Dr. Bunz’s research objective is to understand the genetic basis of common cancers and to determine how recurrent genetic alterations affect treatment with existing and novel therapeutic agents.
Ionizing radiation is a mainstay of therapy for most types of cancer. The DNA strand breaks, crosslinks, adducts and DNA replication intermediates that are caused by ionizing radiation and many other therapeutic agents trigger activation of a complex network of intracellular signaling molecules that ultimately control cell growth and cell death. Employing recently developed technology, the Bunz laboratory studies the signaling molecules and pathways that are activated by DNA damage. The goal of this work is to better understand how current therapies work, and to develop new and improved cancer treatments.
Dr. Bunz’s laboratory studies the molecular basis of cancer therapy. Our goal is to determine how p53 and other mediators of the DNA damage response are activated by therapeutic agents, and to understand how these pathways ultimately control cell growth and death, and mediate tumor suppression.
Learn more about clinical trials at the Johns Hopkins Kimmel Cancer Center.
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Bunz F, Kobayashi R, Stillman B. cDNAs encoding the large subunit of human replication factor C. Proc Natl Acad Sci USA. 1993;90(23):11014-11018.
Bunz F, Dutriaux A, Lengauer C, Waldman T. Zhou S, Brown J P, Sedivy JM, Kinzler KW, and Vogelstein B. Requirement for p53 and p21 to Sustain G2 Arrest After DNA Damage. Science. 1998; 282(5393):1497-1501.
Wilsker D, Petermann E, Helleday T, Bunz F. Essential function of Chk1 can be uncoupled from DNA damage checkpoint and replication control. Proc Natl Acad Sci USA. 2008;105(52):20752-57. PMCID: PMC2634938
Chung JH, Bunz F. Cdk2 is required for p53-independent G2/M checkpoint control. PLoS Genetics. 2010; 6:e1000863. PMCID: PMC2829054
Chung JH, Larsen AR, Chen E, Bunz F. A PTCH1 homolog transcriptionally activated by p53 suppresses hedgehog signaling. J Biol Chem. 2014; 289(47):33020-33031. PMCID: PMC4239647