Zobrazeno 1 - 10
of 12
pro vyhledávání: '"Nicholas J. Panzarino"'
Autor:
Min Peng, Ke Cong, Nicholas J. Panzarino, Sumeet Nayak, Jennifer Calvo, Bin Deng, Lihua Julie Zhu, Monika Morocz, Lili Hegedus, Lajos Haracska, Sharon B. Cantor
Publikováno v:
Cell Reports, Vol 24, Iss 12, Pp 3251-3261 (2018)
Summary: The DNA helicase FANCJ is mutated in hereditary breast and ovarian cancer and Fanconi anemia (FA). Nevertheless, how loss of FANCJ translates to disease pathogenesis remains unclear. We addressed this question by analyzing proteins associate
Externí odkaz:
https://doaj.org/article/935ddf6285564b53bbb87c4cac17d059
Autor:
Sharon B. Cantor, Neil Johnson, Lihua J. Zhu, Bin Deng, Jianhong Ou, Matt Bere, Mihir B. Doshi, Jennifer A. Calvo, Samuel M. Bond, Sumeet U. Nayak, Michelle Mosqueda, Min Peng, Ke Cong, John J. Krais, Nicholas J. Panzarino
Defects in DNA repair and the protection of stalled DNA replication forks are thought to underlie the chemosensitivity of tumors deficient in the hereditary breast cancer genes BRCA1 and BRCA2 (BRCA). Challenging this assumption are recent findings t
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::06de07f4f7ad1796e1fb15bd0f3b947c
https://doi.org/10.1158/0008-5472.c.6512572.v1
https://doi.org/10.1158/0008-5472.c.6512572.v1
Autor:
Sharon B. Cantor, Neil Johnson, Lihua J. Zhu, Bin Deng, Jianhong Ou, Matt Bere, Mihir B. Doshi, Jennifer A. Calvo, Samuel M. Bond, Sumeet U. Nayak, Michelle Mosqueda, Min Peng, Ke Cong, John J. Krais, Nicholas J. Panzarino
Supplemental Figure Legends
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5154b074718c1c75fc74fd60d98c0d25
https://doi.org/10.1158/0008-5472.22427155
https://doi.org/10.1158/0008-5472.22427155
Autor:
Sharon B. Cantor, Neil Johnson, Lihua J. Zhu, Bin Deng, Jianhong Ou, Matt Bere, Mihir B. Doshi, Jennifer A. Calvo, Samuel M. Bond, Sumeet U. Nayak, Michelle Mosqueda, Min Peng, Ke Cong, John J. Krais, Nicholas J. Panzarino
Supplemental Figures 1-6. Figure S1: BRCA-deficient cancer cells fail to restrain replication in the presence of stress and ssDNA gaps develop. Figure S2: Replication restraint, depletion, and PDX controls. Figure S3: Depletion of SMARCAL1 or inhibit
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4895446f2204506ea34735722026f78a
https://doi.org/10.1158/0008-5472.22427161
https://doi.org/10.1158/0008-5472.22427161
Autor:
Ke Cong, John J. Krais, Michelle Mosqueda, Sharon B. Cantor, Sumeet Nayak, Lihua Julie Zhu, Jianhong Ou, Min Peng, Matt Bere, Neil Johnson, Samuel M. Bond, Jennifer A. Calvo, Bin Deng, Nicholas J. Panzarino, Mihir B. Doshi
Publikováno v:
Cancer Res
Defects in DNA repair and the protection of stalled DNA replication forks are thought to underlie the chemosensitivity of tumors deficient in the hereditary breast cancer genes BRCA1 and BRCA2 (BRCA). Challenging this assumption are recent findings t
Autor:
Eli Rothenberg, Ke Cong, Silviana Lee, Nicholas J. Panzarino, Katherine S. Pawelczak, Neil Johnson, Sumeet Nayak, Min Peng, Arne Nedergaard Kousholt, Pamela S. VanderVere-Carozza, Jos Jonkers, Jennifer A. Calvo, Wei Ting C. Lee, John J. Turchi, John J. Krais, Sharon B. Cantor
Publikováno v:
Mol Cell
Mutations in BRCA1 or BRCA2 (BRCA) is synthetic lethal with poly(ADP-ribose) polymerase inhibitors (PARPi). Lethality is thought to derive from DNA double-stranded breaks (DSBs) necessitating BRCA function in homologous recombination (HR) and/or fork
Autor:
Neil Johnson, Nicholas J. Panzarino, Arne Nedergaard Kousholt, Jennifer A. Calvo, Sharon B. Cantor, Matt Bere, Jos Jonkers, Sumeet Nayak, Wei Ting C. Lee, Eli Rothenberg, Ke Cong, Min Peng, John J. Krais
BRCA1 or BRCA2 (BRCA)-deficient tumor cells have defects in DNA double strand break repair by homologous recombination (HR) and fork protection (FP) that are thought to underlie the sensitivity to poly(ADP-ribose) polymerase inhibitor (PARPi). Given
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::11726f93dbf7fe1c10652ca816760bca
https://doi.org/10.1101/781989
https://doi.org/10.1101/781989
Publikováno v:
Clinical Cancer Research. 27:IA-026
Defects in DNA repair and/or the protection of stalled DNA replication forks are thought to underlie the chemosensitivity of tumors deficient in the hereditary breast cancer genes, BRCA1 and BRCA2 (BRCA). Challenging this assumption, recent findings
Autor:
Mónika Mórocz, Sumeet Nayak, Nicholas J. Panzarino, Min Peng, Ke Cong, Sharon B. Cantor, Lihua Julie Zhu, Jennifer A. Calvo, Bin Deng, Lajos Haracska, Lili Hegedus
Publikováno v:
Cell reports
Cell Reports, Vol 24, Iss 12, Pp 3251-3261 (2018)
Cell Reports, Vol 24, Iss 12, Pp 3251-3261 (2018)
SUMMARY The DNA helicase FANCJ is mutated in hereditary breast and ovarian cancer and Fanconi anemia (FA). Nevertheless, how loss of FANCJ translates to disease pathogenesis remains unclear. We addressed this question by analyzing proteins associated
Autor:
Ewa Gogola, Julian R. de Ruiter, Nicholas J. Panzarino, Xia Ding, Anna Vidal Crespo, Linda M. Starnes, Jeremy A. Daniel, Jennifer A. Calvo, Nancy Wong, André Nussenzweig, Ji-Eun Lee, Sharon B. Cantor, Arnab Ray Chaudhuri, Kai Ge, Vanessa Lafarga, Sam John, Oscar Fernandez-Capetillo, Binghui Shen, Jos Jonkers, Alexandra A. Duarte, David Cortez, Shyam K. Sharan, Panagiotis A. Konstantinopoulos, Sven Rottenberg, Amanda Day, Elsa Callen
Publikováno v:
Nature
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) i