Scientific Review Council

The Scientific Review Council (SRC) oversees the peer review of all cancer research applications submitted to CPRIT. Members of the SRC chair the cancer research peer review committees. The SRC must assess the evaluations completed by the cancer research peer review committees and create a final list of proposals recommended for CPRIT grant awards. This list is submitted to CPRIT's executive director. Texas law affords great weight to the review council’s funding recommendations, requiring the executive director’s final recommendations for funding awards to be “substantially based” on the list submitted by the review council.

Richard Kolodner, Ph.D.

  • Chair, Scientific Review Council
    Head, Academic Affairs, Ludwig Institute for Cancer Research, New York Offices
    Member, Ludwig Institute for Cancer Research San Diego Branch and Head of the Laboratory of Cancer Genetics
    Distinguished Professor of Medicine and of Cellular and Molecular Medicine, UCSD School of Medicine
  

The major research interest of Dr. Kolodner’s laboratory is using Saccharomyces cerevisiae as a model organism to study the molecular mechanisms by which cells maintain the stability of their genome and prevent the accumulation of mutations and genome rearrangements. The laboratory also works on inherited defects in human recombination and repair genes to understand how such defects cause cancer susceptibility and to understand the basic human genetics of these genes. These studies have involved the routine use of techniques in S. cerevisiae genetics, protein purification, genomics and human genetics.

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Tom Curran, Ph.D., FRS

  • Chair, Basic Cancer Research Peer Review Panel 1
    Mai and Harry F. West Chair in Pediatric Research
    Deputy Scientific Director, The Children’s Hospital of Philadelphia Research Institute
    Professor of Pathology and Laboratory Medicine, Cell & Developmental Biology, Perelman School of Medicine
    Associate Director Translational Genomics, University of Pennsylvania
  

Dr. Curran discovered the Fos oncogene and its binding partner, p39, which he later showed was the product of the Jun oncogene. His laboratory demonstrated that Fos and Jun function as inducible transcription factors that regulate gene expression in response to extracellular stimuli associated with proliferation, differentiation, cell death and neuronal activation. This work elucidated the signal transduction pathways that go awry in cancer cells and has initiated the use of Fos as a marker for activity-dependent changes in the nervous system.

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Sanjiv “Sam” Gambhir, M.D., Ph.D.

  • Chair, Imaging Technology and Informatics Peer Review Panel
    Chair, Department of Radiology, Stanford University School of Medicine
    Director, Canary Center at Stanford for Cancer Early Detection
    Director, Molecular Imaging Program at Stanford (MIPS)
    Professor, Department of Radiology and Bio-X Program, Stanford University
    Professor, Department of Bioengineering, Stanford University
  

Dr. Gambhir’s research focuses on imaging assays to monitor fundamental cellular/molecular events in living subjects with an emphasis on cancer. Technologies being utilized include micro-positron emission tomography (microPET), bioluminescence imaging, fluorescence optical imaging, Raman optical imaging, ultrasound, and photoacoustics in small animal models. Particular interest of his research and lab is early cancer detection including combining in vivo and in vitro diagnostics.

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Peter Jones, Ph.D.

  • Chair, Cancer Biology Peer Review Panel
    Mark A., J. Ruth, and Stillman F. Sawyer Chair in Cancer Research, Keck School of Medicine of USC, USC Norris Comprehensive Cancer Center
    Professor of Biochemistry & Molecular Biology and Urology, Keck School of Medicine USC
  

A pioneer in the field of epigenetics, Dr. Jones has uncovered basic mechanisms of DNA methylation and its role in cancer. He discovered that 5-azacytidine can induce changes in gene expression and act as a powerful DNA methylation inhibitor, which led to the isolation of the first mammalian determination gene and to the discovery of tumor suppressor genes that are epigenetically silenced in human cancer. The drug 5-azacytadine has been approved for use in treatment of myelodysplastic syndrome.

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Richard J. O’Reilly, M.D.

