Rachel L. Flynn, PhD
Assistant Professor
Boston University School of Medicine
Dept of Pharmacology & Experimental Therapeutics

PhD, Umass Medical School



In the Laboratory of Genomic stability and Cancer Therapeutics we use a combination of biochemical and cell biological approaches to study the function of mammalian telomeres. Telomeres cap the ends of linear chromosomes and provide a molecular barrier for the human genome. Following each cell division, progressive telomere shortening erodes that barrier and compromises the stability of the genome. Critically short, or dysfunctional telomeres induce replicative senescence and/or cell death and ultimately, lead to cellular aging. Cancer cells, however, overcome the replicative senescence associated with critically short telomeres by exploiting mechanisms of telomere elongation. The focus of my lab is to understand the mechanisms regulating mammalian telomere maintenance and to understand how defects in this process contribute to premature aging and cancer progression. The hope is that these studies will allow us to gain the mechanistic insight necessary to define novel targets and/or strategies in the treatment of human disease.

Assistant Professor
Boston University School of Medicine
Medicine
Hematology & Medical Oncology Section

Peter Paul Career Development Professorship
Boston University



2013 Foster Foundation: Award for osteosarcoma research
2012 NIH: K99/R00 Pathway to Independence Award
2012 NIH: Scholarship for Telomere Biology and DNA Repair Conference
2009 NIH: F32 Individual Fellowship (declined for ACS)
2009-2012 ACS: Individual Fellowship
2007 University of Massachusetts Medical School: Graduate School of Biomedical Science Commencement Speaker
2007-2009 NIH: T32 Training Grant by the Department of Pathology under Dr. David Louis
2003 Sigma Xi, The Scientific Research Society of NA


Molecular Mechanisms Regulating the Alternative Lengthening of Telomeres Pathway
08/01/2016 - 07/31/2018 (PI)
NIH/National Cancer Institute
1R01CA201446-01A1

Functional characterization of the telomere repeat containIng RNA, TERRA, in telomere maintenance
03/17/2017 - 02/28/2018 (PI)
NIH/National Cancer Institute
1R01CA214880-01

Defining ATR function in the Alternative Lengthening of Telomeres Pathway
10/01/2015 - 09/30/2017 (PI)
Edward Mallinckrodt, Jr. Foundation

Targeting the Alternative Lengthening of Telomeres Pathway in Cancer
10/01/2015 - 09/30/2016 (PI)
Elsa U. Pardee Foundation

Suppression of genomic instability by tuning the DNA damage response at telomeres
06/01/2013 - 05/31/2016 (PI)
NIH/National Cancer Institute
5R00CA166729-04

Probing the Alternative Lengthening (ALT) Pathway in Osteosarcoma
09/01/2013 - 03/31/2015 (PI)
Foster Foundation



Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Faculty can login to make corrections and additions.

  1. Cox KE, Maréchal A, Flynn RL. SMARCAL1 Resolves Replication Stress at ALT Telomeres. Cell Rep. 2016 Feb 9; 14(5):1032-40.View Related Profiles. PMID: 26832416; DOI: 10.1016/j.celrep.2016.01.011;.
  2. Flynn RL, Cox KE, Jeitany M, Wakimoto H, Bryll AR, Ganem NJ, Bersani F, Pineda JR, Suvà ML, Benes CH, Haber DA, Boussin FD, Zou L. Alternative lengthening of telomeres renders cancer cells hypersensitive to ATR inhibitors. Science. 2015 Jan 16; 347(6219):273-7.View Related Profiles. PMID: 25593184; PMCID: PMC4358324; DOI: 10.1126/science.1257216;.
  3. Flynn RL, Chang S, Zou L. RPA and POT1: friends or foes at telomeres? Cell Cycle. 2012 Feb 15; 11(4):652-7. PMID: 22373525; PMCID: PMC3318101; DOI: 10.4161/cc.11.4.19061;.
  4. Flynn RL, Centore RC, O'Sullivan RJ, Rai R, Tse A, Songyang Z, Chang S, Karlseder J, Zou L. TERRA and hnRNPA1 orchestrate an RPA-to-POT1 switch on telomeric single-stranded DNA. Nature. 2011 Mar 24; 471(7339):532-6. PMID: 21399625; PMCID: PMC3078637; DOI: 10.1038/nature09772;.
  5. Flynn RL, Zou L. ATR: a master conductor of cellular responses to DNA replication stress. Trends Biochem Sci. 2011 Mar; 36(3):133-40. PMID: 20947357; PMCID: PMC3024454; DOI: 10.1016/j.tibs.2010.09.005;.
  6. Centore RC, Havens CG, Manning AL, Li JM, Flynn RL, Tse A, Jin J, Dyson NJ, Walter JC, Zou L. CRL4(Cdt2)-mediated destruction of the histone methyltransferase Set8 prevents premature chromatin compaction in S phase. Mol Cell. 2010 Oct 8; 40(1):22-33. PMID: 20932472; PMCID: PMC2957874; DOI: 10.1016/j.molcel.2010.09.015;.
  7. Flynn RL, Zou L. Oligonucleotide/oligosaccharide-binding fold proteins: a growing family of genome guardians. Crit Rev Biochem Mol Biol. 2010 Aug; 45(4):266-75. PMID: 20515430; PMCID: PMC2906097; DOI: 10.3109/10409238.2010.488216;.
  8. Xie J, Litman R, Wang S, Peng M, Guillemette S, Rooney T, Cantor SB. Targeting the FANCJ-BRCA1 interaction promotes a switch from recombination to poleta-dependent bypass. Oncogene. 2010 Apr 29; 29(17):2499-508. PMID: 20173781; PMCID: PMC2909592; DOI: 10.1038/onc.2010.18;.
  9. Litman R, Gupta R, Brosh RM Jr, Cantor SB. BRCA-FA pathway as a target for anti-tumor drugs. Anticancer Agents Med Chem. 2008; 8(4):426-30.
  10. Peng M, Litman R, Xie J, Sharma S, Brosh RM, 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. PMID: 17581638; PMCID: PMC1914102; DOI: 10.1038/sj.emboj.7601754;.
Showing 10 of 12 results. Show More

This graph shows the total number of publications by year, by first, middle/unknown, or last author.

Bar chart showing 12 publications over 9 distinct years, with a maximum of 4 publications in 2010

YearPublications
20051
20061
20071
20081
20104
20111
20121
20151
20161

Available to Mentor as: (Review Mentor Role Definitions):
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72 E. Concord St Silvio Conte (K)
Boston MA 02118
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