Katharina Schlacher, Ph.D.
Department of Cancer Biology, Division of Discovery Science
About Katharina Schlacher
Dr Schlacher is an Associate Professor in the Department of Cancer Biology at the UT MD Anderson Cancer Center. She is a Rita Allen Foundation Fellow and CPRIT Scholar in Cancer Biology. She received her Ph.D. at the University of Southern California (USC) under Dr. Myron Goodman in biochemistry of error-prone DNA polymerases, after completing her Masters degree at the Karl-Franzens University Graz, Austria, under Dr. Ellen Zechner. During her post-doctoral training as a Damon Runyon Fellow under Dr. Maria Jasin at Memorial Sloan Kettering Cancer Center (NYC), which she performed concomitantly under Dr. Hong Wu at UCLA (Los Angeles), she pioneered investigations on replication fidelity under stress and discovered DNA replication fork protection as a new genome instability pathway. Replication fork protection has since been recognized a major genome instability suppressor and cancer therapy resistance pathway. By employing Fanconi Anemia (FA) as a genetic paradigm disease model in combination with atomic structure guidance, single molecule, single cell and animal models, her research focuses on understanding molecular mechanisms of DNA replication fork stability and stress response in both the mitochondria and nucleus. Importantly, her investigations are delineating how these processes suppress FA associated phenotypes of inflammation, tumorigenesis and diverse diseases including anemia, developmental disease and most recently autism at the molecular level to enable foundational knowledge for effective prevention and advanced treatment strategies.
Present Title & Affiliation
Dual/Joint/Adjunct Appointment
Associate Professor, Department of Cancer Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas
Research Interests
Research in my laboratory focuses on defining molecular mechanisms genome stability pathways during both nuclear and mitochondrial DNA replication. Guided by the teachings of human disease our goal is to develop a rigorous, molecular understanding of these fundamental processes that suppress diverse pathologies to enable new and effective strategies for prediction, prevention and treatment.
To do this, we combine single molecule, single cell and in vivo approaches with focus on Fanconi Anemia (FA) as a disease framework. FA is a prototypic inherited progeroid and cancer pre-dispositioning disease with a strikingly broad spectrum of disease presentations. These span from blood cancers, solid tumors, pancytopenia, developmental abnormalities, infertility, increased risk for diabetes and cardiac disease, and neuroinflammation to hypersensitivity to cancer therapeutics. The FA pathway is furthermore now genetically and phenotypically linked with autism. While scientifically challenging due to this diversity, with its genetically defined mutations FA provides a uniquely powerful opportunity to uncover foundational mechanistic knowledge that links these disease phenotypes at the molecular level.
In my efforts, I am motivated by an unwavering curiosity and passion to create new methods and integrate insights that may overcome limitations from current dogmas to enable expanded understanding. I discovered and defined DNA replication fork protection as a new distinct genome instability pathway involving BRCA1/2 and Fanconi Anemia (FA) tumor susceptibility genes (Cell 2011, Cancer Cell 2012). This insight opened a rich genome stability research field critical for cancer therapy response (discussed in Nature Cell Biology 2017, Nature 2018, Nature Rev Clinical Onc 2024, Nature Cancer 2025). Recently we found that BRCA/FA fork protection functions are mechanistically and genetically mutually exclusive from the DNA repair functions of these proteins (Mol. Cell 2025). This finding explains how mutations in cancer patients that confer fork protection defects are proficient for DNA repair (Nature Comm 2023a) and opens a new conceptual path for targeted treatment strategies. We developed single-cell microscopy assays for nuclear protein-DNA replication reactions, for DNA structures, and for mitochondrial replication reactions (eLife 2017, JCB 2018, Science Advances 2021). We generated unique Rad51c mouse models: we overcame embryonic lethality by creating CRISPR/Cas9 edited hypomorphic Rad51c and polygenic Rad51c+Brca2 FA mutant mice (Nature communications 2023b). Excitingly these develop the full spectrum of phenotypes for the pleiotropic human disease Fanconi Anemia. This includes small stature, infertility, developmental delays, bone marrow failure, high inflammation, chemotherapy sensitivity, and death due to acute T-cell leukemia. Enabled by our developed tools, I discovered that canonically nuclear BRCA/FA proteins are furthermore distinctively required in the mitochondria for mtDNA fork protection (Science Advances 2021). mtDNA fork protection too is physiologically and genetically separable from nuclear replication fork stability, amongst others by activating a unique form of innate immune signaling: a cGAS-dependent, Unphosphorylated-STAT1 (Un-P-STAT1) driven inflammation. Notably this is distinct and independent from canonical, nuclear DNA damage-induced type I interferon responses and linked to chemotherapy resistance, cardiac disease, and neuroinflammation. Our most recent work in FA and Rad51c mutant mice reveals that this mtDNA-mediated inflammation drives sex-specific physiological outcomes, including male-predominant obesity-associated macrophage reprogramming and anemia (BioRxiv 2024, currently under review at Science). Under the conditions tested, estrogen acts as a mitochondria-targeted antioxidant, reducing mtDNA replication stress and suppressing inflammation and anemia. mtDNA instability causing diet-induced anemia of inflammation underscores the physiological importance of this yet largely unexplored mitochondrial genome stability pathway.
