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Adding An additional Study Section in the Oncological Sciences IRG

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Title: Adding An additional Study Section in the Oncological Sciences IRG


1
Adding An additional Study Section in the
Oncological Sciences IRG
  • Elliot Postow, PhD
  • Director
  • Division of Biological Basis of Disease
  • Center for Scientific Review
  • National Institutes of Health

2
Workload Distribution
Review Cycle
3
Chronology of EventsFor a New Study Section
(MONC) in ONC IRG
  • First meeting of Special Emphasis Panel
  • June 27-28, 2005
  • Letter of invitation sent to members of a Working
    Group
  • March 13, 2006
  • Teleconference to develop guidelines
  • April 17, 2006
  • Guidelines finalized
  • May 8, 2006
  • Presentation to PRAC
  • May 22, 2006
  • First meeting of the MONC study section
  • October 16-17, 2006

4
Oncological Sciences MONC-Working Group, 2006
  • Chairperson
  • Korc, Murray, MD
  • Chair,
  • Department of Medicine
  • Dartmouth Medical School
  • Members
  • Augenlicht, Leonard H, PhD
  • Professor of Medicine Cell Biology
  • Albert Einstein College of Medicine
  • Gallick, Gary, PhD
  • Professor
  • Department of Cancer Biology
  • University of Texas MD Anderson Cancer Center
  • Grandis, Jennifer, R., MD
  • Professor
  • Department of Otolaryngology/ Pharmacology
  • Mietz, Judy, PhD
  • Program Director
  • National Cancer Institute
  • Murphy, Maureen E., PhD
  • Member, Department of Pharmacology
  • Fox Chase Cancer Center
  • Spalholz, Barbara, PhD
  • Program Director
  • National Cancer Institute
  • Wellstein, Anton, MD, PhD
  • Professor
  • Department of Oncology
  • Lombardi Cancer Center Georgetown University

5
Cancer Etiology (CE) Guidelines
  • CE reviews grant applications related to the
    causal agents, processes, and cells involved in
    early events in carcinogenesis. Areas included
    within CE involve gene regulation, DNA damage and
    repair mechanisms, chemical and viral
    carcinogenesis. Emphasis is on linking chemistry
    and pathology to study the etiology of cancer.
  • Specific areas covered by CE include
  • Gene regulation including transcription factors,
    RNA stability and processing, as they contribute
    to carcinogenesis.
  • DNA damage and repair mechanisms related to
    carcinogenesis.
  • Chemically- and environmentally-induced
    carcinogenesis.
  • Identification of causal agents such as
    xenobiotics, DNA adducts, endogenous and
    exogenous compounds that modulate early events in
    carcinogenesis.
  • Responses to stress such as free radicals,
    oxidative stress and reactive oxygen species as
    they contribute to the carcinogenic process.
  • Metabolism of endogenous and exogenous compounds
    that lead to carcinogenesis
  • Contribution of viruses, other than HIV/AIDS, to
    carcinogenesis.

6
Molecular Oncogenesis (MONC) Guidelines
  • MONC reviews grant applications that focus on
    the early molecular events that lead to oncogenic
    transformation such as the identification of
    oncogenes and tumor suppressor genes alterations
    in signaling, growth, and cell cycle control
    pathways and protein stability/degradation
    mechanisms. Applications dealing with normal
    developmental processes as they pertain to
    oncogenic transformation are also reviewed.
  • Specific areas covered by MONC include
  • Identification of oncogenes and tumor suppressor
    genes or alterations in their expression or
    function that may contribute to oncogenic
    transformation. (CAMP)
  • Alterations in signal transduction pathways that
    may modulate or lead to oncogenic transformation.
    (CAMP, CE, TCB)
  • Proteasome-mediated degradation Mechanisms
    and/or alterations of protein stability that
    could contribute to transformation, including
    post-translation modification such as
    ubiquitylation or sumoylation. (CE)
  • Cell cycle regulation and dysregulation that may
    contribute to early oncogenic transformation.
    (CAMP, TCB)
  • Mechanisms of immortalization as a prerequisite
    for oncogenic transformation. (CAMP, CE)
  • Biology of progenitor cells, including the
    identification and characterization of cancer
    stem cells that may be involved in oncogenic
    transformation. (CAMP)

7
Cancer Molecular Pathobiology (CAMP) Guidelines
  • CAMP reviews applications involving
    pathology of the malignant cell with the emphasis
    on mechanisms controlling cell growth and death,
    and the molecular events in gene regulation.
  • Specific areas covered by CAMP include
  • Oncogenes and tumor suppressor genes and their
    pathways in oncogenesis.
  • Gene regulation including chromatin structure and
    remodeling, RNA stability, transcription and
    translation relevant to oncogenesis.
  • Signaling transduction pathways related to the
    regulation of cell growth in cancer.
  • Role of characterized stem cells in oncogenesis.
  • Mechanisms of overcoming senescence in the
    context of oncogenesis
  • Cell death pathways (both apoptotic and
    non-apoptotic) in cancer.
  • Mechanisms of oncogenesis mediated by telomeres
    and telomerase.

8
Tumor Cell Biology (TCB) Guidelines
  • TCB reviews grant applications focusing on
    signal transduction and growth factor regulation
    in neoplasias and tumor progression.
  • Specific areas covered by TCB include
  • Signal transduction mediated by protein kinases,
    phosphatases, and other proteins, including
    signaling mediated by hypoxia, inflammation, and
    nutrient sensing mechanisms.
  • Signaling by cell surface receptors, growth
    factors, cytokines, and associated proteins. This
    includes analyses of the composition, formation
    and functioning of signaling complexes in tumor
    progression and in tumor cells.
  • Analysis of interactions among signaling pathways
    in tumor cells and tumor progression.
  • Pathways regulated by oncogenes and tumor
    suppressor genes how these genes alter signaling
    in neoplasms and the consequences of these
    alterations on tumor cell phenotype and
    physiology.
  • Hormonal modulation of carcinogenesis, including
    endocrine signaling as it relates to
    tumorigenesis, steroid metabolism, and hormone
    receptors.
  • Differentiation and transdifferentiation in
    neoplasias.
  • Signal transduction mediated by the cytoskeleton
    as it relates to tumorigenesis and tumor
    progression.

9
Distribution of workload for the 2006/05 review
cycle with and without the new study section
(MONC)
CAMP
Without the new study section
CE
57
TCB
24
19
With the new study section
MONC
10
Discussants
  • Dean E. Brenner, MD
  • Faye Calhoun, PhD
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