Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0006142 (breast cancer)
 160,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sera from a group of patients with ovarian cancer had a statistically significant deficiency of alpha-L-fucosidase activity compared with sera from healthy females or female patients with cervical or breast cancer. Mixing experiments did not identify an inhibitor of alpha-L-fucosidase activity in the sera of ovarian cancer patients. Decreased activity of alpha-L-fucosidases was not associated with stage of disease, tumor burden, histologic type, or grade of differentiation. Unlike alpha-L-fucosidase, beta-man-nosidase and beta-N-acetylglucosamindase in sera of ovarian cancer patients were not deficient in activity. Examination of population data of healthy females and of pedigrees of ovarian cancer patients suggested that the quantitative activity alpha-L-fucosidase in serum was genetically determined. Of 60 healthy females, 4 had low enzyme activity (less than 100 U alpha-L-fucosidase/ml serum), 26 had intermediate activity (100-274 U alpha-L-fucosidase/ml), and 30 had high activity (275 U/ml), whereas of 44 ovarian cancer patients, 11 had low, 29 had intermediate, and 4 had high activity. Application of the Hardy-Weinberg law to these data revealed that low enzyme activity in sera was three times more prevalent in the ovarian cancer group, the allele for this low enzyme activity being two times more common. These observations suggested that deficiency of alpha-L-fucosidase activity in sera of females may be a hereditary condition associated with increased risk for development of ovarian cancer.
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PMID:Frequency of an allele for low activity of alpha-L-fucosidase in sera: possible increase in epithelial ovarian cancer patients. 694 42

Several recent epidemiological studies have shown an increase in breast cancer risk among women who have elevated plasma levels of testosterone, reduced levels of sex hormone-binding globulin (SHBG), and hence elevated levels of bioavailable androgens and estrogens not bound to SHBG. This endocrine profile is generally associated with obesity and chronic hyperinsulinemia, of which it is most likely a result. Lack of physical activity, obesity, and a diet rich in rapidly digestible carbohydrates and poor in fibre favour the development of insulin resistance and hyperinsulinemia. The elevated insulin levels, in turn are related to decreases in plasma and tissue levels of IGFBP-1 and IGFBP-2 (insulin-like growth factor-binding proteins), and this may increase the availability of insulin-like growth factor-I (IGF-I) to its receptors. Like insulin, IGF-I also inhibits the hepatic synthesis of SHBG, whereas both hormones stimulate the ovarian synthesis of sex steroids. Moreover, insulin and IGF-I can both enhance the development of breast tumours, through their cognate receptors within the mammary tissue. Taken together, these observations lead to the hypothesis that breast cancer risk may be increased in women with elevated plasma insulin levels, and/or with elevated levels of bioactive IGF-I. Hyperinsulinemia and an increased IGF-I bioactivity could thus be an important physiological link between a western lifestyle, overnutrition, a hyperandrogenic sex steroid profile, and increased breast cancer risk. Prospective cohort studies will be needed to test this hypothesis, and to study in greater detail the possible relationships of breast cancer risk with plasma levels of IGF-I and IGFBPs. Confirmation of a relationship of breast cancer risk with plasma insulin levels, on the one hand, or with total plasma IGF-I, on the other hand, could open up new perspectives for breast cancer prevention, either by changes in dietary intake patterns and physical activity, or by the use of certain chemopreventive drugs.
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PMID:[Plasma insulin, IGF-I and breast cancer]. 1130 43

We provide an overview of the role of adiposity, physical activity and diet in the risk for breast cancer in Mexican women. Lack of physical activity, diets high in carbohydrates and in glycemic load and low intake of folate and vitamin B12 have been shown to increase the risk of breast cancer in Mexican women, in particular postmenopausal breast cancer. Other dietary factors that may begin to play a more relevant role in breast cancer incidence in Mexico are alcohol intake and vitamin D status. Recommendations to maintain a healthy weight, practice moderate physical activity, decrease intake of rapidly absorbed carbohydrates and increase consumption of fruits and vegetables could have an important impact on the epidemic of breast cancer in Mexico.
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PMID:The role of obesity, physical activity and dietary factors on the risk for breast cancer: Mexican experience. 1996 72