Our long-term interest is to obtain an in-depth molecular understanding of the core mechanisms of DNA Fork Protection in both the nucleus and the mitochondria that drive physiological outcomes in the context of tumorigenesis, cancer treatments, anemia and fertility, and autism spectrum disease in the immediate future. My aspiration is that this new knowledge will provide a powerful scientific framework for advanced biomarker development, predicting disease predisposition, inferring drug treatment responses, and creating novel treatment strategies including smart-design combination therapies for treatment and potentially prevention.
Education & Training
Degree-Granting Education
| 2006 | USC, Los Angeles, California, US, Molecular Biology, Ph.D |
| 2003 | Karl-Franzens University, Graz, AT, Microbiology, Magistra Rerum Naturales |
Postgraduate Training
| 2008-2013 | Post-Doctoral Fellow (concurrently with MSKCC), UCLA, Los Angeles, California |
| 2007-2013 | Post-Doctoral Fellow, Memorial Sloan-Kettering Cancer Center, New York, New York |
Experience & Service
Faculty Academic Appointments
Assistant Professor, Department of Cancer Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas, 2014 - 2020
Administrative Appointments/Responsibilities
Chair of the Mike Hogg Award and Lecture, UT MD Anderson Cancer Center, 2023 - Present
Administrative core director of the CPRIT/BACIS multi-investigator award, UT MD Anderson Cancer Center, Houston, Texas, 2022 - 2024
Chair of the Faculty Senate Research Affairs Committee, UT MD Anderson Cancer Center, Houston, Texas, 2022 - 2023
Faculty Senator, UT MD Anderson Cancer Center, Houston, Texas, 2019 - 2025
Co-director Journal Club, Department of Cancer Biology, UT MD Anderson Cancer Center, Houston, Texas, 2015 - 2017
Co-director, Graduate School of Biological Sciences Core Course, UT MD Anderson Cancer Center an UT Health, Houston, Texas, 2015 - 2016
Other Professional Positions
Senior Research Scientist (concurrently), Memorial Sloan Kettering Cancer Center and University of California, Los Angeles, New York and Los Angeles, New York and California, 2013 - 2014
Senior Research Scientist, University of California, Los Angeles, California, 2013 - 2014
Editorial Activities
Editorial Board Member, eLife, 2020 - 2021
Scientific Editor, eLife, 2018 - 2020
Honors & Awards
| 2016 | Rita Allen Foundation Scholar, Rita Allen Foundation |
| 2016 | Sabin Family Foundation Fellow, Andrew Sabin Family Foundation |
| 2014 | UT Rising STARs Award, University of Texas Systems |
| 2014 | CPRIT Scholar in Cancer Biology, Cancer Prevention and Research Institute of Texas |
| 2012 | MSKCC Postdoctoral Research Award, Memorial Sloan-Kettering Cancer Center |
| 2012 | Nomination to Blavatnik Award, New York Academy of Sciences |
| 2011 | Parvin Foundation Award, University of California, Los Angeles |
| 2011 | Molecular Biology Institute Research Excellence Award, University of California, Los Angeles |
| 2011 | Nomination to Chancellor’s Award for Exceptional Accomplishment in Postdoctoral Research, University of California, Los Angeles |
| 2011 | EMS Best New Investigator Platform Presentation Award, Environmental Mutagen Society |
| 2010 | Award for best oral presentation by a postdoctoral fellow, University of California, Los Angeles |
| 2007 | Berger Foundation Fellowship, Damon Runyon Cancer Research Foundation |
| 2006 | College Doctoral Research Prize in Recognition for Outstanding Research by a Ph.D. student, College of Letters, Arts and Sciences, University of Southern California |
Professional Memberships
Selected Presentations & Talks
Local Presentations
- 2026. BRCA/FA and inflammation – a tale of two genome stabilities. Invited. Allison Institute Research Seminar. Houston, Texas, US.
- 2025. Molecular impacts of nutrition and hormones on BRCA2 – a tale of (more than one) genome stability. Invited. Energy Balance Research Seminar. Houston, Texas, US.
- 2022. Nuclear and mitochondrial genome stability. Invited. DREAM Team meetings. Houston, Texas, US.
- 2021. p53 and BRCA in DNA Replication Fork Stability. Invited. 2021 BACIS Retreat. Houston, Texas, US.
- 2021. Polygenic Brca/Fanc mutations act synergistically during cancer development and Fanconi Anemia. Invited. DREAM Team meetings. Houston, Texas, US.
- 2020. BRCA2 and Replication Instability. Invited. Ovarian Moonshot Work Group. Houston, Texas, US.
- 2020. BRCA and DNA Replication Fork Stability. Invited. 2020 BACIS Retreat. Houston, Texas, US.
- 2020. Replication fork protection and genome instability. Invited. Head & Neck & HPV Biomarkers Meeting. Houston, Texas, US.
- 2020. BRCA/FANC Mitochondrial DNA replication instability causes cGAS-dependent inflammation. Invited. ICON Meeting. Houston, Texas, US.
- 2020. Mitochondrial and Nuclear BRCA/Fanconi Anemia Tumor Suppressors in Disease and Inflammation. Invited. Department of Cancer Biology Seminar Series. Houston, Texas, US.
