Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunoperoxidase staining for human keratin proteins was performed cytologically on samples from 90 patients with malignant tumors, and histologically on samples from 164 patients with malignant tumors. At the cytological level, almost all tumor cells not only in squamous cell carcinoma but also in nonsquamous cell carcinoma were positive for keratin proteins, in contrast with the apparent abscence of keratin proteins in sarcoma. At the histological level, almost all neoplastic cells of squamous cell carcinoma were positive for keratin proteins, the same as at the cytological level. In contrast, among cases of nonsquamous cell carcinoma, the frequency of appearance of keratin proteins varied according to the organ; it tended to be low in tumors with relatively good prognosis, such as carcinomas in the digestive system or thyroid cancer, and to be high in tumor with poor prognosis, such as pulmonary cancer, gallbladder cancer and endometrial cancer. However, there was a marked difference between the frequency of appearance of keratin proteins at the cytological level and that at the histological level, particularly in the cases of gastric cancer.
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PMID:The localization of human keratin proteins at cytological and histological levels in carcinomatous and sarcomatous lesions. 242 10

Carrying excess body fat is a leading cause of cancer. Epidemiologic evidence gives strong clues about the mechanisms that link excess adiposity to risk for several cancer sites. For postmenopausal breast cancer and endometrial cancer, the hyper-estrogenic state that is induced by excess body fatness is the likely cause. For esophageal cancer and gallbladder cancer, chronic local inflammation induced by acid reflux and gallstones is the likely cause, and for liver cancer, local inflammation induced by hepatic fatty infiltration is the likely cause. However, for several other cancers known to be associated with excess adiposity, including cancers of the colon, pancreas, ovary, kidney, and prostate, specific causes are not known. Possible candidates include elevated systemic or local tissue inflammation induced by adiposity and effects of the elevated levels of leptin, insulin, IGFs, and depressed immune function that are seen with excess adiposity. There is growing evidence that intentional weight loss not only reduces circulating levels of cancer-associated factors but that it also reduces cancer incidence and recurrence. Better research is needed to understand the mechanisms that link excess body fat to cancer risk as well as to understand the amount of weight loss needed for substantial cancer risk reduction. Finally, as we develop better understanding of the mediators of the effects of excess body fatness on cancer risk, we should identify pharmacologic interventions that target those mediators so that they can be used to complement weight loss in order to reduce cancer risk.
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PMID:Body fatness as a cause of cancer: epidemiologic clues to biologic mechanisms. 2587 Feb 50

The prevalence of obesity has increased substantially in the past in almost all countries of the world, and a further increase is expected for the future. Besides the well-established effects on type 2 diabetes and cardiovascular disease, there is convincing evidence today that obesity also increases the risk of several types of cancer, including colorectal cancer, postmenopausal breast cancer, endometrial cancer, renal cell carcinoma, esophageal adenocarcinoma, pancreatic cancer, and liver cancer. Obesity probably also increases the risk of ovarian cancer, advanced prostate cancer, gallbladder cancer, and gastric cardia cancer. For some cancer types, there is also some evidence that weight gain during adulthood increases cancer risk, e.g., colorectal cancer, postmenopausal breast cancer, endometrial cancer, and liver cancer. However, for most cancers, it is an open question as to whether vulnerability to weight gain in relation to cancer risk depends on specific life periods. There are a number of plausible mechanisms that may explain the relationship between obesity and cancer risk, including pathways related to insulin resistance, inflammation, and sex hormones. For most cancers, there is only limited evidence that weight loss in adulthood decreases cancer risk, which is primarily due to the limited long-term success of weight loss strategies among obese individuals. There is limited evidence suggesting that obesity may also be associated with poor prognosis among patients with colorectal cancer, breast cancer, endometrial cancer, ovarian cancer, and pancreatic cancer. Taken together, these findings support efforts to prevent weight gain on an individual level as well as on a population level. Whether and to what extent overweight or obese cancer patients benefit from weight loss strategies is unclear and needs to be addressed in future studies.
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PMID:Obesity and Risk of Cancer: An Introductory Overview. 2790 99

In various cancers, high-grade tumor and poor survival rate in patients with upregulated lncRNAs UCA1 have been confirmed. Urothelial carcinoma associated 1 (UCA1) is an oncogenic non-coding RNA with a length of more than 200 nucleotides. The UCA1 regulate critical biological processes that are involved in cancer progression, including cancer cell growth, invasion, migration, metastasis, and angiogenesis. So It should not surprise that UCA1 overexpresses in variety of cancers type, including pancreatic cancer, ovarian cancer, gastric cancer, colorectal cancer, breast cancer, prostate cancer, endometrial cancer, cervical cancer, bladder cancer, adrenal cancer, hypopharyngeal cancer, oral cancer, gallbladder cancer, nasopharyngeal cancer, laryngeal cancer, osteosarcoma, esophageal squamous cell carcinoma, renal cell carcinoma, cholangiocarcinoma, leukemia, glioma, thyroid cancer, medulloblastoma, hepatocellular carcinoma and multiple myeloma. In this article, we review biological function and regulatory mechanism of UCA1in several cancers and also, we will discuss the potential of its as cancer biomarker and cancer treatment.
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PMID:The Functional Role of Long Non-coding RNA UCA1 in Human Multiple Cancers: a Review Study. 3256 Jun 5