# Presentation: 121016

## 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

## Workload Distribution

| Study Section | 2004/10 | 2005/01 | 2005/05 | 2005/10 | 2006/01 | 2006/05 |
| --- | --- | --- | --- | --- | --- | --- |
| CAMP | 103 | 111 | 126 | 100 | 95 | 101 |
| CE | 113 | 102 | 133 | 99 | 115 | 129 |
| TCB | 93 | 108 | 93 | 83 | 80 | 99 |
| ONC-U
(MONC) | N/A | N/A | N/A | 62 | 62 | 84 |

**Review Cycle**

## Chronology of EventsFor 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

## 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
- University of Pittsburgh School of Medicine
**Krauss, Robert S., PhD**
- Associate Professor
- Department of Cell and Developmental Biology
- Mount Sinai School of Medicine

**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
_**Executive Secretary**_
- Postow, Elliot, PhD
- Director
- Division of Biologic Basic of Disease
- Center for Scientific Review
- National institutes of Health

## 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.

## 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)

## 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.

## 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.

## Distribution of workload for the 2006/05 review cycle with and without the new study section (MONC)

**Distribution of workload for the 2006/05 review cycle with and without the new study section (MONC****)**

**CAMP**

**CE**

**TCB**

- Without the new study section

- With the new study section

**MONC**

**57%**

**24%**

**19%**

## Discussants

- Dean E. Brenner, MD
- Faye Calhoun, PhD