Select Cantor Lab Publications

Cong K, MacGilvary, Lee S, MacLeod S.G., Calvo, J, Peng M, Kousholt AN, Day T, Cantor S.B. FANCJ promotes PARP1 activity during DNA replication that is essential in BRCA1 deficient cells. Nature Communications 2024 in press/BioRxiv.

Whalen, J.M. and Cantor S.B. Unveiling the toxicity of single-stranded DNA gap through a yeast model. Nature Structural and Molecular Biology. 2023 July 6th.

Cong K, Cantor SB. Exploiting replication gaps for cancer therapy. Molecular Cell. 2022 May 13. https://doi.org/10.1016/j.molcel.2022.04.023.

Cong K, Peng M, Kousholt AN, Lee WTC, Lee S, Nayak S, Krais J, VanderVere-Carozza PS, Pawelczak KS, Calvo J, Panzarino NJ, Turchi JJ, Johnson N, Jonkers J, Rothenberg E, Cantor SB. Replication gaps are a key determinant of PARP inhibitor synthetic lethality with BRCA deficiency. Mol Cell. 2021 Aug 5;81(15):3128-3144.e7. doi: 10.1016/j.molcel.2021.06.011. Epub 2021 Jul 2.

Panzarino NJ, Krais JJ, Cong K, Peng M, Mosqueda M, Nayak SU, Bond SM, Calvo JA, Doshi MB, Bere M, Ou J, Deng B, Zhu LJ, Johnson N, Cantor SB. Replication Gaps Underlie BRCA Deficiency and Therapy Response. Cancer Research, 2021 Mar 1;81(5):1388-1397. doi: 10.1158/0008-5472.CAN-20-1602. Epub 2020 Nov 12. PMID: 33184108; PMCID: PMC8026497.

Calvo JA, Fritchman B, Hernandez D, Persky NS, Johannessen CM, Piccioni F, Kelch BA, Cantor SB. Comprehensive Mutational Analysis of the BRCA1-Associated DNA Helicase and Tumor-Suppressor FANCJ/BACH1/BRIP1. Mol Cancer Res. 2021 Jun;19(6):1015-1025. doi: 10.1158/1541-7786.MCR-20-0828. Epub 2021 Feb 22. PMID: 33619228; PMCID: PMC8178215.

Cantor SB. Revisiting the BRCA-pathway through the lens of replication gap suppression: "Gaps determine therapy response in BRCA mutant cancer". DNA Repair (Amst). 2021 Nov;107:103209. doi: 10.1016/j.dnarep.2021.103209. Epub 2021 Aug 13. PMID: 34419699; PMCID: PMC9049047.

Nayak S, Calvo JA, Cong K, Peng M, Berthiaume E, Jackson J, Zaino AM, Vindigni A, Hadden MK, Cantor SB. Inhibition of the translesion synthesis polymerase REV1 exploits replication gaps as a cancer vulnerability. Sci Adv. 2020 Jun 10;6(24):eaaz7808. doi: 10.1126/sciadv.aaz7808. PMID: 32577513; PMCID: PMC7286678.

Min Peng, Ke Cong, Nick Panzarino, Sumeet Nayak, Jennifer Calvo, Bin Deng, Lihua Julie Zhu, Monika Morocz, Lili Hegedus, Lajos Haracska, Cantor SB. Opposing roles of FANCJ and HLTF protect forks and restrain replication during stress. Cell Reports. 2018 Sept 18; 24, 3251–3261. PMC6218949

Cantor SB and Calvo J. Fork Protection and Chemoresistance in Hereditary Breast and Ovarian Cancer. Cold Spring Harbor Symposia on Quantitative Biology: Chromosome Segregation & Structure, Volume 82, 2018. 

Arnab Ray Chaudhuri, Elsa Callen, Xia Ding, Ewa Gogola, Alexandra A. Duarte, Ji-Eun Lee, Nancy Wong, Vanessa Lafarga, Jennifer A. Calvo, Nicholas J. Panzarino, Sam John, Amanda Day, Anna Vidal Crespo, Hua-Tang Chen, Binghui Shen, Linda M. Starnes, Jeremy Daniel, Julian R. de Ruiter, Panagiotis A. Konstantinopoulos, David Cortez, Cantor SB, Oscar Fernandez-Capetillo, Kai Ge, Jos Jonkers, Sven Rottenberg, Shyam K. Sharan, André Nussenzweig. Replication Fork Stability Confers Chemoresistance in BRCA-deficient Cells. Nature. 2016 Jul 21; (535), 382–387. PMC4959813

Cantor, SB, Nayak S. FANCJ at the FORK. Mutat Res. 2016 Feb 17. pii: S0027-5107(16)30013-6. doi: 10.1016/j.mrfmmm.2016.02.003.

Guillemette S, Serra R, Peng M, Hayes JA, Konstantinopoulos PA, Green MR, and. Cantor SB, Resistance to therapy in BRCA2 mutant cells due to loss of the nucleosome-remodeling factor CHD4. Genes and Development, 2015 Mar 1;29(5):489-94.

Min Peng, Jenny Xie, Anna Ucher, Janet Stavnezer & Cantor SB, Crosstalk between BRCA-Fanconi anemia and mismatch repair pathways prevents MSH2-dependent aberrant DNA damage responses. EMBO J. 2014 June 25: 10.15252/embj.201387530.