  • Chair, Translational Cancer Research Peer Review Panel
    Chair, Department of Pediatrics and Director of the Bone Marrow Transplantation Program, Memorial Sloan-Kettering Cancer Center
  

Dr. Richard J. O'Reilly has been engaged in clinical research and experimental therapeutics focused on allogeneic hematopoietic cell transplantation.  He pioneered the development of curative marrow transplantation approaches for the treatment of children with severe combined immune deficiency who lack an HLA matched sibling donor.  He introduced the use of matched unrelated donors and T-cell depleted transplants from HLA half matched donors in order to provide a normal blood system without graft vs host disease (GvHD) to patients afflicted with lethal immune deficiencies and leukemia, and subsequently performed the first successful transplants of unrelated marrow for the treatment of leukemia. He and his colleagues developed an approach employing soy bean lectin agglutination and E-rosette depletion for elimination of T lymphocytes from bone marrow allografts.  Thereafter, they verified the potential of allogeneic T cell-depleted transplants to prevent GvHD in primate models.  Beginning in 1980, they introduced trials of transplants from haplotype matched parents depleted of T-cells by this technique as a treatment for children with severe combined immune deficiency. This experience, which is now one of the world’s largest, clearly demonstrates that such transplants can reconstitute immunity and abrogate GvHD.  Indeed, 70% of the patients in the entire series are surviving with immune reconstitution and without GvHD.

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Carol Prives, Ph.D.

  • Chair, Basic Cancer Research Peer Review Panel 2
    Professor, Department of Biological Sciences, Columbia University
  

Dr. Prives’s research has focused on the p53 tumor suppressor since the late 1980’s when she established conditions for purifying and characterizing the p53 protein biochemically and was among the first to show that p53 is a sequence specific transcriptional activator. Her research found that tumor derived mutant forms of p53, especially those that are mutated with high frequency, are defective in such transactivation. Dr. Prives continued to study p53 as a DNA binding transactivator, with special focus on mechanisms by which p53 selects its target genes; and she also provided the first model for stabilization of p53 by genotoxic stress when her group showed that p53 becomes phosphorylated after DNA damage at sites that weaken its interaction with its negative regulator Mdm2. They have continued to study the structure and functional regulation of Mdm2 and its relationship to p53.  After the p53 homologues, p63 and p73, were identified, she developed and tested the hypothesis that one of the modes by which some tumor derived mutant forms of p53 elicit pro-oncogenic activities is through down-regulation of the apoptotic functions of p63/p73. Since then, her work has focused on many aspects of the p53 family and on mutant p53. Recently, she has examined mutant p53 pro-oncogenic activities in breast cancer cell lines using the “3D” culture protocol.

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Thomas A. Sellers, Ph.D., M.P.H

  • Chair,Cancer Prevention Research Peer Review Panel
    Executive Vice President and Center Director, H. Lee Moffitt Cancer Center & Research Institute
    Adjunct Professor, Department of Epidemiology and Biostatistics, College of P.H., University of South Florida
    Adjunct Professor, Department of Oncologic Sciences, College of Medicine, University of South Florida
    Adjunct Professor, Department of Epidemiology and Health Policy Research, University of Florida
  

Dr. Sellers’ research program seeks to integrate a basic science background in nutrition and genetics with observational research methods to try to understand questions such as, why do less than 20% of cigarette smokers develop lung cancer and why is a proven effective cancer treatment beneficial to only a subset of patients? His studies are based on genetic analysis of germline DNA and the increasing incorporation of acquired (somatic) events. The primary focus of his research is ovarian cancer, which is a devastating disease with no clear warning signs and high mortality rates. Dr. Sellers also has active collaborations that involve cancers of the breast, lung and prostate. The underlying theme is identifying individual differences in cancer susceptibility and using that information to facilitate approaches to cancer prevention, early detection and precision medicine to enhance outcomes after diagnosis. Critical to the success of this effort is team science, necessitating collaborations with geneticists, pathologists, biostatisticians, biomedical informaticists and clinicians.

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Margaret A. Tempero, M.D.

  • Chair, Clinical and Translational Cancer Research Peer Review Panel
    Director, UCSF Pancreas Center
    Rombauer Family Distinguished Professorship in Pancreas Cancer Clinical and Translational Science
  

Dr. Tempero’s research career has focused on pancreatic ductal adenocarcinoma, especially in the area of investigational therapeutics. She was a pioneer in the use of antibody-based therapies and helped develop the fixed dose rate concept for gemcitabine. Her group has developed effective gemcitabine combinations and provided a foundation for using CA19-9 as a surrogate for survival in clinical trials, and currently is assessing molecular subtypes and molecular enrichment for selecting new drugs for clinical evaluation.

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