John P. Murnane, PhD

A B C D E F G H I J K L M N O P Q R S T U V W X Y Z
John P. Murnane, PhD

Professor, Department of Radiation Oncology, UCSF
Wun-Kon Fu Endowed Chair in Radiation Oncology, UCSF

jmurnane@radonc.ucsf.edu

Phone: (415) 476-9083 (voice)
Box 0806, UCSF
San Francisco, CA 94143-0806

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Cancer Center Membership

Program Member ยป Cancer Genetics

Research Summary

My interests for many years have been mechanisms of DNA damage, DNA repair, and chromosome instability, and their relationship to cancer. My early work was the first to demonstrate that cell cycle regulation is important in protecting cells against DNA damage (Nature 285:326, 1980). My work was also the first to demonstrate that human cells can become immortal by maintaining telomeres through a process other than telomerase, and to propose that this mechanism involves recombination (EMBO J 13:4953, 1994). My laboratory was the first to establish a model system to demonstrate and monitor the ability of mammalian cells to stabilize broken chromosomes through the addition of new telomeres, called chromosome healing (PNAS 96:6781, 1999). My recent studies are focused on the role of telomere loss in the chromosome instability leading to human cancer cell progression and resistance to anti-cancer therapy. Our studies address the mechanism of sensitivity of subtelomeric regions to DNA double-strand breaks, and I have proposed that this sensitivity of telomeric regions to double-strand breaks is an important factor in chromosome instability in cancer (Cancer Res 70:4255, 2010). My laboratory is now involved in an in-depth analysis of the mechanisms responsible for this sensitivity of telomeric regions to double strand breaks and how to exploit this sensitivity and the ability of human cells to perform chromosome healing to limit the chromosome instability leading to tumor progression and resistance to cancer therapy.

Education

California State University, Northridge, B.S., 1971, Chemistry
University of California, Los Angeles, Ph.D., 1980, Microbiology and Immunology


Professional Experience

  • 1980-1983
    Postdoctoral Fellow, Laboratory of Radiobiology & Environmental Health, University of California, San Francisco
  • 1983-1984
    Asst. Research Biochemist, Laboratory of Radiobiology & Environmental Health, University of California, San Francisco
  • 1991-1995
    Associate Professor, Laboratory of Radiobiology & Environmental Health, University of California, San Francisco
  • 1995-1998
    Associate Professor, Department of Radiation Oncology, University of California, San Francisco
  • 2000-2004
    Assistant Professor, Laboratory of Radiobiology & Environmental Health, University of California, San Francisco
  • 1998-present
    Professor, Department of Radiation Oncology, University of California, San Francisco
  • 2007-present
    Vice Chairman, Department of Radiation Oncology, UCSF

Honors & Awards

  • 2007
    Margolis Lifetime Teaching Award, Department of Radiation Oncology, UCSF
  • 2009
    Wun-Kon Fu Endowed Chair in Radiation Oncology, Dept. of Radiation Oncology, UCSF

Selected Publications

  1. Replication Stress and Telomere Dysfunction Are Present in Cultured Human Embryonic Stem Cells. Cytogenet Genome Res. 2015; 146(4):251-60.
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  2. Processing by MRE11 is involved in the sensitivity of subtelomeric regions to DNA double-strand breaks. Nucleic Acids Res. 2015 Sep 18; 43(16):7911-30.
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  3. In memoriam. Radiat Res. 2015 Mar; 183(3):e49-50.
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  4. Numerical chromosomal instability mediates susceptibility to radiation treatment. Nat Commun. 2015; 6:5990.
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  5. Effect of radiation quality on mutagenic joining of enzymatically-induced DNA double-strand breaks in previously irradiated human cells. Radiat Res. 2014 Nov; 182(5):573-9.
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  6. DNA-Damage Response during Mitosis Induces Whole-Chromosome Missegregation. Cancer Discov. 2014 Nov; 4(11):1281-9.
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  7. Increased mutagenic joining of enzymatically-induced DNA double-strand breaks in high-charge and energy particle irradiated human cells. Radiat Res. 2013 Jul; 180(1):17-24.
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  8. The role of ATM in the deficiency in nonhomologous end-joining near telomeres in a human cancer cell line. PLoS Genet. 2013 Mar; 9(3):e1003386.
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  9. Mechanisms of telomere loss and their consequences for chromosome instability. Front Oncol. 2012; 2:135.
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  10. PIF1 disruption or NBS1 hypomorphism does not affect chromosome healing or fusion resulting from double-strand breaks near telomeres in murine embryonic stem cells. DNA Repair (Amst). 2011 Nov 10; 10(11):1164-73.
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  11. Telomere dysfunction and chromosome instability. Mutat Res. 2012 Feb 1; 730(1-2):28-36.
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  12. Subtelomeric regions in mammalian cells are deficient in DNA double-strand break repair. DNA Repair (Amst). 2011 May 5; 10(5):536-44.
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  13. Telomere loss as a mechanism for chromosome instability in human cancer. Cancer Res. 2010 Jun 1; 70(11):4255-9.
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  14. Effect of telomere proximity on telomere position effect, chromosome healing, and sensitivity to DNA double-strand breaks in a human tumor cell line. Mol Cell Biol. 2010 Feb; 30(3):578-89.
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  15. Increased sensitivity of subtelomeric regions to DNA double-strand breaks in a human cancer cell line. DNA Repair (Amst). 2009 Aug 6; 8(8):886-900.
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  16. Telomerase-dependent and -independent chromosome healing in mouse embryonic stem cells. DNA Repair (Amst). 2008 Aug 2; 7(8):1233-49.
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  17. Telomeres acquire distinct heterochromatin characteristics during siRNA-induced RNA interference in mouse cells. Curr Biol. 2008 Feb 12; 18(3):183-7.
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  18. Telomeric transgenes are silenced in adult mouse tissues and embryo fibroblasts but are expressed in embryonic stem cells. Stem Cells. 2007 Dec; 25(12):3085-92.
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  19. Suppression of anchorage-independent growth by expression of the ataxia-telangiectasia group D complementing gene, ATDC. Biochem Biophys Res Commun. 2006 Sep 22; 348(2):728-34.
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  20. Telomeres and chromosome instability. DNA Repair (Amst). 2006 Sep 8; 5(9-10):1082-92.
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