanism that will enable early detection of premalignant and also develop therapies for patients diagnosed with pancreatic cancer. In the year 2008, pancreatic carcinoma killed over 37,000 Americans. Regarding prognosis, infiltrating ductal adenocarcinoma has a five-year survival rate that is less than five percent. This article will discuss pancreatic adenocarcinoma characteristics at the cellular level, progression through the body, the morphological difference between its cell and cells, treatment modalities/options and preventive measures.
"Pancreatic cancer" that denotes the infiltrating ductal adenocarcinoma is the fourth commonest cause of mortality after lung, colon and breast cancers. It is the most invasive cancer and carries the highest mortality rate. The pancreatic carcinoma affects head, body, and tail at 60%, 15%, and 5% proportion respectively. However, about 20% of the pancreatic carcinoma affects the gland in entirety. The cancer is a hard poorly defined mass that affects the ducts and the parenchyma of the pancreas. The majority are ductal carcinomas that to some level affect normal ducts of the pancreas (Makohon-Moore & Iacobuzio-Donahue, 2016).
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Just as there is a definitive progression from adenoma-invasive carcinoma in colorectal cancer, there are precursor lesions called pancreatic intraepithelial neoplasia(PanINs)The genetic alterations that are found in these precursor lesions are the same as those found in invasive cancer. The epithelial cells in the precursor lesions show shortening of the telomere. There is a progression of normal pancreatic cells to invasive carcinoma through PanINs-1A, 1B, PanINs-2, PanINs-3. The carcinoma is characteristically very invasive and triggers a non-neoplastic reaction that comprises fibroblasts, extracellular matrix, and lymphocytes. As it progresses through the head of the pancreas, the carcinoma obstructs the distal common bile duct, and the patient develops jaundice. There is marked distention of the biliary tree. They grow along the nerves and spread into the retroperitoneum. However, there is direct spread into the spleen, adrenals, transverse colon, and the stomach. Gastric, omental and peri-pancreatic lymph are affected frequently. Distant spread occurs in the liver, lungs, and bones respectively (Makohon-Moore, & Iacobuzio-Donahue, 2016).
In terms of characteristics, there is no difference between the carcinoma of the head, body, and tail. When compared to the normal cells, pancreatic cancerous cells have moderate to poor differentiation that forms abortive tubular structures. They also show a group of cells that are aggressive into the deep parenchyma. There is also fibrosis of the stroma of pancreas. In terms of morphology, lymphoid cells are also visualized. The glands of the pancreas that are invaded by malignancy have cells that are cuboidal or columnar in appearance.
The most commonly affected system is that encoded by the KRAS and the P16/CDKN2A. For KRAS, there is point mutation that invariably affects the guanosine triphosphatase activity. The P16/CDKN2A gene is affected by inactivation in 95% cases of pancreatic carcinoma. This makes it the most affected tumor suppressor gene. The p16 plays a crucial role in the cell cycle, and when affected there is a failure of checkpoints in the cell cycle. The gastrointestinal system is the one frequently affected as the pancreas is one of the organs found in the system. The glucose regulation is affected, and most of these patients develop diabetes mellitus, and the insulin production of the pancreas is affected. When the disease metastasizes to the liver, gluconeogenesis is invariably affected (Zavoral et al., 2011).
Detecting pancreatic carcinoma early using screening tumor markers such as Carcinoembryonic Antigen and CA 19-9 is helpful in early treatment. Surgery is the mainstay of treatment of this malignancy. Whipple procedure is done as a curative resection. Total or distal pancreatectomy is also an option for a cure. When the disease is advanced, there is an option for chemotherapy and/or radiotherapy. The chemotherapeutic regimen commonly used is Gemcitabine, capecitabine, and docetaxel (Dave, 2004).
The strongest environmental risk factor is smoking of cigarettes. Avoiding cigarette smoking or Smoking cessation will go a long way in preventing pancreatic carcinoma. Minimal consumption of dietary fats is also a preventive activity. Avoiding risk factors that predispose to chronic pancreatitis and diabetes will decrease chances of pancreatic carcinoma as these two are implicated. Smoking and alcohol are the underlying factors of chronic pancreatitis.
References
Dave, S. S. et al. (2004). Prediction of survival in follicular lymphoma based on molecular features of tumor-infiltrating immune cells. N Engl J Med 351:2159-2169.
Makohon-Moore, A., &Iacobuzio-Donahue, C.A. (2016).Pancreatic cancer biology and genetics from an evolutionary perspective. Nature reviews cancer16, 553-565. www.nature.com/nrc/journal/v16/n9/full/nrc.2016.66.html?oxtrotcallback=true
Zavoral, M., Minarikova, P., Zavada, F., Salek, C., & Minarik, M. (2011). Molecular biology of pancreatic cancer. World Journal of Gastroenterology: WJG, 17(24), 2897-2908. http://doi.org/10.3748/wjg.v17.i24.2897
