Cancer Epigenetics: Tumor Heterogeneity, Plasticity of Stem-like States, and Drug Resistance DOI Creative Commons
Hariharan Easwaran, Hsing-Chen Tsai,

Stephen B. Baylin

et al.

Molecular Cell, Journal Year: 2014, Volume and Issue: 54(5), P. 716 - 727

Published: June 1, 2014

Language: Английский

Cancer Genome Landscapes DOI
Bert Vogelstein, Nickolas Papadopoulos, Victor E. Velculescu

et al.

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

7295

Genomic Classification and Prognosis in Acute Myeloid Leukemia DOI Open Access

Elli Papaemmanuil,

Moritz Gerstung, Lars Bullinger

et al.

New 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

3536

Clonal evolution in cancer DOI
Mel Greaves, Carlo C. Maley

Nature, Journal Year: 2012, Volume and Issue: 481(7381), P. 306 - 313

Published: Jan. 1, 2012

Language: Английский

Citations

2943

Clonal Heterogeneity and Tumor Evolution: Past, Present, and the Future DOI Creative Commons
Nicholas McGranahan, Charles Swanton

Cell, Journal Year: 2017, Volume and Issue: 168(4), P. 613 - 628

Published: Feb. 1, 2017

Language: Английский

Citations

2348

Tumour heterogeneity and cancer cell plasticity DOI

Corbin E. Meacham,

Sean J. Morrison

Nature, Journal Year: 2013, Volume and Issue: 501(7467), P. 328 - 337

Published: Sept. 17, 2013

Language: Английский

Citations

2287

The causes and consequences of genetic heterogeneity in cancer evolution DOI
Rebecca A. Burrell, Nicholas McGranahan, Jiří Bártek

et al.

Nature, Journal Year: 2013, Volume and Issue: 501(7467), P. 338 - 345

Published: Sept. 17, 2013

Language: Английский

Citations

2168

Evolution of the Cancer Stem Cell Model DOI Creative Commons

Antonija Kreso,

John E. Dick

Cell stem cell, Journal Year: 2014, Volume and Issue: 14(3), P. 275 - 291

Published: March 1, 2014

Language: Английский

Citations

2039

Clonal evolution in relapsed acute myeloid leukaemia revealed by whole-genome sequencing DOI Creative Commons
Li Ding, Timothy J. Ley, David E. Larson

et al.

Nature, 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

1945

Intra-tumour heterogeneity: a looking glass for cancer? DOI
Andriy Marusyk, Vanessa Almendro, Kornélia Polyák

et al.

Nature reviews. Cancer, Journal Year: 2012, Volume and Issue: 12(5), P. 323 - 334

Published: April 19, 2012

Language: Английский

Citations

1864

The Life History of 21 Breast Cancers DOI Creative Commons
Serena Nik‐Zainal, Peter Van Loo, David C. Wedge

et al.

Cell, Journal Year: 2012, Volume and Issue: 149(5), P. 994 - 1007

Published: May 1, 2012

Language: Английский

Citations

1402