Weight gain has been reported in early stage breast cancer patients during chemotherapy, but the involved mechanisms remain unclear. A chemotherapy-induced decrease of brown adipose tissue (BAT) activity may partly contribute to weight gain in these patients. A positron emission tomography/computed tomography scan was performed at baseline and after 1 course of docetaxel + trastuzumab treatment in 26 breast cancer women. Variation of the maximal standardized uptake value of BAT in the cervical and supraclavicular regions between the 2 measures was assessed according to weight changes. Overall, (18)F-FDG uptakes in BAT decreased by 11.3% after 1 course of chemotherapy (p = 0.03). No correlation was found between the baseline values of (18)F-FDG uptake and body mass index or age of patients, but as expected (18)F-FDG uptake was dependent on season period. Among the patients, 35% gained weight, 25% lost weight, and 40% remained stable. Women who gained weight during chemotherapy experienced a significant decrease of (18)F-FDG uptake in BAT (p = 0.005). Decreased activity of BAT was associated with body weight gain during chemotherapy. These original data suggest for the first time that BAT modulation by chemotherapy would be a potential contributor to body weight gain through blunted thermogenesis in breast cancer patients.
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PMID:Brown adipose tissue activity in relation to weight gain during chemotherapy in breast cancer patients: a pilot study. 2515 43

Calcitonin Gene-related Peptide (CGRP), Vasoactive Intestinal Peptide (VIP) and Substance P (SP) are sensory neuropeptides which may alter cancer growth through modulation of chronic inflammation. We recently reported that SP suppresses breast cancer growth and metastasis through neuroimmune modulation. These neuropeptides are hydrolyzed by Neprilysin (NEP) to bioactive fragments. Decreased activity of NEP was reported in clear cell and chromophobe type renal cell carcinoma (RCC). It is however not known how the levels of neuropeptides hydrolyzed with NEP changes in RCC. Decrease activity of SP and CGRP containing sensory nerve endings was previously reported to increase cancer metastasis in animal models. It is however not known how peptidergic nerve endings are altered in RCC. Hence we here evaluated the levels of neuronal and non-neuronal neuropeptides and NEP activity in RCC including papillary type as well as neighboring uninvolved kidney. A cross-sectional study was conducted in 57 patients undergoing radical nephrectomy and diagnosed with RCC. NEP activity, levels and expression were determined using flourogenic substrate, western blot and qPCR respectively in freshly-frozen tissues. Immunohistochemical analyses were also performed. Neuronal and non-neuronal levels of CGRP, SP and VIP levels were determined using two-step acetic acid extraction. Levels and activity of NEP were markedly decreased in RCC regardless of subtype. Similar levels of VIP were detected in first and second extractions. VIP levels were higher in clear cell and papillary RCC compared to nearby kidney tissue. VIP levels of neighboring kidney tissue of papillary type RCC was significantly lower compared to kidney samples from clear cell RCC. CGRP levels were higher in second extraction. Similar to VIP levels, CGRP levels of neighboring kidney tissue from clear cell and chromophobe type RCC was significantly lower compared to corresponding tumor samples, an effect observed in the second extraction. VIP and CGRP levels of nearby kidney tissue varied subtype dependently demonstrating that different subtypes of RCC alter their local environment differently. Furthermore NEP-induce hydrolysis of VIP creates selective VPAC-1 receptor agonist which has anti-proliferative and anti-inflammatory effects. Hence loss of NEP activity may prevent anti-tumoral effects of VIP on RCC.
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PMID:Neuropeptide Levels as well as Neprilysin Activity Decrease in Renal Cell Carcinoma. 2776 99