- 2020. Mitochondrial and Nuclear BRCA/Fanconi Anemia Tumor Suppressors in Disease and Inflammation. Invited. Work-In-Progress series. Houston, Texas, US.
- 2019. BRCA and DNA replication fork Stability. Invited. 2019 BACIS retreat. Houston, Texas, US.
- 2018. BRCA and Fanconi Anemia promote genomic stability to suppress tumorigenesis. Invited. Breast Cancer Grand Rounds. Houston, Texas, US.
- 2018. BRCA/Fanconi Anemia in DNA replication fork stability and tumorigenesis. Invited. Prostate Cancer Moon Shots. Houston, Texas, US.
- 2016. DNA replication fork protection and genomic instability to suppress tumorigenesis. Invited. Department of Cancer Biology. Houston, Texas, US.
- 2015. Mechanisms of DNA Replication Fork Protection and Tumorigenesis. Invited. Distinguished Lecture in Molecular and Cellular Oncology. Houston, Texas, US.
- 2015. Targeting the DNA Replication Fork Protecteome for Therapy and Diagnostics. Invited. Breast and Ovarian Moon Shots. Houston, Texas, US.
- 2015. Protection of Replication Fork Stability. Invited. Future of Cancer Science Symposium. Houston, TX, US.
- 2015. Replication Fork Protection. Invited. DREAM Team meetings. Houston, Texas, US.
- 2015. Taking a fresh look at breast tumor suppressors: the BRCA/PTEN protecteome prevents genomic instability at the DNA replication forks. Invited. Breast Medical Oncology Wednesday Morning Meeting. Houston, Texas, US.
- 2015. The BRCA-PTEN protecteome suppresses genomic instability at the DNA replication fork,. Invited. Department of Genetics seminar series. Houston, Texas, US.
- 2015. A Phosphatase-Independent PTEN Activity Controls 53BP1 Recruitment to Stalled Replication Forks. Invited. Prostate Cancer Moon Shots. Houston, Texas, US.
- 2014. The BRCA-PTEN protecteome suppresses genomic instability at the DNA replication fork. Invited. Department of Cancer Biology Research Seminar. Houston, Texas, US.
Regional Presentations
- 2025. BRCA2 structure and disease – a tale of two genome stabilities. Invited. The Genome Instability Group. Houston, Texas, US.
- 2024. BRCA structure and disease: More than (one) genome stability. Invited. Discover Biomedicine Series. Houston, Texas, US.
- 2024. BRCA2 structure and disease: More than (one) genome stability. Invited. The Genome Instability Group. Houston, Texas, US.
- 2023. From mechanisms to biomarkers: Fueling translational research in energy balance. Invited. Center for Energy Balance Day of Science. Houston, Texas, US.
- 2023. Diet induced mitochondrial replication instability uncovers gender-bias in anemia of inflammation ..or why women are better (off). Invited. Annual MIMIG meeting. Houston, Texas, US.
- 2023. RAD51C structure to disease: A tale of two genome stabilities. Invited. Baylor Breast Disease Seminar. Houston, Texas, US.
- 2022. BRCA/FANC Tumor Suppressors Protect Mitochondrial DNA Forks From MRE11 Dependent cGAS Immune Signaling. Invited. MIMIG monthly meeting series. virtual, US.
- 2022. Hypomorphic BRCA/FANC mutations suppress T-ALL and mitochondrial instability. Invited. GCC 2nd Annual Future of Immunology Symposium.
- 2022. Mitochondrial and nuclear replication fork stability. Invited. The Genome Instability Group. Virtual, US.
- 2020. Harnessing Fanconi Anemia cell and mouse models to delineate cancer treatment strategies. Invited. Texas conference on genome repair. San Antonio, Texas, US.
- 2018. RAD51C in Mitochondria. Invited. The Genome Instability Group. Houston, Texas, US.
- 2016. Genomic Replication Fork Stability And Anemia. Invited. The Genome Instability Group. Houston, Texas, US.
- 2016. Replication Fork Protection and Therapy Response. Invited. 2016 DNA Damage Response and Cancer Therapy Joint Symposium. Houston, Texas, US.
- 2015. The BRCA-PTEN protecteome suppresses genomic instability at the DNA replication fork. Invited. The Genome Instability Group. Houston, Texas, US.
- 2014. The BRCA-PTEN protecteome. Invited. The Genome Instability Group. Houston, Texas, US.
- 2010. BRCA2/FANCD1 independent of HR protects stalled replication forks from 3’-5’ degradation by MRE11 via a conserved C-ter RAD51 binding domain. Invited. UCLA pharmacology Retreat. Huntington Beach, California, US.
- 2010. BRCA2 (FANCD1) protects stalled replication forks from degradation, a novel pathway shared with BRCA1 and Fanconi Anemia. Invited. Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Retreat. Asilomar, California, US.
- 2006. DNA pol V transactivation by RecA protein resolves mysteries of SOS damage-induced mutations. Invited. Department of Molecular and Computational Biology retreat. Laguna Beach, California, US.
National Presentations
- 2025. BRCA2 structure and disease; a tale of two genome instabilities. Invited. Seminar series. Durham, North Carolina, US.
