Replication fork stability confers chemoresistance in BRCA-deficient cells

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Standard

Replication fork stability confers chemoresistance in BRCA-deficient cells. / Chaudhuri, Arnab Ray; Callen, Elsa; Ding, Xia; Gogola, Ewa; Duarte, Alexandra A; Lee, Ji-Eun; Wong, Nancy; Lafarga, Vanessa; Calvo, Jennifer A; Panzarino, Nicholas J; John, Sam; Day, Amanda; Crespo, Anna Vidal; Shen, Binghui; Starnes, Linda M; de Ruiter, Julian R; Daniel, Jeremy A; Konstantinopoulos, Panagiotis A; Cortez, David; Cantor, Sharon B; Fernandez-Capetillo, Oscar; Ge, Kai; Jonkers, Jos; Rottenberg, Sven; Sharan, Shyam K; Nussenzweig, André.

I: Nature, Bind 535, Nr. 7612, 2016, s. 382-7.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Chaudhuri, AR, Callen, E, Ding, X, Gogola, E, Duarte, AA, Lee, J-E, Wong, N, Lafarga, V, Calvo, JA, Panzarino, NJ, John, S, Day, A, Crespo, AV, Shen, B, Starnes, LM, de Ruiter, JR, Daniel, JA, Konstantinopoulos, PA, Cortez, D, Cantor, SB, Fernandez-Capetillo, O, Ge, K, Jonkers, J, Rottenberg, S, Sharan, SK & Nussenzweig, A 2016, 'Replication fork stability confers chemoresistance in BRCA-deficient cells', Nature, bind 535, nr. 7612, s. 382-7. https://doi.org/10.1038/nature18325

APA

Chaudhuri, A. R., Callen, E., Ding, X., Gogola, E., Duarte, A. A., Lee, J-E., Wong, N., Lafarga, V., Calvo, J. A., Panzarino, N. J., John, S., Day, A., Crespo, A. V., Shen, B., Starnes, L. M., de Ruiter, J. R., Daniel, J. A., Konstantinopoulos, P. A., Cortez, D., ... Nussenzweig, A. (2016). Replication fork stability confers chemoresistance in BRCA-deficient cells. Nature, 535(7612), 382-7. https://doi.org/10.1038/nature18325

Vancouver

Chaudhuri AR, Callen E, Ding X, Gogola E, Duarte AA, Lee J-E o.a. Replication fork stability confers chemoresistance in BRCA-deficient cells. Nature. 2016;535(7612):382-7. https://doi.org/10.1038/nature18325

Author

Chaudhuri, Arnab Ray ; Callen, Elsa ; Ding, Xia ; Gogola, Ewa ; Duarte, Alexandra A ; Lee, Ji-Eun ; Wong, Nancy ; Lafarga, Vanessa ; Calvo, Jennifer A ; Panzarino, Nicholas J ; John, Sam ; Day, Amanda ; Crespo, Anna Vidal ; Shen, Binghui ; Starnes, Linda M ; de Ruiter, Julian R ; Daniel, Jeremy A ; Konstantinopoulos, Panagiotis A ; Cortez, David ; Cantor, Sharon B ; Fernandez-Capetillo, Oscar ; Ge, Kai ; Jonkers, Jos ; Rottenberg, Sven ; Sharan, Shyam K ; Nussenzweig, André. / Replication fork stability confers chemoresistance in BRCA-deficient cells. I: Nature. 2016 ; Bind 535, Nr. 7612. s. 382-7.

Bibtex

@article{80c8d45a321344b6a801a33ea26bdb50,
title = "Replication fork stability confers chemoresistance in BRCA-deficient cells",
abstract = "Cells deficient in the Brca1 and Brca2 genes have reduced capacity to repair DNA double-strand breaks by homologous recombination and consequently are hypersensitive to DNA-damaging agents, including cisplatin and poly(ADP-ribose) polymerase (PARP) inhibitors. Here we show that loss of the MLL3/4 complex protein, PTIP, protects Brca1/2-deficient cells from DNA damage and rescues the lethality of Brca2-deficient embryonic stem cells. However, PTIP deficiency does not restore homologous recombination activity at double-strand breaks. Instead, its absence inhibits the recruitment of the MRE11 nuclease to stalled replication forks, which in turn protects nascent DNA strands from extensive degradation. More generally, acquisition of PARP inhibitors and cisplatin resistance is associated with replication fork protection in Brca2-deficient tumour cells that do not develop Brca2 reversion mutations. Disruption of multiple proteins, including PARP1 and CHD4, leads to the same end point of replication fork protection, highlighting the complexities by which tumour cells evade chemotherapeutic interventions and acquire drug resistance.",
keywords = "Journal Article, Research Support, N.I.H., Intramural, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, Non-P.H.S.",
author = "Chaudhuri, {Arnab Ray} and Elsa Callen and Xia Ding and Ewa Gogola and Duarte, {Alexandra A} and Ji-Eun Lee and Nancy Wong and Vanessa Lafarga and Calvo, {Jennifer A} and Panzarino, {Nicholas J} and Sam John and Amanda Day and Crespo, {Anna Vidal} and Binghui Shen and Starnes, {Linda M} and {de Ruiter}, {Julian R} and Daniel, {Jeremy A} and Konstantinopoulos, {Panagiotis A} and David Cortez and Cantor, {Sharon B} and Oscar Fernandez-Capetillo and Kai Ge and Jos Jonkers and Sven Rottenberg and Sharan, {Shyam K} and Andr{\'e} Nussenzweig",
year = "2016",
doi = "10.1038/nature18325",
language = "English",
volume = "535",
pages = "382--7",
journal = "Nature",
issn = "0028-0836",
publisher = "nature publishing group",
number = "7612",

