2 Crazy Information On Transducin
001). Correlation of p-mTOR expression with outcome in PCa showed a significant association with pathological stage (P?=?0.003) but Staurosporine chemical structure not pre-operative PSA (P?=?0.271) or Gleason score (P?=?0.105). Conclusions: This study demonstrates that p-mTOR signalling has a potential role in the initiation and progression of PCa and is associated with advanced stage disease. These data not only provide further support for the use of rapamycin analogues in the treatment of prostate cancer, but identify mTOR as a potential target for chemoprevention. J. Tie1,2,3, I. Kinde4, H.-L. Wong1,3,5, J. McKendrick5, M. Singh6, C. Karapetis7, J. Desai1,3,8, B. Tran1,2,3, J. Roebert9, K. Kinzler4, B. Vogelstein4, P. Gibbs1,2,3,10 1The Royal Melbourne Hospital, Melbourne, Australia, 2Western Hospital, Melbourne, Australia, 3Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia, 4Ludwig Center for Cancer Genetics and Therapeutics, Howard Hughes Medical Institute at Johns Hopkins Kimmel Cancer Center, Philadelphia, USA, 5Box Hill Hospital, Melbourne, Australia, 6Andrew Love Cancer Centre, Melbourne, Australia, 7Flinders Medical Centre, Adelaide, Australia, 8Peter MacCallum Cancer Centre, Melbourne, Australia, 9MIA Victoria, Melbourne, Australia, 10BioGrid Australia, Melbourne, Australia Background: Prognostic and predictive biomarkers in mCRC are urgently needed. Analysis of ctDNA has shown promise as a liquid biopsy, click here reflecting the evolving mutational status of the tumour. Here we explored baseline ctDNA as a prognostic marker, and early changes in ctDNA as a marker of chemotherapy response. Methods: Serial plasma samples and CEA were collected at baseline, day 3 (D3) and cycle 2 day 1 (C2D1) from 40 mCRC patients receiving standard combination chemotherapy. Restaging scans performed at 8 weeks were centrally assessed using RECIST criteria. Samples were analysed at Johns Hopkins Kimmel Cancer Center. Tumour tissue was analysed for hotspot mutations in TP53, APC, KRAS, BRAF, PIK3CA, FBXW7 and SMAD4. The same mutation was queried and quantified in plasma using a massively parallel sequencing platform (Safe-SeqS). Results: Preliminary data Transducin is available on 31 patients in this ongoing study. At least 1 mutation was found in 30 of 31 (97%) tumours, with matching ctDNA found in 28 of 30 patients (93%). Median baseline cell-free DNA (cfDNA) and ctDNA levels were 8.6?ng/ml (0.7�C168.7) and 238 copies/ml (0�C27,778), respectively. Patients with baseline cfDNA of ��35 compared with