- 2025. BRCA in Mitochondrial and Nuclear Replication Stability, Inflammation and Disease. Invited. Spring Seminar. Chapel Hill, North Carolina, US.
- 2024. BRCAness and the tale of two genome instabilities. Invited. Social DNAing Seminar Series. virtual, US.
- 2023. RAD51C: a tale of two genome stabilities. Invited. Annual meeting. Virtual, US.
- 2023. BRCA mediated nuclear and mitochondrial DNA replication instability in inflammation and disease. Invited. Boston, Massachusetts, US.
- 2021. BRCA/FANC Tumor Suppressors in Mitochondria and Inflammation. Invited. Microbiology and Molecular Genetics Department. Virtual, US.
- 2021. BRCA/FANC in replication instability and inflammation. Invited. Cancer Development and Progression Program. virtual, US.
- 2019. (Mitochondrial) DNA replication instability in disease, cancer and inflammation. Invited. Rita Allen Foundation Scholars Symposium. Cold Spring Harbor, NY, US.
- 2019. FANC and mitochondria. Invited. MDACC-BCM Drug Development Symposia. Houston, TX, US.
- 2019. Nuclear and mitochondrial DNA replication instability in disease and inflammation. Invited. 2019 Baylor-MDACC Joint Symposium. Houston, Texas, US.
- 2019. BRCA and Fanconi anemia from mechanism to disease. Invited. Bethesda, Maryland, US.
- 2019. BRCA, p53 and FANC in the replication fork stability. Invited. New York, New York, US.
- 2019. BRCA, p53 and FANC in the replication fork stability. Invited. New York, New York, US.
- 2019. BRCA, p53, FANC in the mechanism of disease. Invited. Los Angeles, California, US.
- 2018. FANCO/RAD51C protects mitochondrial DNA replication forks to suppress inflammation. Invited. Rita Allen Foundation Scholars Symposium. Princeton, New Jersey, US.
- 2015. The BRCA-PTEN protecteome suppresses genomic instability at the DNA replication fork. Invited. Seminar series. San Antonio, TX, US.
- 2012. Fork protection by BRCA and Fanconi Anemia as a new genome instability pathway. Boston, Massachusetts, US.
- 2009. BRCA2 (FANCD1) protects stalled replication forks from degradation, a novel pathway shared with BRCA1 and Fanconi Anemia. Invited. Damon Runyon Cancer Research Foundation Annual Retreat. Cape Cod, Massachusetts, US.
- 2007. Taking on SSA, a mutagenic DNA repair pathway induced in familial-inherited breast cancer. Invited. Damon Runyon Cancer Research Foundation Annual Retreat. Marshall, California, US.
International Presentations
- 2027. BRCA: two genome instabilities in inflammation and disease. Invited. Dynamic Mechanisms of Genome Replication and Repair — From Molecular Machines to Human Disease.
- 2026. BRCA: two genome stabilities in Inflammation and disease. Invited. Frontiers in Immunity and Inflammation (International series). Rochester, US.
- 2026. CHAMP1 in mitochondria. Invited. CHAMP1 Research Challenge 2026. Philadelphia, US.
- 2026. The FA protecteome: Structure, mechanism and disease. Invited. 7th Fusion Repair/Replication Structures and Cancer Recombination mechanisms. Playa Mujeres, MX.
- 2025. The BRCA/FA protecteome – a tale of two genome stabilities. Invited. Gene Center Seminar. Munich, DE.
- 2025. The BRCA/FA protecteome – a tale of two genome stabilities. Invited. IFOM Seminar. Milan, IT.
- 2025. CHAMP1 protein interactors in mitochondria associated inflammation as disease mechanism?. Invited. CHAMP1 Research Challenge 2025.
- 2025. BRCA2 structure and disease: More than (one) genome stability. Invited. Inter-organelle Stress Communication in Inflammation & Disease Conference. Malta, MT.
- 2025. The FA protecteome: Structure, mechanism and disease. Invited. 2nd Fusion Recombination mechanisms. Crete, GR.
- 2025. FA protecteome: mechanism in disease and inflammation. Invited. DNA Replication Gaps, Cancer and Disease. Daejeon, KR.
- 2025. BRCA structure, mechanism and disease: More than (one) genome stability. Invited. GRC DNA repair: Fundamental mechanism and human biology. Ventura, US.
- 2024. Telltale disease overlaps between CHAMP1/ASD and Fanconi Anemia to understand molecular mechanism?. Invited. CHAMP1 Family and Science Engagement Conference. Orlando, US.
- 2024. BRCA in Mitochondrial and nuclear genome stability for novel therapeutic targets. Invited. 4th Exploring DNA Repair Pathways as Targets for Cancer Therapy Conference 2024. St. Julian's, MT.
- 2024. Structure guided control of mitochondrial and nuclear BRCA in inflammation and disease. Invited. Princess Margaret-MD Anderson Joint Symposium. Toronto, CA.
- 2024. BRCA2 structure and disease: More than (one) genome stability. Invited. 6th DNA Repair/Replication Structures and Cancer Conference. Cancun, MX.
