Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence from case-control and cohort studies and animal research is reviewed to examine whether oral contraceptive (OC) use is related to cancer of the kidney, colon, rectum, gall bladder, extrahepatic bile ducts, benign or malignant pituitary tumors or prolactinemia. While animal research suggests possible hormone sensitivity, there are only 2 cohort studies available on renal adeno-carcinoma; result are contradictory. Colon and rectal cancer are sometimes studied separately and sometimes together despite different etiologic factors. Colon cancer is less common in women of higher parity, and associated with other female sex hormone related cancers. 3 case-control studies have produced no consistent results except for a possible higher risk of right colon cancer in OC users. Cohort studies on colorectal cancer resulted in very few cases and no significant increase in risk for these very common malignancies among OC users. Gallbladder cancer is associated with gallstones, a condition known to be enhanced by estrogens, yet 1 case-control study found no change in risk. In contract, cancer of the extrahepatic bile duct, usually more common in men, was found to be elevated in OC users in 1 small study. The question of pituitary tumors is complicated by difficulties in diagnosis, differentiating between hyperplasia, microadenomas, galactorrhea, prolactinemia and cycle irregularity. Basic research indicates that estrogens stimulate prolactin secretion and development of pituitary tumors. Yet of 6 case-control studies only 2 reported relative risks significantly above 1. Only 6 cases have been found in 3 large cohort studies. Therefore it is probable that any association of pituitary tumors with pills is largely due to their prescription for women with menstrual irregularity, some of whom had pre-existing pituitary adenomas.
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PMID:Oral contraceptives and skin neoplasia. 186 36

We examined the cytosolic estrogen receptor (ER) level in tumor tissue from 77 patients: 36 meningiomas, 20 gliomas (12 glioblastomas, 2 cerebellar astrocytomas, 2 ependymomas, and 4 medulloblastomas), 8 neurinomas, 7 pituitary adenomas (2 prolactin-producing adenomas, 1 growth hormone-producing adenoma, and 4 nonfunctioning adenomas), and 6 metastatic brain tumors (1 from breast cancer, 4 from lung cancers, and 1 from colon cancer). Nuclear ER levels were assayed in 11 meningiomas and 2 glioblastomas. ER was determined by the dextran-coated charcoal method and calculated by Scatchard analysis. Cytosolic ER was detected in 100% of the pituitary adenomas, 50% of the meningiomas, 50% of the metastatic brain tumors, 25% of the neurinomas, and 15% of the gliomas. In gliomas, only medulloblastomas had ER activity. Nuclear ER was found in three premenopausal women with meningioma. The dissociation constant of the ER complex was, in each case, less than 10(-9) M. These observations suggest that some brain tumors may be responsive to estrogen via the cellular ER.
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PMID:Estrogen receptors in brain tumors. 650 47

Fifteen consecutive patients with recently diagnosed colorectal cancer were studied for plasma and tumor tissue prolactin content. In eight patients (four men and four postmenopausal females), preoperative high plasmatic prolactin was found (mean 1553 nmol; range 516-3677 nmol). In three of them, prolactin was also present in the tumor cells. All plasma prolactin levels returned to normal after tumor resection and remained so during a three-month follow-up. The tumor stage by Duke distribution was similar for both high and normal plasmatic prolactin patients. The role of prolactin in the pathogenesis of colorectal cancer, and as a marker of the tumor, remains to be established. This is the first time that prolactin has been detected in human colon cancer.
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PMID:Plasma and tumor prolactin in colorectal cancer patients. 755 57

The primary nutritionally linked diseases are coronary heart disease, stroke and cancers of the stomach, colon, pancreas, prostate, breast, ovary, and endometrium. Dietary fats operate through a promoting mechanism. An S-shaped dose-response curve with a threshold has been demonstrated in models of breast and colon cancer in which the standard Western fat intake of 40% of energy yields a high level of promotion, and reduction of fat to 10% to 20% of energy (the traditional Japanese fat intake) has a low promoting action. In models of breast and colon cancer, saturated fats such as beef fat or lard, and monounsaturated oils, such as olive oil, display only a weak promoting effect, with the incidence of induced tumors being similar at intake levels of 40% and 10% of energy. On the other hand, the n-6-polyunsaturated oils display a strong promoting effect. Such findings may have a parallel in the low but definitely increasing slope of postmenopausal breast cancer incidence in the past 30 years as the American public decreased saturated fat intake to avoid heart disease and increased use of the n-6-polyunsaturated oils. Mechanisms underlying the cancer-promoting effect in the colon stem from increased hepatic production of bile acids, which are transferred to the intestinal tract via the bile. Ingestion of 40% fat calories yields higher concentrations of bile acids in the colon than lower levels of dietary fat ingestion. Cancer in the mammary gland is promoted through higher concentrations of fats and phospholipids in the gland as well as increased levels of estrogen secondary to production by the ovary and other endocrine tissues that, in turn, affect the generation of pituitary hormones such as prolactin and growth hormone. The n-3-fats, as found in fish and fish oils, have a pronounced inhibitory effect in models of colon and breast cancer, presumably through their shifting of prostaglandin metabolism to the generation of prostaglandins, which lower cell proliferation potential and, thus, decrease promotional effects. The role of dietary fat as a promoter can be modified by other nutritional components. Finally, one of the best pieces of evidence for an enhancing effect of many dietary fats in the nutritionally linked cancers is the current increase in the incidence of these diseases in Japan as the nutritional habits of people in that country become more Westernized.
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PMID:Dietary fat and risk of chronic disease: mechanistic insights from experimental studies. 921 63

