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)

Galectin-3, a member of the beta-galactoside-binding lectin family, is involved in several biological events including binding to the basement membrane glycoprotein laminin. Although the exact role of galectin-3 during the interactions between cells and laminin is not yet known, it has recently been observed that its expression is down-regulated at both the protein and the mRNA level in colon cancer tissues in correlation with progression of the disease. This study investigated the possibility that breast cancer cells might also exhibit decreased galectin-3 expression in association with their aggressiveness. The expression of galectin-3 was examined by immunoperoxidase staining, using a polyclonal antibody raised against recombinant galectin-3, in a collection of 98 human breast lesions including 12 fibroadenomas, 15 fibrocystic disease lesions, 22 in situ carcinomas, and 49 infiltrating ductal carcinomas, 19 of which had positive axillary lymph nodes. Normal breast tissue adjacent to the lesions was present in 59 biopsies. Normal breast tissue expressed high levels (3+) of galectin-3. High expression (2+ to 3+) was also found in most benign lesions examined. The expression of galectin-3 was significantly decreased in in situ carcinoma and this down-regulation was more pronounced in invasive ductal carcinoma, particularly when associated with infiltration of axillary lymph nodes. These data constitute the first observation that galectin-3 is down-regulated in breast cancer and suggest the decreased expression of this galactoside-binding lectin is associated with the acquisition of the invasive and metastatic phenotype.
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PMID:Decreased expression of galectin-3 is associated with progression of human breast cancer. 869 44

Bile acid conjugates are found in human breast cyst fluid in average concentrations about 50-fold greater than those in blood. Because epidemiologic studies have linked colon and breast cancer and aberrant bile acid profiles are associated with colon cancer risk, we decided to study the influence of bile acid conjugates (glycochenodeoxycholic acid, glycodeoxycholic acid, glycocholic acid, and glycolithocholic acid) on thymidine incorporation into DNA in cancer (MCF-7) and noncancer (MCF-10A) human mammary cell lines. The two lines responded differently. In MCF-7, bile acids, except for glycolithocholic acid, stimulated thymidine incorporation. Estradiol caused even greater stimulation, an effect that was not influenced further by the addition of bile acids. Bile acids suppressed incorporation in MCF-10A cells. Estradiol at 1 nM had no effect, but 10 nM estradiol was stimulatory. In most cases bile acids appeared to diminish the incorporations observed with estradiol alone, but not significantly. The relevance of these studies to the possible impact of bile acids on the course of fibrocystic disease of the breast would require further investigation.
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PMID:Effect of bile acids and estradiol on thymidine incorporation into DNA in MCF-7 and MCF-10A breast cell lines. 938 10