- 2023. FANCO/RAD51C from structure to disease: A tale of two genome stabilities. Invited. 2023 Annual FARF Symposium. Vancouver, CA.
- 2023. Mitochondrial DNA stability-dependent inflammatory signalling reveals gender disparity in diet induced anemia of inflammation. Invited. 2nd Mitochondria Conference. Lisbon, PT.
- 2023. RAD51C from structure to disease. Invited. Genome instability and DNA repair. Whistler, CA.
- 2022. Polygenic stress models mimic the pleiotropic disease of Fanconi Anemia. Invited. 2022 Annual FARF Symposium. Austin, US.
- 2022. Mitochondrial and nuclear genome instability in BRCA/FANC disease and cancer. Invited. 5th DNA Repair/Replication Structures and Cancer Conference. Cancun, MX.
- 2022. BRCA/FANC Tumor Suppressors Protect Mitochondrial DNA Forks From MRE11 Dependent cGAS Immune Signaling. Invited. 2022 Mitox Meeting. virtual, US.
- 2021. MRE11-Dependent Instability in Mitochondrial DNA Fork Protection Activates a CGAS Immune Signaling Pathway. Invited. 12th World Congress on Targeting Mitochondria. virtual, US.
- 2020. BRCA/FANC and mitochondria. Invited. Chromosomal Instability as a Driver of Human Disease. Lisbon, PT.
- 2020. Polygenic Mutations Model the Pleiotropic Disease of Fanconi Anemia. Invited. Keystone Genome Stability and DNA Repair. Virtual, US.
- 2020. Bigenic mutations in Brca2 and Rad51c model human Fanconi Anemia disease phenotypes in mice. Invited. Polygenic mutations model the pleiotropic disease of Fanconi Anemia. Virtual, US.
- 2020. Mitochondrial DNA Fork Protection by Fanconi Anemia Genes Suppresses cGAS Activation by MRE11 nuclease. Invited. Adaptive ROS Signaling in Physiology and Disease. canceled, US.
- 2020. Mitochondrial and nulcear DNA Fork Protection by Fanconi Anemia Genes Suppresses * meeting canceled. Invited. Nucleotide Excision Repair and Crosslink Repair. Smolenice, SK.
- 2020. Breast Cancer and Fanconi Anemia disease prediction and modeling. Invited. 4th DNA Repair/Replication Structures and Cancer Conference. Nassau, US.
- 2020. Genome Instability and DNA repair. Invited. Keystone Symposium. Whistler, CA.
- 2019. Nuclear and Mitochondrial DNA replication instability in disease and inflammation. Invited. Radiation Research Society Annual Meeting. San Diego, US.
- 2019. Mitochondrial DNA replication fork protection by the Fanconi Anemia pathway suppresses inflammation and disease. Invited. DNA damage response in cell physiology and disease workshop. Sounion, GR.
- 2019. Biallelic compound mutations in DNA replication mutant mice recapitulate Fanconi anemia patient phenotypes. Poster. Eukaryotic DNA Replication & Genome Maintenance. Cold Spring Harbor, US.
- 2019. Biallelic compound mutations in DNA replication mutant mice recapitulate Fanconi anemia patient phenotypes. Poster. FARF Annual research Symposium. Chicago, US.
- 2019. mtDNA replication forks protection by the Fanconi Anemia pathway suppresses inflammation and disease. Invited. The Mitochondrial Biogenesis and Dynamics in Health and Disease Conference. Palm Spring, US.
- 2019. FANC is a compound mutation disease. Invited. 18th Annual International AT Workshop. Houston, US.
- 2019. The Fanconi Anemia pathway proteins protect mitochondrial DNA replication fork to suppress inflammation. Invited. Mitochondria: From Basic Biology to Mechanisms of Disease Conference. Nassau, BS.
- 2019. The Fanconi Anemia Pathway Protects Mitochondrial DNA Replication Forks to Suppress Inflammation and Disease. Invited. Genome Maintenance: Mechanisms of Repair, Consequences of Failure for Human Disease and Opportunities for Therapeutic Intervention. Ventura, US.
- 2019. Mitochondria in Aging and Age-Related Disease. Invited. Mitochondria in Aging and Age-Related Disease. Keystone, US.
- 2018. BRCA1/2/3 and p53 in replication fork stability. Invited. AACR San Antonio Breast Cancer Symposium. San Antonio, US.
- 2018. BRCA and Fanconi Anemia mediated DNA replication instability and disease. Invited. invited speaker. Vienna, AT.
- 2018. Mitochondrial DNA fork protection by FANCO/RAD51C suppresses inflammation. Invited. Annual Fanconi Anemia Research Foundation Symposium. San Diego, US.
- 2018. Mitochondrial DNA fork protection by FANCO/RAD51C suppresses metabolic reprogramming and inflammation. Invited. GRC Mutagenesis. Newry, US.
- 2018. RAD51C in DNA Fork Protection and Stability. Invited. 3rd DNA Replication/Repair Structures and Cancer Conference. Cancun, MX.
- 2017. P53 suppresses mutagenic RAD52 and POLq pathways by orchestrating DNA replication restart homeostasis. Invited. CSHL Eukaryotic DNA Replication & Genome Maintenance meeting. Cold Spring Harbor, US.
