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Cantor Lab Publications

Nicholas J. Panzarino, John Krais, Min Peng, Michelle Mosqueda, Sumeet Nayak, Samuel Bond, Jennifer Calvo, Ke Cong, Mihir Doshi, Matt Bere, Jianhong Ou, Bin Deng, Lihua Julie Zhu, Neil Johnson, Sharon B. Cantor. Replication gaps underlie BRCA-deficiency and therapy response.  Cancer Res 2020

Sumeet NayakJennifer A. Calvo, Ke CongMin PengEmily BerthiaumeJessica JacksonAngela M. ZainoAlessandro VindigniM. Kyle Haddenm Sharon B. Cantor Inhibition of the translesion synthesis polymerase REV1 exploits replication gaps as a cancer vulnerability.  Science Advances 2020 June 10.

Cantor SB. TPX2 joins 53BP1 to maintain DNA repair and fork stability. J Cell Biology 2019 Jan 11.

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. 

Wang Y, Ung M, Cantor SB, and Cheng C. Computational Investigation of Homologous Recombination DNA Repair Deficiency in Sporadic Breast Cancer. Scientific Reports, 2017 volume 7, 15742.

Suzuki S, Racine RR, Manalo NA, Cantor SB, Raffel GD. Impairment of fetal hematopoietic stem cell function in the absence of Fancd2.Experimental hematology. 2017; 48:79-86. PMID: 27915139 PMCID: PMC5362321

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 FORKMutat 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 CHD4Genes 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 responsesEMBO J. 2014 June 25: 10.15252/embj.201387530.

Guillemette S, Branagan A, Peng M, Dhruva A, Schärer OD, CantorSBFANCJ 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 ResponseMol 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.BFANCJ/BACH1 acetylation at lysine 1249 promotes a robust DNA Damage ResponsePLoS 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 SyndromeEMBOJ. 2011, Feb 16;30(4):692-705.

Jenny Xie, Min Peng, Shawna Guillemette, Candice Gilbert, Andrew Buermeyer,and Cantor, SBAn MLH1 mutation links FANCJ to colon cancer, MMR signaling, and insight towards directed therapyCancer 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 bypassOncogene, 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 exchangeJ Biol Chem. 2009 Mar 20;284(12):7505-17.

Siehler,Y.S, Marra, G, CantorSB, Gerischer, U, Schrauder, M, and Wiesmuller, L. Human MutL-Complexes Monitor Homologous Recombination Independently of Mismatch RepairDNA Repair. 2009 Feb 1;8(2):242-52.

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 proteinBlood. 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.

Gupta, R, Sharma, S, Doherty, KM, Sommers, JA, Cantor, SB., Brosh, RM Jr. Inhibition of BACH1 (FANCJ) helicase by backbone discontinuity is overcome by increased motor ATPase or length of loading strandNucleic Acids Res. 2006; 34:6673–6683.

Peng, M, Litman, R, Jin, Z, Fong, G, and Cantor, SB. BACH1 is a DNA repair protein supporting BRCA1 damage responseOncogene. 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 complexesGenes 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 FANCJCancer 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 cancerJ 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 mutationsProc Natl Acad Sci USA. 2004; 101:2357–62.

Joo, WD, Jeffrey, PD, Cantor, SB, Finnin, MS, Livingston, DM, Pavletich, N. Structure of the 3BP1 BRCT region bound to p53 and its comparison to the BRCA1 BRCT structureGenes Dev. 2002; 16:592–593.

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.

Chen, J, Silver, D, Cantor, SB, Livingston, DM, Scully, R. BRCA1, BRCA2, and Rad51 operate in a common DNA damage response pathwayCancer Res. 1999; 1752s–1756s.

Chen, J, Silver, D, Walpita, D, Cantor, SB, Gazdar, A, Tomlinson, G, Couch, F, Weber, B, Ashley, T, Livingston, D, Scully, R.  Stable interaction between the products of the BRCA1 and BRCA2 tumor suppressor genes in mitotic and meiotic cellsMol Cell. 1998; 2:317–328.

Feig, A, Urano, T, Cantor, SBEvidence for a Ras/Ral signaling cascadeTrends in Biochemical Sciences. 1996; 251:438–41.

Cantor, SB, Urano, T, Feig, LA.  Identification and characterization of RalBP1, a potential downstream target of RAL GTPasesMol Cell Biol. 1995; 15:4578– 84.

Complete List of Published Work in My Bibliography:
https://www.ncbi.nlm.nih.gov/sites/myncbi/sharon.cantor.2/bibliography/47668311/public/?sort=date&direction=ascending