John P. Murnane

John P. Murnane, Ph.D.

Department of Radiation Oncology

Mount Zion Cancer Research Building
2340 Sutter St., Room S329
San Francisco, CA 94143-1331
Phone: (415) 476-9083
Fax: (415) 476 9069
Email: JMurnane[at]

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Professional Focus

John Murnane’s interests are the study of the mechanisms of DNA damage, 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). His 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). Telomeres are the caps on the ends of chromosomes, and acquiring the ability to maintain telomeres is an important step in cancer progression. His laboratory was also the first to establish a model system to demonstrate the ability of mammalian cells to stabilize broken chromosomes through the addition of new telomeres, called chromosome healing (PNAS 96:6781, 1999). He is currently investigating whether the regulation of chromosome healing can be used as a method for preventing chromosome instability in cancer cells, and selectively sensitize cancer cells to ionizing radiation. More recently his work has demonstrated that regions near telomeres are highly sensitive to DNA double-strand breaks, and has proposed that this sensitivity of telomeric regions to DNA double-strand breaks is an important factor in chromosome instability, which is important in tumor cell progression and resistance to classical and targeted therapies (Cancer Res 70:4255, 2010). His laboratory is now involved in the analysis of the mechanisms and proteins responsible for the sensitivity of telomeric regions to DNA double strand breaks, and how this sensitivity can be exploited to prevent chromosome instability or selectively kill cancer cells demonstrating chromosome instability.


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

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


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