- 2017. Epigenetics-Enabled MRE11 Replication restart by p53 promotes replication pathway homeostasis to suppress opportunistic transcription reprogramming. Invited. DNA replication and disease. Rome, IT.
- 2017. molecular tools and mechanism of FANC/BRCA disease suppressors. Invited. Graz, AT.
- 2017. Genomic Stability by MRE11 fork restart to suppresses BRCA-survival Pathways. Invited. Genome Stability and DNA Repair. Santa Fe, US.
- 2017. P53 promotes replication genome stability by epigenetics-enabled MRE11 restart. Poster. AACR Annual Meeting. Washington, US.
- 2017. p53 Promotes Genomic Stability and Replication Pathway Homeostasis by Epigenetics enabled MRE11 replication restart. Invited. 2nd Exploring DNA Repair Pathways as Targets for Cancer Therapy. Cancun, MX.
- 2015. A Phosphatase-Independent PTEN Activity Controls 53BP1 Recruitment to Stalled Replication Forks for Replication Restart and Stability. Invited. DNA Replication and Recombination. Whistler, CA.
- 2015. Recruitment of 53bp1 for replication fork restart and stability depends upon a phosphatase-independent PTEN activity. Invited. Exploring DNA Repair Pathways as Targets for Cancer Therapy. Cancun, MX.
- 2014. PTEN regulates 53BP1 activity to suppress DNA replication instability by promoting unexpected NHEJ-mediated restart of stalled forks. Invited. Maintenance of Genomic Stability, KN.
- 2013. The replication protecteome suppresses genomic instability. Invited. 11th International Conference on Environmental Mutagens. Foz do Iguassu, BR.
- 2013. Replisome isolation by FA/BRCA Gene-network Protects against Short-circuiting Replication and Repair. Invited. DNA replication and repair. Banff, CA.
- 2011. Repair-independent Pathway Connects Fanconi Anemia Tumor Suppressors to RAD51 and BRCA1/2 to protect stalled replication forks. Invited. 23st Annual FARF Symposium. Barcelona, ES.
- 2011. A New Pathway Independent of Repair Connects Fanconi Anemia Tumor Suppressors to RAD51 and BRCA1/2 to protect stalled replication forks. Invited. 42nd Annual Meeting Environmental Mutagen Society. Montreal, CA.
- 2011. Replication fork protection provides a mechanistic link between breast cancer and Fanconi anemia susceptibility. Invited. GRCGenetic Toxicology. Lucca, IT.
- 2011. Double-Strand Break Repair Independent Role For BRCA2 In Blocking Stalled Replication Fork Degradation By MRE11. Invited. ASBMB annual meeting. Washington, US.
- 2011. Double-Strand Break Repair Independent Role For BRCA2 In Blocking Stalled Replication Fork Degradation By MRE11. Invited. Chromosomal Instability and DNA Repair. Keystone, US.
- 2010. BRCA2/FANCD1 independent of HR protects stalled replication forks from 3’-5’ degradation by MRE11 via a conserved C-ter RAD51 binding domain. Invited. 22nd Annual Fanconi Anemia Research Fund Scientific Symposium. Minneapolis, US.
- 2010. BRCA2 protects stalled replication forks from degradation, a novel pathway shared with BRCA1 and Fanconi Anemia. Invited. International Ataxia-Telangiectasia Workshop. Long Beach, US.
- 2010. BRCA2 (FANCD1) protects stalled replication forks from degradation, a novel pathway shared with BRCA1 and Fanconi Anemia. Invited. Maintenance of Genomic Stability. Jolly Beach Resort, AG.
- 2009. BRCA2 (FANCD1) protects stalled replication forks from degradation, a novel pathway shared with BRCA1 and Fanconi Anemia. Invited. Telomere Biology and DNA repair. Ashmore, AU.
- 2009. BRCA2 (FANCD1) protects stalled replication forks from degradation, a novel pathway shared with BRCA1 and Fanconi Anemia. Invited. 21st Annual Fanconi Anemia Research Fund Scientific Symposium. Baltimore, US.
- 2008. RecFOR proteins prevent template switching during D-loop mediated replication restart. Invited. Recombination Mechanism. Il Ciocco, IT.
- 2007. Mechanisms integrating Recombination, Replication and Repair. Poster. Genetic Recombination and Genome Rearrangement. Snowmass Village, US.
- 2006. RecA protein activates DNA polymerase V in trans to promote SOS-induced mutagenesis. Poster. Mutagenesis. Newport, US.
- 2006. Pol V and RecA protein, a minimal mutasome. Poster. Nucleic Acid Enzymes. Taos, US.
- 2004. RecA’s third role is the activation of pol V, which is acquired by two physically distinct protein-interactions. Poster. GRC Mutagenesis. Oxford, GB.
Formal Peers
- 2019. RRS Annual Symposium, lecture for CME credits. Visiting. San Diego, CA, US.
- 2018. San Antonio Breast Cancer Symposium, for CME credits. Visiting. San Antonio, TX, US.
- 2018. Breast Cancer Grand Rounds. Visiting. Houston, TX, US.
