نتایج جستجو برای: polyposis colorectal cancer
تعداد نتایج: 932929 فیلتر نتایج به سال:
BACKGROUND Young-onset colorectal cancer is clinicopathologically different from older-onset colorectal cancer and tends to occur in patients with hereditary germline conditions such as Lynch syndrome and familial adenomatous polyposis. CASE REPORT We describe the case of a 44-year-old man with a paternal history of colon polyps, a personal 2-year history of hematochezia, and a diagnosis of r...
Hereditary non-polyposis colorectal cancer: current risks of colorectal cancer largely overestimated
Numerous experimental, epidemiologic, and clinical studies suggest that nonsteroidal anti-inflammatory drugs (NSAIDs), particularly the highly selective cyclooxygenase (COX)-2 inhibitors, have promise as anticancer agents. NSAIDs restore normal apoptosis in human adenomatous colorectal polyps and in various cancer cell lines that have lost adenomatous polyposis coli gene function. NSAIDs also i...
Colorectal cancer (CRC) is the second leading cause of cancer death in the United States. Annually, approximately 130,200 individuals will be diagnosed and 56,300 will die from this disease.1 In general, CRC evolves in an “adenoma to carcinoma” sequence during which a series of somatic alterations accumulate in the DNA of the tumor tissue. Since 1987, significant strides have been made in chara...
Familial adenomatous polyposis (FAP), due to germ-line mutation of the adenomatous polyposis coli (APC) gene, is characterized by development of colorectal adenomas and ultimately colorectal cancer. The usefulness of ornithine decarboxylase (ODC) activity and polyamine levels in normal-appearing colorectal mucosa to stratify risk for colorectal neoplasia by discriminating presymptomatic individ...
Familial adenomatous polyposis (FAP) and MUTYH-associated polyposis (MAP) are inherited disorders associated with multiple colorectal adenomas that lead to a very high risk of colorectal cancer. The somatic mutations that drive adenoma development in these conditions have not been investigated comprehensively. In this study we performed analysis of paired colorectal adenoma and normal tissue DN...
Attenuated familial adenomatous polyposis (AFAP) is a variant of familial adenomatous polyposis with fewer than one hundred colorectal polyps and a later age of onset of the cancer. Here, we report two cases of AFAP within family members. Each patient demonstrated the same novel germ line mutation in exon 15 of the adenomatous polyposis coli (APC) gene and was successfully managed with sulindac...
Cyclooxygenase-2 (COX-2), an inducible prostaglandin G/H synthase, is overexpressed in pre-neoplastic tissues and several human cancers including colorectal cancer. Evidence linking COX-2 activity to carcinogenesis was derived from epidemiologic studies and animal models with defect adenomatous polyposis coli (APC) gene. PGE2 induced by COX-2 exerts several biological properties that may be adv...
Familial colorectal cancer type X (FCCTX) is characterized by clinical features of hereditary non-polyposis colorectal cancer with a yet undefined genetic background. Here we identify the SEMA4A p.Val78Met germline mutation in an Austrian kindred with FCCTX, using an integrative genomics strategy. Compared with wild-type protein, SEMA4A(V78M) demonstrates significantly increased MAPK/Erk and PI...
A number of hereditary conditions have been identified that predispose to colorectal cancer. Most inherited forms of colorectal cancer can be placed into two groups, those that are associated with a pre-malignant phenotype (the “polyposis” syndromes) and those do not have a pre-malignant phenotype (generally termed “non-polyposis”). The polyposis syndromes can be further subdivided into two gro...
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