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John P. Murnane, Ph.D.

Professor
Department of Radiation Oncology

Meet Dr. Murnane

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John Murnane’s interests are the study of the mechanisms of DNA repair and chromosome instability and their relationship to cancer. His early work was the first to demonstrate that cell cycle regulation is important in protecting cells against DNA damage (Nature 285:326, 1980), that human cells can become immortal by maintaining telomeres through an alternate mechanism other than telomerase and propose that this mechanism involves recombination (EMBO J 13:4953, 1994), and that broken chromosomes in mammalian cells can be stabilized by de novo telomere addition (PNAS 96:6781, 1999). More recently his work has demonstrated that chromosome instability in cancer cells results from spontaneous telomere loss, and has proposed that this increased rate of telomere loss in cancer cells results from the sensitivity of telomeric regions to DNA double-strand breaks (reviewed in Cancer Res 70:4255, 2010). His laboratory has more recently shown that this sensitivity of telomeric regions to DNA double-strand breaks is due to inappropriate processing which inhibits repair (Nucleic Acids Res 10.1093, 2015). His laboratory has now developed a high throughput assay based on these results that is being used to identify small molecule inhibitors that can be used to selectively kill cancer cells demonstrating chromosome instability.
Education

Education

1971 California State University, Northridge BS Chemistry
1977 UCLA    
1980 UCLA PhD Microbiology
Professional Experience

Professional Experience

2007-present UCSF Professor in Residence, Vice Chair Department of Radiation Oncology
1998-2007 UCSF Adjunct Professor  
1996-1998 UCSF Associate Adjunct Professor Department of Radiation Oncology
1991-1996 UCSF Associate Adjunct Professor  
1984-1991 UCSF Assistant Adjunct Professor Laboratory of Radiobiology & Environmental Health
1983-1984 UCSF Asst. Research Biochemist with Dr. Robert Painter Laboratory of Radiobiology & Environmental Health
1980-1983 UCSF Postdoctoral Fellow with Dr. Robert B. Painter Laboratory of Radiobiology & Environmental Health
Publications

Recent Significant Publications

Murnane, J. P. Telomere loss as a mechanism for chromosome instability in human cancer. Cancer Res., 70:4255-4259 (2010).

Reynolds, G.E., Gao, Q., Miller, D., Snow, B.E., Harrington, L.A., and Murnane J.P. The role of PIF1 and NBS1 in chromosome healing and fusion resulting from double-strand breaks near telomeres in murine embryonic stem cells. DNA Repair, 10:1164-1173 (2011).

Miller, D., Reynolds, G.E., Mejia, R., Stark, J.M., and Murnane, J.P. Subtelomeric regions in mammalian cells are deficient in DNA double-strand break repair. DNA Repair10:536-544 (2011).

Murnane, J.P. Telomeric dysfunction and chromosome instability. Mutat. Res. 730:28-36 (2012).

Muraki, K., Nyhan, K., Han, L., and Murnane, J.P. Mechanisms of telomere loss and their consequences for chromosome instability. Front. Oncol. 2:135 (2012).

Muraki, K., Han, L., Miller, D., and Murnane, J.P. The role of ATM in the deficiency in nonhomologous end-joining near telomeres in a human cancer cell line. PLoS Genetics, 9:e1003386 (2013).

Li, Z., Hudson, F.Z., Wang, H., Wang, Y., Bian, Z., Murnane, J.P., and Dynan, W.S. Increased mutagenic joining of enzymatically-induced DNA double-strand breaks in high-charge and energy particle irradiated human cells. Radiation Res. 180:17 (3013).

Li, Z., Wang, H., Wang, Y., Murnane, J.P., and Dynan, W.S. Effect of radiation quality on mutagenic joining of enzymatically-induced DNA double-strand breaks in previously irradiated human cells. Radiation Res. In press (2014).

Bakhoum, S.F., Kabeche, L., Murnane, J.P., Zaki, B.I., and Compton, D.A. DNA-damage response during mitosis induces whole-chromosome missegregation. Cancer Discov. 4:1281-9 (2014).

Bakhoum, S.F., Kabeche, L., Wood, M.D., Laucius, D., Qu, D., Laughney, A.M., Reynolds, G.E., Louie, R.J., Phillips, J., Chan, D.A., Bassem, I.Z., Murnane, J.P., Petritsch, C., and Compton, D.A. Numerical chromosomal instability mediates susceptibility to radiation treatment. Nature Commun. 6:5990 (2015).

Muraki, K., Han, L, Miller, D., and Murnane, J. P. Processing by MRE11 is involved in the sensitivity of subtelomeric regions to DNA double-strand breaks. Nucleic Acids Res. doi: 10.1093/nar/gkv714 (2015).

View my research on PubMed

Redefining Possible