Rs with the h Chsten levels of Met with basal subtypes correlated, and breast cancer are Met with a signature transcriptional activation code in the first instance PCI-24781 CRA-02478 within the cluster core. Among these tumors, had an active Met expression profiling survive a worse prognosis and shorter disease free. Thesis of data transcription were recently best CONFIRMS through the analysis of genome copy number in cell lines BLBC Although cation focus MET amplification was not detected rkung that was ect designed to enrich the way of HGF / Met refl it, h INDICATIVE copy number gains and overexpression of the key adapter molecules downstream signal transducer and m possible.
In sum, offer studies on cell lines patientderived material, and in animal models shows clearly that preferably expressed in terms of BLBCs other subtypes SU11274 c-Met inhibitor of breast cancer Met While this is certainly correct to point out that the overexpression of Met fa can be observed is also nonbasal than in sporadic tumors: for example, an hour heres ma of Met in some F cases of HER2-positive and ER-positive breast cancers detected. Same holds true for other receptor tyrosine kinases EGFR and c-Kit includes: her expression is strongly correlated with BLBCs theseoncogenes but not only in this subtype of tumor expressed. In fact, if taken alone, none of the markers in the cluster core as independent Can operate Independent Press Predictors of k. Thesis marker but not defined in the rule kidney an algorithm which isolates of F BLBCs signifi cant in comparison to other facilities for breast cancer.
Met gene BRCA1 mutant cancer and basal basal Ph Phenotype as Th e group go Ren also a kind of familial Ren breast cancer in BRCA1 mutation carrier hunter. Th e presence of germline BRCA1 mutations increased The risk of developing breast and ovarian cancer in young women ht. Th e pathological and molecular characteristics of breast cancer in BRCA1 mutation carrier are spacious comparable to those observed in the basal like subtype: These tumors have a high-grade histology, high proliferation index and the limits, and the lack of ER, progesterone receptor and HER2 expression. The molecular function of one of the most important activity Th of the BRCA1 BRCA1 encompasses the regulation of doppelstr Ngigen DNA break repair through the process of homologous recombination.
Tumor cells which are not the expression of the BRCA1 gene are relatively sensitive to DNA beautiful digestion agent. Thesis cells are particularly sensitive to chemical inhibition of the polymerase poly, the accumulation of the DNA single strand, which is then converted to breaks in the DNA double strand w leads During replication. In normal cells, the DNA breaks doppelstr are Xed Independent fi by repair mechanisms with BRCA1 in cells lacking BRCA1, these L Emissions caused by fehleranf repaired Llige systems, as non-homologous end-joining, with the accumulation of complex chromosomal rearrangements and mutations to the closing Lich lead to cell death. Tumors in patients with mutated BRCA1 result by the presence of somatic inactivating mutations of the gene is p53. Genomic instability t would be caused by the loss of BRCA1 normally to cell cycle arrest by the checkpoint p53-mediated DNA-Sch Lead to, and eventually to apoptosis Lich. Th e simultaneous loss of p53 function aff ords the cell