Why Chemotherapy Does Not Work: Cancer Genome Evolution and the Illusion of Oncogene Addiction

2016 ◽  
pp. 177-190
Author(s):  
Aleksei Stepanenko ◽  
Vadym Kavsan
Keyword(s):  
Genome Evolution ◽  
Cancer Genome ◽  
Oncogene Addiction

scholarly journals Predicting Human Genetic Interactions from Cancer Genome Evolution

PLoS ONE ◽  
2015 ◽  
Vol 10 (5) ◽  
pp. e0125795 ◽  
Author(s):  
Xiaowen Lu ◽  
Wout Megchelenbrink ◽  
Richard A. Notebaart ◽  
Martijn A. Huynen
Keyword(s):  
Genome Evolution ◽  
Cancer Genome ◽  
Genetic Interactions

scholarly journals Pervasive lesion segregation shapes cancer genome evolution

Nature ◽  
2020 ◽  
Vol 583 (7815) ◽  
pp. 265-270 ◽  
Author(s):  
Sarah J. Aitken ◽  
◽  
Craig J. Anderson ◽  
Frances Connor ◽  
Oriol Pich ◽  
...  
Keyword(s):  
Genome Evolution ◽  
Cancer Genome

scholarly journals Structural variant evolution after telomere crisis

2020 ◽  
Author(s):  
S.M Dewhurst ◽  
X Yao ◽  
Joel Rosiene ◽  
Huasong Tian ◽  
Julie Behr ◽  
...  
Keyword(s):  
Genome Evolution ◽  
Wide Spectrum ◽  
Cancer Genome ◽  
Short Telomere ◽  
Structural Variant ◽  
Evolutionary Lineages

AbstractTelomere crisis contributes to cancer genome evolution, yet only a subset of cancers display breakage-fusion-bridge (BFB) cycles and chromothripsis, hallmarks of previous experimental telomere crisis studies. We examine the spectrum of SVs instigated by natural telomere crisis. Spontaneous post-crisis clones from prior studies had both complex and simple SVs without BFB cycles or chromothripsis. In contrast, BFB cycles and chromothripsis occurred in clones that escaped from telomere crisis after CRISPR-controlled telomerase activation in MRC5 fibroblasts. This system revealed convergent evolutionary lineages altering one allele of 12p, where a short telomere likely predisposed to fusion. Remarkably, the 12p chromothripsis and BFB events were stabilized by independent fusions to 21. Telomere crisis can therefore generate a wide spectrum of SVs, and lack of BFB patterns and chromothripsis does not indicate absence of past crisis.

scholarly journals Tolerance of Whole-Genome Doubling Propagates Chromosomal Instability and Accelerates Cancer Genome Evolution

2014 ◽  
Vol 4 (2) ◽  
pp. 175-185 ◽  
Author(s):  
Sally M. Dewhurst ◽  
Nicholas McGranahan ◽  
Rebecca A. Burrell ◽  
Andrew J. Rowan ◽  
Eva Grönroos ◽  
...  
Keyword(s):  
Genome Evolution ◽  
Chromosomal Instability ◽  
Cancer Genome ◽  
Whole Genome ◽  
Genome Doubling ◽  
Whole Genome Doubling

scholarly journals TRPS1 drives heterochromatic origin refiring and cancer genome evolution

Cell Reports ◽  
2021 ◽  
Vol 34 (10) ◽  
pp. 108814
Author(s):  
Jianguo Yang ◽  
Xiaoping Liu ◽  
Yunchao Huang ◽  
Lin He ◽  
Wenting Zhang ◽  
...  
Keyword(s):  
Genome Evolution ◽  
Cancer Genome

scholarly journals DNA secondary structures and epigenetic determinants of cancer genome evolution

2010 ◽  
Vol 11 (Suppl 1) ◽  
pp. P10
Author(s):  
Subhajyoti De ◽  
Franziska Michor
Keyword(s):  
Genome Evolution ◽  
Secondary Structures ◽  
Cancer Genome ◽  
Dna Secondary Structures

scholarly journals Mechanisms Generating Cancer Genome Complexity: Back to the Future

Cancers ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3783
Author(s):  
Franck Toledo
Keyword(s):  
Genome Evolution ◽  
Fluorescent In Situ Hybridization ◽  
Chromosome Breakage ◽  
Cancer Genome ◽  
Hybridization Data ◽  
Genome Complexity ◽  
Amplification Mechanism ◽  
Cell Genome ◽  
Single Cell Genome

Understanding the mechanisms underlying cancer genome evolution has been a major goal for decades. A recent study combining live cell imaging and single-cell genome sequencing suggested that interwoven chromosome breakage-fusion-bridge cycles, micronucleation events and chromothripsis episodes drive cancer genome evolution. Here, I discuss the “interphase breakage model,” suggested from prior fluorescent in situ hybridization data that led to a similar conclusion. In this model, the rapid genome evolution observed at early stages of gene amplification was proposed to result from the interweaving of an amplification mechanism (breakage-fusion-bridge cycles) and of a deletion mechanism (micronucleation and stitching of DNA fragments retained in the nucleus).

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