The hyperactive PARP can also be the release of apoptosis Factor induction of cell death and mitochondria and cause necrosis. PARP inhibitors mimic more NAD ԧ block and inhibit the binding of the PARP enzyme and base excision repair NAD . In tumor cells with BRCA and BRCA AZD1152-HQPA Barasertib deficiency in DSB repair is crossed out Gardens colleagues adversely recombination repair pathways Chtigt. Also blocking PARP inhibitor-induced SSB, replication forks blocked, and persistent CSD ultimately lead to cell cycle arrest and apoptosis. Erh Hte block cell death by repair of SSB and DSB is caused as synthetic lethality t known. r about his In the excision of the base Sch The in DNA, PARP was also in other important functions, the growth of cancer, such as tumor angiogenesis, thanks to the modulation part of tumor hypoxia inducible factor release and Vaskul Ren endothelial growth factor Given the BRCA Seen pathway dysfunction in sporadic TNBC should theoretically PARP inhibitors.
not only in the tumors of tears liked the BRCA gene mutations effective, but also in sporadic TNBC as well Currently, clinical trials immerse the effectiveness of PARP inhibitors in both groups of patients w While Telaprevir experimental research into the mechanisms of suppression of tumor growth and pr Predictive marker for response to treatment with PARP inhibitor. The anti-angiogenic VEGF anti Visible in TNBC, Vaskul Ren Endothelial growth factor, which increased a key role in angiogenesis Can be ht play an r Important in the progression of the disease given TNBC subtype, s preference for the high proliferation.
VEGF stimulates the proliferation and migration of epithelial cells, inhibits apoptosis of endothelial tissue, erh Ht Gef Permeability t And vasodilation. Bevacizumab, is the best known angiogenic agents Anti a humanized monoclonal Body that binds to VEGF and prevents interaction with Vaskul Have Ren endothelial bevacizumab shown value is, when combined with chemotherapy patients combined negative breast cancer in hormone receptor, but as a group benefit and toxicity t of anti-angiogenesis in the treatment of breast cancer has not been clearly defined. EGFR EGFR anti Although SA is not a specific marker base as breast cancer, its overexpression has been found, and these tumors can survive a prognostic marker in significant long-term. In Similar way, an over-expression of EGFR found in TNBC estrogen and may be an inverse relationship between the expression of receptors for EGFR amplification and be.
TNBC cell growth and survival may be assisted by ligands by signaling via EGFR expression and increased FITTINGS concentrations. TIMP expression, an endogenous inhibitor of several matrix elements and ADAM metalloproteinase family, erb B inhibits ligand and receptor shedding by tumor and tumor suppression in vivo. In many human tumors, the expression of TIMP reduced in correlation with the thwart diseases. These results suggest that ADAM inhibitor INCB and TMI, a specific inhibitor of ADAM inhibit downstream signaling of all members of the EGFR family. Drugs have been developed to both the extracellular Re Dom ne of the EGFR and the intracellular targeting Re Dom ne. Clinical studies that cetuximab, a humanized antique Body anti-EGFR antique IgG panitunumab body, a human antique Body comprehensive fight against EGFR, gefitinib and erlotinib, both sm Tyrosine kinase inhibitors in TNBC all
molecules are encouraging.