PubMed · 5339920
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A Lambert, J P Deffez, B Bonnet, F Alliot. [Buccal localization disclosing reticulo-sarcoma].. https://pubmed.ncbi.nlm.nih.gov/5339920/
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HER-2 (c-erbB2, neu) receptor is the molecular marker of ductal breast cancer although it is verexpressed in other adenocarcinoma as well (e.g.endometrial, colorectal and lung cancers). The increased receptor expression is most frequently (90-97%) due to gene amplification. Detection of the overexpression of HER-2 helps to determine prognosis, to predict chemoresistance and to select for Herceptin therapy. HER-2 overexpression can be estimated either by immunohistochemistry or by fluorescent in situ hybridisation (FISH). Standardization of the immunohistochemical HER-2 tests is the best in HercepTest DAKO), however, the frequent 2+level requires complementary FISH test to verify gene amplification. This combination is not necessary at low (0-1+) or high (3+) level of immunohistochemical reactions, because the correlation with gene amplification status is acceptably high. Recently several new anti-HER-2 antibodies have been introduced into HER-2 diagnostics in various countries. According to our experiences we recommend to combine rationally the immunohistochemistry and FISH techniques to determine the HER-2 status in breast cancer.
Staurosporine and its derivative 7-hydroxystaurosporine are protein kinase inhibitors that are being considered for treatments of cancers. Several recent studies have shown that cells with defective pRB protein are resistant to the G(1) cell cycle-inhibiting effects of staurosporine compounds. In this study, we examined the effect of staurosporine on two breast cancer-derived and three lung cancer-derived cell lines characterized by deficiencies in the p16 tumor suppressor. All of these p16-deficient cell lines are highly sensitive to staurosporine-induced inhibition of pRB phosphorylation and induction of arrest in G(1). This response is similar to that seen in cultured normal human bronchial epithelial cells and normal mammary epithelial cells, but strikingly different than the staurosporine resistance seen in cancer cells with defective pRB. Interestingly, inhibition of pRB phosphorylation could be seen within 4 h of treatment, suggesting that this inhibition is a consequence of direct effects of staurosporine on protein kinase(s) rather than a result of induction of other cyclin-dependent kinase inhibitors. Our findings suggest that different types of cancer cells have vastly different responses to the staurosporine class of agents, and that evaluation of pRB and p16 will help predict the response of the cancer cells to these agents.
This study determined the selective cytotoxicity of eight coumarin compounds to human renal carcinoma cells, relative to non-carcinoma proximal tubular cells. Selectivity cytotoxicity was observed following exposure to 6-nitro-7-hydroxycoumarin (6-NO(2)-7-OHC) and 7,8-dihydroxycoumarin (7,8-OHC). 6-NO(2)-7-OHC induced cytotoxicity was irreversible in both cell lines, unlike 7,8-OHC, which was reversible in the carcinoma cells only. Mobility shift and BrdU incorporation assays showed that both compounds did not intercalate DNA but had a concentration-dependent inhibitory effect on its synthesis. All coumarins studied were found to be non-mutagenic using the standard Ames test. These results would suggest that 6-NO(2)-7-OHC and 7,8-OHC might have a therapeutic role to play in the treatment of renal cell carcinoma.