Guillemette S, Branagan A, Peng M, Dhruva A, Schärer OD, CantorSB. FANCJ localization by mismatch repair is vital to maintain genomic integrity after UV irradiation.Cancer Res. 2014 Feb 1;74(3):932-44. doi: 10.1158/0008-5472.CAN-13-2474. Epub 2013 Dec 18.

Avvaru N. Suhasini, Joshua A. Sommers, Parameswary A. Muniandy, Yan Coulombe, Cantor, SB., Jean-Yves Masson, Michael M. Seidman and Robert M. Brosh, Jr. Fanconi Anemia Group J Helicase and MRE11 Nuclease Interact to Facilitate the DNA Damage Response. Mol Cell Biol., 2013; 11, 2212-2227.

Jenny Xie, Min Peng, Shawna Guillmette, Steven Quan, Stephanie Maniatis Aditya Venkatesh, Scott Shaffer Yuliang Wu, Robert M. Brosh Jr, and Cantor, S.B.  FANCJ/BACH1 acetylation at lysine 1249 promotes a robust DNA Damage Response. PLoS Genetics.  2012 Jul;8(7).

Avaru N. Suhasini, Nina A. Rawtani, Yuliang Wu, Joshua A.  Sommers, Sudha Sharma, Georgina Mosedale, Phillip S. North, Cantor, S B, Ian D. Hickson, and Robert M. Brosh, Jr., Interaction between the Helicases Genetically Linked to Fanconi Anemia Group J and Bloom’s Syndrome. EMBOJ. 2011, Feb 16;30(4):692-705.

Jenny Xie, Min Peng, Shawna Guillemette, Candice Gilbert, Andrew Buermeyer,and Cantor, SB.  An MLH1 mutation links FANCJ to colon cancer, MMR signaling, and insight towards directed therapy. Cancer Prevention Research, 2010 Nov;3(11):1409-16.* featured on journal cover * subject of a perspective review

Jenny Xie, Rachel Litman,Shu Wang, Min Peng, Shawna Guillemette, Timothy Rooney, and Cantor, SB. Targeting the FANCJ-BRCA1 interaction promotes a switch from recombination to polη-dependent bypass. Oncogene, 2010;29(17):2499-508.

Sommers JA, Rawtani N, Gupta R, Bugreev DV, Mazin AV, Cantor, SB, Brosh RM. FANCJ uses its motor ATPase to disrupt protein-DNA complexes, unwind triplexes, and inhibit rad51 strand exchange. J Biol Chem. 2009 Mar 20;284(12):7505-17.

Barber, LJ, Youds, JL, Ward, JD, McIlwraith, MJ, O’Neil, N, Petalcorin, M, Martin, J, Collis,S, Cantor, SB, Auclair, M, Tissenbaum, H , West, S, Rose, A & Boulton, S. SPAR1/RTEL maintains genomic stability by suppressing homologous recombination.  Cell. 2008 Oct 17;135(2):261-71.

Gupta,R, Sharma, S, Sommers, J, Kenny, M, Cantor, SB, and Brosh, RM Jr.BACH1 (FANCJ) Helicase Forms DNA Damage Inducible Foci with Replication Protein A and Interacts Physically and Functionally with the Single–Stranded  DNA binding protein. Blood. 2007 Oct 1;110(7):2390-8.

Peng, M, Litman, R,Xie, X, Sharma, S, Brosh, RM Jr. and Cantor, SB. The FANCJ/MutLalpha interaction is required for correction of the cross-link response in FA-J cells.  EMBO J. 2007 Jul 11;26(13):3238-49.

Peng, M, Litman, R, Jin, Z, Fong, G, and Cantor, SB. BACH1 is a DNA repair protein supporting BRCA1 damage response. Oncogene. 2006; 25:2245–53.

Greenberg, R.A, Sobhian, B., Pathania, S, Cantor, SB., Nakatani, Y. and Livingston,D. Multifactorial contributions to an acute DNA damage response by BRCA1/BARD1–containing complexes. Genes and Dev. 2006; 20:34–4.  

Litman, R, Peng, M, Jin, Z, Zhang, F, Zhang, J, Powell, S, Andreassen, PR, Cantor, SB. BACH1 is critical for homologous recombination and appears to be the Fanconi anemia gene product FANCJ. Cancer Cell. 2005; 8:255–265

Gupta, R, Sharma, S, Sommers, JA, Jin, Z, Cantor, SB, Brosh, RM Jr. Analysis of the DNA substrate specificity of the human BACH1 helicase associated with breast cancer. J Biol Chem. 2005; 280:25450–60.

Cantor, SB, Drapkin, R, Zhang, F, Lin, Y, Han, J, Pamidi, S, Livingston, DM. The BRCA1–associated protein BACH1 is a DNA helicase targeted by clinically relevant inactivating mutations. Proc Natl Acad Sci USA. 2004; 101:2357–62.

Cantor, SB, Bell, D, Ganesan, S, Kass, E, Drapkin, R, Grossman, S, Wahrer, D, Sgroi, D, Lane, W, Haber, D, Livingston, D. BACH1, a novel helicase–like protein, interacts directly with BRCA1 and contributes to its DNA repair function. Cell. 2001; 105:149–160.