Two recent studies reported that many patients with colorectal carcinoma have elevated serum prolactin (PRL) concentrations and have suggested ectopic PRL secretion as the cause. In the present study, serum PRL was minimally elevated in 16 of 116 colon cancer patients and 2 of 25 control subjects; medications or chemotherapy appeared to be responsible for the PRL elevations in 11 of 16 cancer patients. Serum PRL was not correlated with either plasma carcinoembryonic antigen or disease stage. Preoperative and postoperative serum PRL concentrations were similar in 26 evaluated patients. None of 19 colorectal tumors was positive for PRL staining by immunohistochemistry. Thus, we could not confirm previous reports of frequent hyperprolactinemia in patients with colorectal cancer; factors such as medications, anxiety, pain, and nausea may have raised serum PRL in these earlier studies. Serum PRL is not a useful marker for colon carcinoma, at least in patients in the United States.
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PMID:Lack of association between hyperprolactinemia and colon carcinoma. 1070 75

The M(r) 16,000 NH(2)-terminal fragment of human prolactin (16K hPRL) is a potent antiangiogenic factor inhibiting endothelial cell function in vitro and neovascularization in vivo. The present study was undertaken to test the ability of 16K hPRL to inhibit the growth of human HCT116 colon cancer cells transplanted s.c. into Rag1(-/-) mice. For this purpose, HCT116 cells were stably transfected with an expression vector encoding a peptide that included the signal peptide and first 139 amino acid residues of human prolactin (HCT116(16K)). Stable clones of HCT116(16K) cells secreted large amounts of biologically active 16K hPRL into the culture medium. Growth of HCT116(16K) cells in vitro was not different from wild-type HCT116 (HCT116(wt)) or vector-transfected HCT116 (HCT116(vector)) cells. Addition of recombinant 16K hPRL had no effect on the proliferation of HCT116(wt) cells in vitro. Tumor growth of HCT116(16K) cells implanted into Rag1(-/-) mice was inhibited 63% in four separate experiments compared with tumors formed from HCT116(wt) or HCT116(vector) cells. Inhibition of tumor growth of HCT116(16K) cells was correlated with a decrease in microvascular density by 44%. These data demonstrate that biologically active 16K hPRL can be expressed and secreted from human colon cancer cells using a gene transfer approach and that production of 16K hPRL by these cells was capable of inhibiting tumor growth and neovascularization. These findings support the potential of 16K hPRL as a therapeutic agent for the treatment of colorectal cancer.
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PMID:Expression of the antiangiogenic factor 16K hPRL in human HCT116 colon cancer cells inhibits tumor growth in Rag1(-/-) mice. 1158 77

Serum concentrations of prolactin, a trophic hormone produced by the pituitary gland, have been shown to be raised in certain group of patients with cancer. Prolactin was detected in 0-20% of the colon cancer by immunohistochemistry and in plasma in 6-53% of the patients. These conflicting results do not support the hypothesis of an ectopic prolactin production by colon carcinoma. The aim of this study was to confirm the reported incidence of hyper-prolactinemia in colorectal cancer and to find further evidence for an ectopic prolactin production by the tumor. Thirty consecutive patients with colon carcinoma were studied. Before surgery all the patients underwent blood sample collection to assay plasma prolactin levels. All patients underwent colectomy. All the neoplastic specimens were tested with antiprolactin antibody. In none of the patients were significantly high preoperative levels of plasma prolactin found. Prolactin immunostaining was not identified in any of the tumor specimens. We could not confirm previous reports of frequent hyperprolactinemia in patients with cancer. This is the first report in which the incidence of both hyperprolactinemia and prolactin positive immunostaining was 0%. Our study was unable to demonstrate the synthesis of prolactin by colorectal cancers. The tumor is unlikely to be the source of hormone production. Our results suggest that circulating prolactin levels cannot be used as prognostic marker in patients with colon cancer.
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PMID:Plasma and tissue prolactin detection in colon carcinoma. 1160 64

Adult stem/progenitor cells are found in many tissues, where their primary role is to maintain homeostasis. Recent studies have evaluated the regulation of adult stem/progenitor cells by prolactin in various target tissues or cell types, including the mammary gland, the prostate, the brain, the bone marrow, the hair follicle, and colon cancer cells. Depending on the tissue, prolactin can either maintain stem cell quiescence or, in contrast, promote stem/progenitor cell expansion and push their progeny towards differentiation. In many instances, whether these effects are direct or involve paracrine regulators remains debated. This minireview aims to overview the current knowledge in the field.
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PMID:Minireview: prolactin regulation of adult stem cells. 2579 5