Nonpolyposis Colorectal Cancer
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What is hereditary nonpolyposis colorectal cancer?
Hereditary nonpolyposis colorectal cancer, often called HNPCC or Lynch syndrome, is a type of inherited cancer of the digestive tract, particularly the colon (large intestine) and rectum. People with hereditary nonpolyposis colorectal cancer have an increased risk of cancers of the stomach, small intestine, liver, gallbladder ducts, upper urinary tract, brain, skin, and prostate. Women with this disorder also have a greatly increased risk of endometrial and ovarian cancer. Even though the disorder is described using the term nonpolyposis, people with hereditary nonpolyposis colorectal cancer may have occasional noncancerous growths called colon polyps. These colon polyps occur at an earlier age than do colon polyps in the general population. Although the polyps do not occur in greater numbers than in the general population, they are more prone to become cancerous.
How common is hereditary nonpolyposis colorectal cancer?
In the United States, about 160,000 new cases of colorectal cancer are diagnosed each year. Hereditary nonpolyposis colorectal cancer is responsible for approximately 2 percent to 7 percent of all diagnosed cases of colorectal cancer.
What genes are related to hereditary nonpolyposis colorectal cancer?
Variations of the MLH1, MSH2, MSH6, and PMS2 genes increase the risk of developing hereditary nonpolyposis colorectal cancer.
All of these genes are involved in the repair of mistakes made when DNA is copied (DNA replication) in preparation for cell division. Mutations in any of these genes prevent the proper repair of DNA replication mistakes. As the abnormal cells continue to divide, the accumulated mistakes can lead to uncontrolled cell growth and possibly cancer. Although mutations in these genes predispose individuals to cancer, not all people who carry these mutations develop cancerous tumors.
How do people inherit hereditary nonpolyposis colorectal cancer?
Hereditary nonpolyposis colorectal cancer risk is inherited in an autosomal dominant pattern, which means one inherited copy of the altered gene is sufficient to increase cancer risk. It is important to note that people inherit an increased risk of cancer, not the disease itself. Not all people who inherit mutations in these genes will develop cancer.
Source: National Institutes of Health
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New colon cancer data have been reported by scientists at Cornell University
2009 MAY 18 - (NewsRx.com) -- According to recent research from the United States, "The incidence of colorectal carcinoma has increased among patients < 40 years of age for unclear reasons. In this study, we describe the clinical. pathologic, and molecular features of colorectal carcinomas that developed in young patients." "We compiled a study group of 24 patients < 40 years of age with colorectal carcinoma, and 45 patients >= 40 years of age served as controls. Cases were evaluated for clinical risk factors of malignancy and pathologic Features predictive of outcome. The tumors were immunohistochemically stained for O-6-methylguanine methyltransferase, MLH-1, MSH-2, MSH-6, beta-catenin, chemokine (C-X-C motif) receptor 4, epidermal growth factor receptor, TP53, p16, survivin, and alpha-methylacyl-CoA racemase; assessed for microsatellite instability and mutations in beta-catenin, APC, EGFR, PIK3CA, KRAS, and BRAF; evaluated for micro-RNA expression (miR-21, miR-20a, miR-183, miR-192, miR-145, miR-106a, miR-181b, and miR-203); and examined for evidence of human papillomavirus infection. One study patient each had ulcerative colitis and hereditary nonpolyposis colorectal cancer. Ninety-two percent of tumors from young patients occurred in the distal colon (P = 0.006), particularly the rectum (58%, P = 0.02), and 75% were stage III or IV. Tumors from young patients showed more frequent lymphovascular (81%, P = 0.03) and/or venous (48%, P = 0.003) invasion, an infiltrative growth pattern (81%, P = 0.03), and alpha-methylacyl-CoA racemase expression (83%, P = 0.02) compared with controls. Carcinomas in this group showed significantly increased expression of miR-21, miR-20a, miR-145, miR-181b, and miR-203 (P <= 0.005 for all comparisons with controls). These results indicate that early-onset carcinomas commonly show pathologic features associated with aggressive behavior," wrote R.K. Yantiss and colleagues, Cornell University. The researchers concluded: "Posttranslational regulation of mRNA and Subsequent protein expression may be particularly important to the development of colorectal carcinomas in young patients." Yantiss and colleagues published their study in American Journal of Surgical Pathology (Clinical, Pathologic, and Molecular Features of Early-onset Colorectal Carcinoma. American Journal of Surgical Pathology, 2009;33(4):572-582). For additional information, contact R.K. Yantiss, Cornell University, Weill Med College, Dept. of Pathology & Laboratory Medical, 525 E 68th St., New York City, NY 10021, USA. Publisher contact information for the American Journal of Surgical Pathology is: Lippincott Williams & Wilkins, 530 Walnut St., Philadelphia, PA 19106-3621, USA. Keywords: United States, New York, Colon Cancer, Colon Carcinoma, Colorectal, Enzyme Research, Gastroenterology, Methyltransferase, Microsatellite Instability, Oncology, Pathology, Racemase, Cornell University. This article was prepared by Clinical Oncology Week editors from staff and other reports. Copyright 2009, Clinical Oncology Week via NewsRx.com.
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