Grant & Contract Support
| Date: | 2027 - 2032 |
| Title: | Decoupling RAD51 Functions to test a Novel Cancer Therapeutic Approach |
| Funding Source: | NIH |
| Role: | PI |
| Date: | 2027 - 2030 |
| Title: | BRCA2 DNA Fork Protection As An Untapped Treatment and Prevention Opportunity |
| Funding Source: | DOD |
| Role: | PI |
| Date: | 2027 - 2028 |
| Title: | Harnessing novel USTAT1 Post-Translational Modifications as Biomarkers for Inflammation-Driven Cancer Resistance |
| Funding Source: | ACS |
| Role: | PI |
| Date: | 2026 - 2029 |
| Title: | Targeting Replication Fork Protection to Overcome Therapy Resistance in BRCA cancers |
| Funding Source: | CPRIT |
| Role: | PI |
| Date: | 2026 - 2029 |
| Title: | A Preclinical Path to Cancer Prevention Using Native Human Proteins |
| Funding Source: | CPRIT |
| Role: | Co-I |
| Date: | 2026 - 2028 |
| Title: | Mitochondria-targeted estrogen as a strategy to suppress anemia and decouple it from genomic instability in Fanconi Anemia |
| Funding Source: | Harrington Discovery Institute |
| Role: | PI |
| Date: | 2026 - 2028 |
| Title: | CHAMP1 and mitochondria |
| Funding Source: | NIH |
| Role: | PI |
| ID: | 1R21HD119755-01A1 |
| Date: | 2026 - 2029 |
| Title: | Developing Precision Peptide Chemical Switches of DNA Stress Responses to Control Organelle-specific Inflammation |
| Funding Source: | Welch Foundation |
| Role: | PI |
| Date: | 2026 - 2031 |
| Title: | Delineating BRCA2 function at DNA forks and breaks |
| Funding Source: | NIH |
| Role: | PI |
| Date: | 2026 - 2031 |
| Title: | Molecular Mechanism of RAD51C in mtDNA genome stability |
| Funding Source: | NIH |
| Role: | PI |
| Date: | 2025 - 2029 |
| Title: | Unexpected modulators of pediatric T-cell leukemia |
| Funding Source: | CPRIT |
| Role: | PI |
| Date: | 2025 - 2028 |
| Title: | Mitochondrial Replication Fork Instability as a Unified Driver of Immune Checkpoint Response |
| Funding Source: | AACR |
| Role: | PI |
| Date: | 2025 - 2028 |
| Title: | Mitochondrial Replication Fork Instability as a Unified Driver of Immune Checkpoint Response |
| Funding Source: | AACR |
| Role: | PI |
| Date: | 2025 - 2026 |
| Title: | Exploring non-canonical roles of CHAMP1 |
| Funding Source: | CHAMP1 Research Foundation |
| Role: | PI |
| Date: | 2025 - 2026 |
| Title: | Ordering intrinsically disordered protein regions by physiologically relevant tumor-suppressor complex formation |
| Funding Source: | Mark Foundation for Cancer Research |
| Role: | PI |
| Date: | 2025 - 2030 |
| Title: | Mechanism of RAD51C fork protection and environmental carcinogenesis |
| Funding Source: | NIH |
| Role: | PI |
| Date: | 2025 - 2030 |
| Title: | Delineating BRCA2 function at DNA forks and breaks |
| Funding Source: | NIH |
| Role: | PI |
| Date: | 2025 - 2029 |
| Title: | Molecular signaling in T-cell leukemia |
| Funding Source: | NIH |
| Role: | PI |
| Date: | 2025 - 2027 |
| Title: | CHAMP1 and mitochondria |
| Funding Source: | NIH |
| Role: | PI |
| Date: | 2024 - 2026 |
| Title: | Bridge Funding "Mechanism of RAD51C fork protection and environmental carcinogenesis" |
| Funding Source: | UT MD Anderson Cancer Center |
| Role: | PI |
| Date: | 2024 - 2029 |
| Title: | Inter-organelle dependent genome stability |
| Funding Source: | NIH |
| Role: | PI |
| Date: | 2024 - 2029 |
| Title: | Mechanism of RAD51C fork protection and environmental carcinogenesis |
| Funding Source: | NIH |
| Role: | PI |
| Date: | 2024 - 2028 |
| Title: | Unexpected modulators of pediatric T-cell leukemia |
| Funding Source: | CPRIT |
| Role: | PI |
| Date: | 2023 - 2028 |
| Title: | IBIS - Integrating BRCA and Inflammatory Signaling |
| Funding Source: | NIH |
| Role: | PI |
| Date: | 2023 - 2028 |
| Title: | The Un-phosphorylated STAT1 response and inflammaging |
| Funding Source: | NIH |
| Role: | PI |
| Date: | 2023 - 2028 |
| Title: | Unexpected mechanism of immune checkpoint therapy modulators |
| Funding Source: | Cancer Research Institute |
| Role: | PI |
| Date: | 2023 - 2028 |
| Title: | Mitochondrial and Nuclear Protein Translocations Linking the Foundational Hallmarks of Aging |
| Funding Source: | NIH |
| Role: | PI |
| Date: | 2023 - 2026 |
| Title: | Androgen mediated mitochondrial instability mediated synergies with BRCA2 in male-specific cancer |
