PROSTATE TUMORS CAN CHANGE THE FUNCTION OF IMMUNE CELLS IN MICE

From an NIH press release:

PROSTATE TUMORS CAN CHANGE THE FUNCTION OF IMMUNE CELLS IN MICE

Researchers have discovered that prostate tumors in mice can cause immune cells known as CD8+ T cells to change their function from cells that have antitumor activity to cells that suppress immune responses. This finding, by researchers at the National Cancer Institute (NCI), part of the National Institutes of Health, has important implications for the design of immune-based therapies for cancer. The new study, available online, appears in the Oct. 15, 2009, issue of the Journal of Immunology.

"The conversion of CD8+ T cells into suppressor cells may be one of the mechanisms by which tumors restrict the immune system's ability to control tumor growth," said Arthur A. Hurwitz, Ph.D., head of the Tumor Immunity and Tolerance Group at NCI's Center for Cancer Research. "Studying this process in mice may help explain why some cancer patients have an initial response from their immune-based therapy, but this response fails with time."

In mice and humans, when the immune system encounters a pathogen or other foreign invader, it responds by mounting an immune response. Part of this response involves the recruitment and activation of CD8+ T cells, which are also called cytotoxic T cells or killer T cells, to help destroy the invader. CD8+ T cells also play a role in immune responses against tumor cells. Other T cells, known as CD4+ T regulatory cells, work to suppress CD8+ T cell activity. Immune suppression by these regulatory T cells helps prevent the body from attacking its own cells. A high level of CD4+ T regulatory cells is also associated with poor prognosis of some cancers. Moreover, research in mice has shown that blocking the immune suppressive activity of these regulatory T cells enhances the body's immunity against tumors, causing tumor growth to slow and improving the antitumor immune responses elicited by cancer vaccines.

Recent evidence in mice has suggested that CD8+ T cells can develop suppressive activities similar to those of CD4+ T regulatory cells. In addition, CD8+ suppressor cells have been found in cancer patients. The presence of these suppressor cells could explain earlier findings by Hurwitz's team that prostate tumor-specific CD8+ T cells injected into prostate tumor-bearing mice migrate to the tumors but then become unresponsive, or tolerized, to the tumor cells. It remained unclear, however, whether the suppressive CD8+ T cells have suppressor activity before they reach the tumor or whether they are converted into suppressor cells by the tumor.

In the new research, Hurwitz's team found that CD8+ T cells acquire immune suppressive functions after they enter the mouse tumor microenvironment, which encompasses nearby noncancerous cells and immune cells in addition to tumor cells. The researchers found that tumor-specific CD8+ T cells isolated from the tumors were able to suppress the proliferative capacity of nonspecific T cells, whereas tumor-specific CD8+ T cells isolated from lymph nodes of the mice were unable to do so.

This anti-proliferative activity appeared to be caused, in part, by substances secreted by the CD8+ T cells after they had been converted to suppressor cells. One of these substances, TGF-beta, is a protein that controls cell proliferation and differentiation and plays a role in cancer and other diseases. TGF-beta is thought to be involved in the immune-suppressive activity of CD4+ T-regulatory cells.

Next, the team investigated whether the conversion of tumor-specific CD8+ T cells to suppressor cells could be prevented. To do this, they administered tumor-specific CD4+ and CD8+ T cells to prostate tumor-bearing mice. Some CD4+ T cells act as helper cells and enhance the activity of other immune cells, including CD8+ T cells. The researchers found that, under these conditions, CD8+ T cells isolated from the prostate tumors no longer suppressed the proliferation of other T cells. Moreover, these cells produced less TGF-beta than cells that were not exposed to CD4+ T cells.

The researchers propose that activated CD4+ T cells that enter tumors may secrete factors that support the CD8+ T cell antitumor functions, or may help other immune cells located in the tumor block the processes by which CD8+ T cells acquire their suppressive activity.

Future work by this team will focus on defining the mechanisms by which tumor-specific CD8+ T cells gain their suppressive functions upon entering the mouse tumor microenvironment. "It is important to understand how these cells become suppressive and how they mediate suppression to find approaches to block these processes," said Hurwitz. "This will enhance our ability to generate more effective antitumor T cell responses in mice, which then might be translated to human."

For more information on Dr. Hurwitz's research, please go to .

NCI leads the National Cancer Program and the NIH effort to dramatically reduce the burden of cancer and improve the lives of cancer patients and their families, through research into prevention and cancer biology, the development of new interventions, and the training and mentoring of new researchers. For more information about cancer, please visit the NCI Web site at or call NCI's Cancer Information Service at 1-800-4-CANCER (1-800-422-6237).

