An analogy between the evolution of drug resistance in bacterial communities and malignant tissues

被引：123

作者：

Lambert, Guillaume ^{[3
]}

Estevez-Salmeron, Luis ^{[1
,2
]}

Oh, Steve ^{[1
,2
]}

Liao, David ^{[1
,2
]}

Emerson, Beverly M. ^{[4
]}

Tlsty, Thea D. ^{[1
,2
]}

Austin, Robert H. ^{[3
]}

机构：

[1] Univ Calif San Francisco, Dept Pathol, San Francisco, CA 94143 USA

[2] Univ Calif San Francisco, Ctr Comprehens Canc, San Francisco, CA 94143 USA

[3] Princeton Univ, Dept Phys, Princeton, NJ 08544 USA

[4] Salk Inst Biol Studies, Regulatory Biol Lab, La Jolla, CA 92037 USA

来源：

NATURE REVIEWS CANCER | 2011年 / 11卷 / 05期

关键词：

HIGH MUTATION-RATES; PSEUDOMONAS-AERUGINOSA; PREDICTS PROGRESSION; CYSTIC-FIBROSIS; CANCER-CELLS; BIOFILMS; GROWTH; MUTAGENESIS; MECHANISMS; HYPERMUTATION;

D O I：

10.1038/nrc3039

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Cancer cells rapidly evolve drug resistance through somatic evolution and, in order to continue growth in the metastatic phase, violate the organism-wide consensus of regulated growth and beneficial communal interactions. We suggest that there is a fundamental mechanistic connection between the rapid evolution of resistance to chemotherapy in cellular communities within malignant tissues and the rapid evolution of antibiotic resistance in bacterial communities. We propose that this evolution is the result of a programmed and collective stress response performed by interacting cells, and that, given this fundamental connection, studying bacterial communities can provide deeper insights into the dynamics of adaptation and the evolution of cells within tumours.

引用

页码：375 / U138

页数：8

共 89 条

[21] VEGF-targeted therapy: mechanisms of anti-tumour activity [J].

Ellis, Lee M. ;

Hicklin, Daniel J. .

NATURE REVIEWS CANCER, 2008, 8 (08) :579-591

[22] Reconstruction of biochemical networks in microorganisms [J].

Feist, Adam M. ;

Herrgard, Markus J. ;

Thiele, Ines ;

Reed, Jennie L. ;

Palsson, Bernhard O. .

NATURE REVIEWS MICROBIOLOGY, 2009, 7 (02) :129-143

[23] Identification of additional genes belonging to the LexA regulon in Escherichia coli [J].

Fernández de Henestrosa, AR ;

Ogi, T ;

Aoyagi, S ;

Chafin, D ;

Hayes, JJ ;

Ohmori, H ;

Woodgate, R .

MOLECULAR MICROBIOLOGY, 2000, 35 (06) :1560-1572

[24] DNA Damage Drives an Activin A-Dependent Induction of Cyclooxygenase-2 in Premalignant Cells and Lesions [J].

Fordyce, Colleen ;

Fessenden, Tim ;

Pickering, Curtis ;

Jung, Jason ;

Singla, Veena ;

Berman, Hal ;

Tlsty, Thea .

CANCER PREVENTION RESEARCH, 2010, 3 (02) :190-201

[25] Why do cancers have high aerobic glycolysis? [J].

Gatenby, RA ;

Gillies, RJ .

NATURE REVIEWS CANCER, 2004, 4 (11) :891-899

[26] Costs and benefits of high mutation rates: Adaptive evolution of bacteria in the mouse gut [J].

Giraud, A ;

Matic, I ;

Tenaillon, O ;

Clara, A ;

Radman, M ;

Fons, M ;

Taddei, F .

SCIENCE, 2001, 291 (5513) :2606-2608

[27] Mutability and Importance of a Hypermutable Cell Subpopulation that Produces Stress-Induced Mutants in Escherichia coli [J].

Gonzalez, Caleb ;

Hadany, Lilach ;

Ponder, Rebecca G. ;

Price, Mellanie ;

Hastings, P. J. ;

Rosenberg, Susan M. .

PLOS GENETICS, 2008, 4 (10)

[28] Error-prone repair DNA polymerases in prokaryotes and eukaryotes [J].

Goodman, MF .

ANNUAL REVIEW OF BIOCHEMISTRY, 2002, 71 :17-50

[29] A microfluidic chemostat for experiments with bacterial and yeast cells [J].

Groisman, A ;

Lobo, C ;

Cho, HJ ;

Campbell, JK ;

Dufour, YS ;

Stevens, AM ;

Levchenko, A .

NATURE METHODS, 2005, 2 (09) :685-689

[30] Modelling the molecular circuitry of cancer [J].

Hahn, WC ;

Weinberg, RA .

NATURE REVIEWS CANCER, 2002, 2 (05) :331-341

← 1 2 3 4 5 6 7 8 9 →