BMS-387032 is that. PARPi only selective Abbot Tion of cancer cells that are not competent human resources without the repair cells This observation was quickly into clinical trials in which PARPi showed good anti-cancer activity of t In patients with BRCA1 and BRCA2 breast, ovarian and prostate cancer with only moderate toxicity Translated th. Human resources is a complex and multi-path components and pr Clinical data show that PARPi be useful in tumors without any of a number of these important proteins. The identification of these tumors potentially sensitive PARPi is the n HIGHEST challenge. Gene expression signatures and audit of the HR function can perform this function, but they are currently co Expensive and circumstances Spoken to be in clinical practice. Modern therapeutics against cancer of non-specific cytotoxic agents that affect both normal and cancer cells develop targeted therapies and personalized medicine.
Targeted therapies at the molecular signatures unique cancer Evodiamine cells directed produce more efficiency with less toxicity t. The development and use of therapeutic products as we resembled erm Practicing personalized medicine. Improving the treatment of cancer In this paper we summarize the pr clinical and clinical development of three large en Targeted Therapies: Murine double minute 2, anaplastic lymphoma kinase and polymerase inhibitors poly. Murine double minute 2 MDM2, also known as HDM2 in humans, is a negative regulator of the p53 tumor suppressor. Encodes a protein with 90 kDa MDM2 Bindungsdom Ne of p53 at the N-terminus and a RING Dom ne at the C-terminal, to be responsible for the E3 ligase p53 ubiquitination. When wild-type p53 by various stimuli, such as DNA-Sch Capitalized, MDM2 binds to p53 at the N-terminus of inhibiting the transcriptional activation of p53 and f Rdern the degradation of p53 by the ubiquitin-proteasome pathway.
MDM2 in various human tumors confinement, Lich melanoma, non-small cell lung cancer, breast cancer, cancer feeder run, Leuk mie, Non-Hodgkin’s lymphoma, and sarcoma s overexpressed. MDM2 is st with p53-mediated apoptosis and growth arrest of the tumor, t the most important oncogenic activity MDM2 Ren. Zus Tzlich MDM2 can cause carcinogenesis independently Ngig of p53. In the p53 mutant tumors with homozygous loss of MDM2, which mimics the inhibition of p53 MDM2 interaction can stabilize mutant p53 and increased Hte occurrence of metastases. overexpression of MDM2 was a positive correlation with a poor prognosis in sarcomas, gliomas and acute leukemia shown mie Lymphoma. In NSCLC, there were conflicting results as to whether the overexpression of MDM2 is associated with a poorer prognosis or the best, but subset analysis showed a poor prognosis for patients at an early stage NSCLC, especially those with an epidermal carcinoma with. Restore inhibition of MDM2 k P53 activity can t contains in cancers Lt wild-type p53, leading to the anti-tumor effect of apoptosis and inhibition of growth. Animal studies have shown, r