| Funding Source: | CureBRCA |
| Role: | PI |
| Date: | 2023 - 2025 |
| Title: | Deciphering unexpected genetic and molecular determinants of T-cell leukemia |
| Funding Source: | Mark Foundation for Cancer Research |
| Role: | PI |
| Date: | 2020 - 2025 |
| Title: | Communication between nuclear and mitochondrial genome stability |
| Funding Source: | NIH |
| Role: | PI |
| Date: | 2020 - 2020 |
| Title: | Bridge funding, Compound Fanconi Anemia mutations for gamma irradiation treatment response prediction |
| Funding Source: | MDACC |
| Role: | PI |
| Date: | 2020 - 2022 |
| Title: | Mathers foundation application (invited for full application) |
| Funding Source: | Mathers Foundation |
| Role: | PI |
| Date: | 2019 - 2021 |
| Title: | Molecular dissection of PARPi-induced anemia for improved therapy efficacy |
| Funding Source: | Ovarian Moonshot MDACC |
| Role: | PI |
| Date: | 2018 - 2025 |
| Title: | Mechanism of RAD51C fork protection and environmental carcinogenesis |
| Funding Source: | NIH/NCI |
| Role: | PI |
| ID: | 1RO1ES029680 |
| Date: | 2018 - 2023 |
| Title: | Compound Fanconi Anemia mutations for gamma irradiation treatment response prediction |
| Funding Source: | NIH/NCI |
| Role: | PI |
| Date: | 2018 - 2023 |
| Title: | Mitochondrial DNA replication stability |
| Funding Source: | NIH/NIGMS |
| Role: | PI |
| Date: | 2018 - 2023 |
| Title: | Defining BRCA2-p53 cooperation at the replication fork |
| Funding Source: | NIH/NCI |
| Role: | PI |
| Date: | 2018 - 2024 |
| Title: | BRCA Answers from Cancer Interactome Structures (BACIS) |
| Funding Source: | CPRIT |
| Role: | Co-PI |
| ID: | RP180463 |
| Date: | 2018 - 2021 |
| Title: | Compound heterozygous mutations in pediatric cancer predisposition |
| Funding Source: | CPRIT |
| Role: | PI |
| ID: | RP180463 |
| Date: | 2018 - 2022 |
| Title: | DNA Replication Fork Stability and Breast Cancer Prognostics |
| Funding Source: | DOD |
| Role: | PI |
| Date: | 2018 - 2020 |
| Title: | Diagnostic and resistance replication biomarkers for ovarian cancer, LOI |
| Funding Source: | OCRFA |
| Role: | PI |
| Date: | 2017 - 2022 |
| Title: | Replication Fork Protection and Mutation Penetrance in Breast/Ovarian Cancer |
| Funding Source: | NIH |
| Role: | PI |
| Date: | 2017 - 2020 |
| Title: | RAD51C in mitochondrial genome instability and Metabolic Warburg Switching |
| Funding Source: | AACR |
| Role: | PI |
| Date: | 2016 - 2021 |
| Title: | Distinct Breast/Ovarian Cancer Mutations and replication fork protection, resubmission, 18th percentile |
| Funding Source: | NCI |
| Role: | PI |
| Date: | 2016 - 2019 |
| Title: | Metabolic Switching Driven by Mitochondrial DNA Replication Protection Instability |
| Funding Source: | NIH |
| Role: | PI |
| Date: | 2016 - 2019 |
| Title: | Integrating Mechanisms of Mitochondrial DNA Fork Protection, Suppression of Metabolic Switching and Disease |
| Funding Source: | Pew Scholar |
| Role: | PI |
| Date: | 2016 - 2021 |
| Title: | Distinct Breast/Ovarian Cancer Mutations and replication fork protection |
| Funding Source: | NIH |
| Role: | PI |
| Date: | 2016 - 2023 |
| Title: | BRCA 1/2 and Fanconi Anemia Suppressor-mediated DNA Fork Protection in Mitochondrial DNA instability and disease |
| Funding Source: | Rita Allen Foundation |
| Role: | PI |
| ID: | 19142 |
| Date: | 2016 - 2018 |
| Title: | Replication Fork Protection as a Novel Tumor Suppressor Pathway Target |
| Funding Source: | Andrew Sabin Family Foundation |
| Role: | PI |
| Date: | 2016 - 2019 |
| Title: | DNA Fork Protection in Suppressing Mitochondrial DNA Instability and disease |
| Funding Source: | Searle Scholar |
| Role: | PI |
| Date: | 2015 - 2017 |
| Title: | Deciphering Replication Fork Protection: A Novel Tumor Suppressor Pathway |
| Funding Source: | UT Regents |
| Role: | PI |
| Date: | 2014 - 2019 |
| Title: | Recruitment First-Time Tenure Track Faculty |
| Funding Source: | CPRIT |
| Role: | PI |
| Date: | 2013 - 2016 |
| Title: | Cellular and Molecular Tumorsuppressor Processes Uncovered by DNA Fork Protection |
| Funding Source: | NIH/NCI |
| Role: | PI |
| ID: | 5 K22 CA175262 |
Patient Reviews
CV information above last modified July 22, 2026