
Molecular Cell, Journal Year: 2014, Volume and Issue: 54(5), P. 716 - 727
Published: June 1, 2014
Language: Английский
Molecular Cell, Journal Year: 2014, Volume and Issue: 54(5), P. 716 - 727
Published: June 1, 2014
Language: Английский
Science, Journal Year: 2013, Volume and Issue: 339(6127), P. 1546 - 1558
Published: March 28, 2013
Over the past decade, comprehensive sequencing efforts have revealed genomic landscapes of common forms human cancer. For most cancer types, this landscape consists a small number "mountains" (genes altered in high percentage tumors) and much larger "hills" infrequently). To date, these studies ~140 genes that, when by intragenic mutations, can promote or "drive" tumorigenesis. A typical tumor contains two to eight "driver gene" mutations; remaining mutations are passengers that confer no selective growth advantage. Driver be classified into 12 signaling pathways regulate three core cellular processes: cell fate, survival, genome maintenance. better understanding is one pressing needs basic research. Even now, however, our knowledge genomes sufficient guide development more effective approaches for reducing morbidity mortality.
Language: Английский
Citations
7295New England Journal of Medicine, Journal Year: 2016, Volume and Issue: 374(23), P. 2209 - 2221
Published: June 8, 2016
Recent studies have provided a detailed census of genes that are mutated in acute myeloid leukemia (AML). Our next challenge is to understand how this genetic diversity defines the pathophysiology AML and informs clinical practice.
Language: Английский
Citations
3536Nature, Journal Year: 2012, Volume and Issue: 481(7381), P. 306 - 313
Published: Jan. 1, 2012
Language: Английский
Citations
2943Cell, Journal Year: 2017, Volume and Issue: 168(4), P. 613 - 628
Published: Feb. 1, 2017
Language: Английский
Citations
2348Nature, Journal Year: 2013, Volume and Issue: 501(7467), P. 328 - 337
Published: Sept. 17, 2013
Language: Английский
Citations
2287Nature, Journal Year: 2013, Volume and Issue: 501(7467), P. 338 - 345
Published: Sept. 17, 2013
Language: Английский
Citations
2168Cell stem cell, Journal Year: 2014, Volume and Issue: 14(3), P. 275 - 291
Published: March 1, 2014
Language: Английский
Citations
2039Nature, Journal Year: 2012, Volume and Issue: 481(7382), P. 506 - 510
Published: Jan. 1, 2012
The sequencing of AML genomes eight patients before and after relapse reveals two major patterns clonal evolution, with chemotherapy appearing to have a role in both patterns. Many acute myeloid leukaemia (AML) achieve remission, but it is often short-lived the returned disease usually refractory therapy. Genome tumour cell evolution. founding clone survives all patients, and, one pattern, acquires new mutations expands at relapse. In other, subclone surviving from original then mutations. Comparisons relapse-specific primary point an increase transversions, implying DNA damage caused by cytotoxic chemotherapy. This work demonstrates that genome individual patient presents moving target, highlights importance striving eradicate its subclones. Most die progressive relapse, which associated evolution cytogenetic level1,2 . To determine mutational spectrum we sequenced validated hundreds somatic using deep sequencing; this allowed us define clonality precisely addition discovering novel, recurrently mutated genes (for example, WAC, SMC3, DIS3, DDX41 DAXX) AML, also found during relapse: (1) gained evolved into clone, or (2) survived initial therapy, additional expanded cases, failed clone. comparison versus cases revealed probably due These data demonstrate shaped, part, receive establish maintain remissions.
Language: Английский
Citations
1945Nature reviews. Cancer, Journal Year: 2012, Volume and Issue: 12(5), P. 323 - 334
Published: April 19, 2012
Language: Английский
Citations
1864Cell, Journal Year: 2012, Volume and Issue: 149(5), P. 994 - 1007
Published: May 1, 2012
Language: Английский
Citations
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