Adaptive mutability of colorectal cancers in response to targeted therapies | Zendy

Mariangela Russo | Zendy; Giovanni Crisafulli | Zendy; Alberto Sogari | Zendy; Nicole M. Reilly | Zendy; Sabrina Arena | Zendy; Simona Lamba | Zendy; Alice Bartolini | Zendy; Vito Amodio | Zendy; Alessandro Magrì | Zendy; Luca Novara | Zendy; Ivana Sarotto | Zendy; Zachary D. Nagel | Zendy; Cortt G. Piett | Zendy; Alessio Amatu | Zendy; Andrea SartoreBianchi | Zendy; Salvatore Siena | Zendy; Andrea Bertotti | Zendy; Livio Trusolino | Zendy; Mattia Corigliano | Zendy; Marco Gherardi | Zendy; Marco Cosentino Lagomarsino | Zendy; Federica Di Nicolantonio | Zendy; Alberto Bardelli | Zendy

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Adaptive mutability of colorectal cancers in response to targeted therapies

Author(s) -

Mariangela Russo,

Giovanni Crisafulli,

Alberto Sogari,

Nicole M. Reilly,

Sabrina Arena,

Simona Lamba,

Alice Bartolini,

Vito Amodio,

Alessandro Magrì,

Luca Novara,

Ivana Sarotto,

Zachary D. Nagel,

Cortt G. Piett,

Alessio Amatu,

Andrea SartoreBianchi,

Salvatore Siena,

Andrea Bertotti,

Livio Trusolino,

Mattia Corigliano,

Marco Gherardi,

Marco Cosentino Lagomarsino,

Federica Di Nicolantonio,

Alberto Bardelli

Publication year - 2019

Publication title -

science

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 12.556

H-Index - 1186

eISSN - 1095-9203

pISSN - 0036-8075

DOI - 10.1126/science.aav4474

Subject(s) - microsatellite instability , homologous recombination , colorectal cancer , dna mismatch repair , cancer research , biology , dna repair , mutation , epidermal growth factor receptor , drug resistance , mutant , cancer , gene , homologous chromosome , dna damage , dna , genetics , microsatellite , allele

A cross-kingdom tale of drug resistance Physicians who treat bacterial infections and those who treat cancer often face a common challenge: the development of drug resistance. It is well known that when bacteria are exposed to antibiotics, they temporarily increase their mutation rate, thus increasing the chance that a descendant antibiotic-resistant cell will arise. Russoet al. now provide evidence that cancer cells exploit a similar mechanism to ensure their survival after drug exposure (see the Perspective by Gerlinger). They found that human colorectal cancer cells treated with certain targeted therapies display a transient up-regulation of errorprone DNA polymerases and a reduction in their ability to repair DNA damage. Thus, like bacteria, cancer cells can adapt to therapeutic pressure by enhancing their mutability.Science , this issue p.1473 ; see also p.1458

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