Posts Tagged ‘cancer’
Nongenic cancer-risk SNPs affect oncogenes, tumour-suppressor genes, and immune function
February 8, 2020Tobacco smoking and somatic mutations in human bronchial epithelium
February 1, 2020https://www.nature.com/articles/s41586-020-1961-1
Tobacco smoking and somatic mutations in human bronchial epithelium
Kenichi Yoshida, Kate H. C. Gowers, Henry Lee-Six, Deepak P. Chandrasekharan, Tim Coorens, Elizabeth F. Maughan, Kathryn Beal, Andrew Menzies, Fraser R. Millar, Elizabeth Anderson, Sarah E. Clarke, Adam Pennycuick, Ricky M. Thakrar, Colin R. Butler, Nobuyuki Kakiuchi, Tomonori Hirano, Robert E. Hynds, Michael R. Stratton, Iñigo Martincorena, Sam M. Janes & Peter J. Campbell
Inherited determinants of early recurrent somatic mutations in prostate cancer | Nature Communications
December 29, 2019Germline finding of a genetic variant that could be linked to SPOP mutations. https://www.nature.com/articles/s41467-017-00046-0
interesting perspective on cancer research in wsj + upcoming book
October 8, 2019The focus is on improving detection vs. treatment of late stage disease.
https://www.wsj.com/articles/cancer-is-still-beating-uswe-need-a-new-start-11570206319
Attached: Cancer Therapy Advisor Q&A
March 17, 2019February 13, 2019
Q&A With Mark B. Gerstein, PhD, on Diagnostic Genomic vs Exomic Sequencing Bryant Furlow
https://www.cancertherapyadvisor.com/home/cancer-topics/general-oncology/qa-with-mark-b-gerstein-phd-on-diagnostic-genomic-vs-exomic-sequencing/
Sequence of events in prostate cancer
October 5, 2018Sequence of events in prostate #cancer, by @MarkARubin1
http://www.Nature.com/articles/d41586-018-06029-5 Discusses the high prevalence of AR-enhancer amplifications in recent studies
QT:{{”
“Quigley and colleagues performed whole-genome sequencing of 101 samples of metastatic, castration-resistant prostate-cancer tissue obtained from previous studies11,12. The most frequently altered genomic site identified was the AR-enhancer region, which was amplified in 81% of samples. The high prevalence of this type of amplification is notable because enhancer amplifications identified so far for other cancer types generally arise at much lower
frequency13–16. Moreover, the high prevalence of this AR-enhancer amplification in the data presented by Viswanathan and Quigley contrasts with its occurrence in only 1 of 54 previously published whole-genome sequences of prostate-cancer samples obtained before clinical treatment had commenced17.”
“}}
The Cancer Genome Atlas: Creating Lasting Value beyond Its Data
June 15, 2018Commentary
The Cancer Genome Atlas: Creating Lasting Value beyond Its Data Carolyn Hutter + Jean Claude Zenklusen
https://www.sciencedirect.com/science/article/pii/S009286741830374X