Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04626 (erbB-2)
 5,251 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Metachronous or synchronous breast carcinoma following or co-existing with colorectal carcinoma are well recognised clinicopathological entities, and the risk of developing both possibly underlines the similarities in carcinogenesis pathways for these carcinomas. We present a 60-year-old housewife with a history of a treated primary colon carcinoma (Duke's C) 15 years previously. Six months ago, during the follow-up care a small sub-areolar lesion was determined in a mammogram. A lumpectomy was performed under local anaesthesia, which revealed an infiltrating ductal carcinoma (6 mm in greatest diameter). Immuno-histochemical assays for oestrogen and progesterone receptors and c-erb B2 ongoprotein were performed. Axillary lymphadenectomy showed 1/11 positive node. She received adjuvant radiotherapy and hormone manipulation. To date, seven months later she is disease free. The aim of this report is to emphasise the risk of metachronous second malignancy of breast or colorectal carcinoma following colorectal carcinomas. A second primary colonic malignancy following breast primary carcinoma is more frequent than inverse clinical form.
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PMID:Metachronous breast carcinoma (second malignancy), following "cure" from colorectal carcinoma. 1565 96

We examined the mechanism through which leptin increases Na(+), K(+)-ATPase activity in the rat kidney. Leptin was infused under anaesthesia into the abdominal aorta proximally to the renal arteries and then Na(+), K(+)-ATPase activity was measured in the renal cortex and medulla. Leptin (1mug/kgmin) increased Na(+), K(+)-ATPase activity after 3h of infusion, which was accompanied by the increase in urinary H(2)O(2) excretion and phosphorylation level of extracellular signal regulated kinase (ERK). The effect of leptin on ERK and Na(+), K(+)-ATPase was abolished by catalase, specific inhibitors of epidermal growth factor (EGF) receptor, AG1478 and PD158780, as well as by ERK inhibitor, PD98059, and was mimicked by both exogenous H(2)O(2) and EGF. The effect of leptin was also prevented by the inhibitor of Src tyrosine kinase, PP2. Leptin and H(2)O(2) increased Src phosphorylation at Tyr(418). We conclude that leptin-induced stimulation of renal Na(+), K(+)-ATPase involves H(2)O(2) generation, Src kinase, transactivation of the EGF receptor, and stimulation of ERK.
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PMID:H2O2 and Src-dependent transactivation of the EGF receptor mediates the stimulatory effect of leptin on renal ERK and Na+, K+-ATPase. 1697 40