}

RIS

TY - JOUR

T1 - Replication fork stability confers chemoresistance in BRCA-deficient cells

AU - Chaudhuri, Arnab Ray

AU - Callen, Elsa

AU - Ding, Xia

AU - Gogola, Ewa

AU - Duarte, Alexandra A

AU - Lee, Ji-Eun

AU - Wong, Nancy

AU - Lafarga, Vanessa

AU - Calvo, Jennifer A

AU - Panzarino, Nicholas J

AU - John, Sam

AU - Day, Amanda

AU - Crespo, Anna Vidal

AU - Shen, Binghui

AU - Starnes, Linda M

AU - de Ruiter, Julian R

AU - Daniel, Jeremy A

AU - Konstantinopoulos, Panagiotis A

AU - Cortez, David

AU - Cantor, Sharon B

AU - Fernandez-Capetillo, Oscar

AU - Ge, Kai

AU - Jonkers, Jos

AU - Rottenberg, Sven

AU - Sharan, Shyam K

AU - Nussenzweig, André

PY - 2016

Y1 - 2016

N2 - Cells deficient in the Brca1 and Brca2 genes have reduced capacity to repair DNA double-strand breaks by homologous recombination and consequently are hypersensitive to DNA-damaging agents, including cisplatin and poly(ADP-ribose) polymerase (PARP) inhibitors. Here we show that loss of the MLL3/4 complex protein, PTIP, protects Brca1/2-deficient cells from DNA damage and rescues the lethality of Brca2-deficient embryonic stem cells. However, PTIP deficiency does not restore homologous recombination activity at double-strand breaks. Instead, its absence inhibits the recruitment of the MRE11 nuclease to stalled replication forks, which in turn protects nascent DNA strands from extensive degradation. More generally, acquisition of PARP inhibitors and cisplatin resistance is associated with replication fork protection in Brca2-deficient tumour cells that do not develop Brca2 reversion mutations. Disruption of multiple proteins, including PARP1 and CHD4, leads to the same end point of replication fork protection, highlighting the complexities by which tumour cells evade chemotherapeutic interventions and acquire drug resistance.

AB - Cells deficient in the Brca1 and Brca2 genes have reduced capacity to repair DNA double-strand breaks by homologous recombination and consequently are hypersensitive to DNA-damaging agents, including cisplatin and poly(ADP-ribose) polymerase (PARP) inhibitors. Here we show that loss of the MLL3/4 complex protein, PTIP, protects Brca1/2-deficient cells from DNA damage and rescues the lethality of Brca2-deficient embryonic stem cells. However, PTIP deficiency does not restore homologous recombination activity at double-strand breaks. Instead, its absence inhibits the recruitment of the MRE11 nuclease to stalled replication forks, which in turn protects nascent DNA strands from extensive degradation. More generally, acquisition of PARP inhibitors and cisplatin resistance is associated with replication fork protection in Brca2-deficient tumour cells that do not develop Brca2 reversion mutations. Disruption of multiple proteins, including PARP1 and CHD4, leads to the same end point of replication fork protection, highlighting the complexities by which tumour cells evade chemotherapeutic interventions and acquire drug resistance.

KW - Journal Article

KW - Research Support, N.I.H., Intramural

KW - Research Support, Non-U.S. Gov't

KW - Research Support, U.S. Gov't, Non-P.H.S.

U2 - 10.1038/nature18325

DO - 10.1038/nature18325

M3 - Journal article

C2 - 27443740

VL - 535

SP - 382

EP - 387

JO - Nature

JF - Nature

SN - 0028-0836

IS - 7612

ER -

ID: 164136217