The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit .

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REFERENCE:
Shafer-Weaver, KA, Anderson, MJ, Stagliano K, Malyguine, A, Greenberg, NM, and Hurwitz AA. Cutting Edge: Tumor-Specific CD8+ T Cells Infiltrating Prostatic Tumors Are Induced to Become Suppressor Cells. J Immunol. Oct. 15, 2009. Vol. 183, No. 8.


U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
National Cancer Institute (NCI)
For Immediate Release: Wednesday, October 7, 2009

CONTACT: NCI Office of Media Relations, 301-496-6641,

MicroRNAS IN BLOOD MAY BE BIOMARKERS OF PANCREATIC CANCER

We desperately need this new test for pancreatic cancer and we need a cure ASAP. - BRH.

MicroRNAS IN BLOOD MAY BE BIOMARKERS OF PANCREATIC CANCER

Small molecules known as microRNAs, which can be detected in blood samples, have the potential to help identify patients with pancreatic cancer, a study finds. The study, by researchers at The University of Texas M.D. Anderson Cancer Center in Houston, was supported by the Early Detection Research Network (EDRN) of the National Cancer Institute (NCI), part of the National Institutes of Health. The paper appeared online Sept. 1, 2009, in Cancer Prevention Research.

Pancreatic cancer is a highly fatal disease that is difficult to detect at early stages. In most patients, symptoms do not appear until the cancer is locally advanced or has spread to other parts of the body. The absence of symptoms in early-stage disease and the current lack of effective, minimally invasive screening and diagnostic techniques limit the available treatment options. Both contribute to the high mortality rate observed for patients with pancreatic cancer.

"The development of a minimally invasive test for the early detection and diagnosis of pancreatic cancer is greatly needed," said Sudhir Srivastava, Ph.D., chief of the Cancer Biomarkers Research Group in NCI's Division of Cancer Prevention. "An important step is to identify biomarkers for pancreatic cancer, such as microRNAs, circulating in the bloodstream that can be used to distinguish individuals with pancreatic cancer from individuals without the disease."

MicroRNAs, or miRNAs, are short strands of RNA. The miRNAs regulate gene expression by controlling the translation of a specific type of RNA called messenger RNA which relays the genetic instructions for making proteins. Previous research has indicated that miRNAs play important roles in regulating normal cell proliferation and in cancer. Altered patterns of miRNA expression have been seen in pancreatic cancer as well as many other cancers. In addition, it has recently been reported that tumor-derived miRNAs can be detected in blood and that these molecules are stable in stored samples. Thus, miRNAs circulating in the blood may have the potential to serve as novel biomarkers for the detection and diagnosis of pancreatic cancer.

To evaluate the feasibility of using miRNAs in the blood as biomarkers for pancreatic cancer, the researchers selected a set of four miRNAs that have been associated with pancreatic cancer -- miR-21, miR-210, miR-155, and miR-196a. Among these, miR-155 has been identified as a candidate biomarker for early pancreatic cancer, and expression of miR196a has been shown to increase during disease progression. Levels of all four miRNAs were assessed in blood samples from 28 pancreatic cancer patients and 19 healthy volunteers. The study population consisted of patients with pathologically confirmed pancreatic cancer and healthy disease free individuals recruited at the M.D. Anderson Cancer Center between 2002 and 2008. The team found that sensitivity -- or ability to accurately detect pancreatic cancer -- using the panel of four miRNAs was 64 percent. The panel also showed an 89 percent specificity, which indicates the proportion of study participants who did not have pancreatic cancer and were correctly identified as being disease free.

"Our results demonstrate proof of principle in developing a blood test based on miRNA signatures for pancreatic cancer," said senior author Subrata Sen, Ph.D., of M.D. Anderson's Department of Molecular Pathology. "More work is needed to evaluate this strategy in different grades and stages of the disease. We are in the process of initiating such studies in collaboration with members of EDRN." For example, the researchers will test the ability of the miRNAs to detect pancreatic cancer in separate patient populations.

Pancreatic cancer, the fourth most common cause of cancer death in the United States, has a poor survival rate compared with that of other types of cancer. Less than five percent of the patients with pancreatic cancer survive five years past diagnosis.

For more information about the Department of Molecular Pathology at M.D. Anderson, please go to .

For more information on NCI's EDRN, please go to: .

NCI leads the National Cancer Program and the NIH effort to dramatically reduce the burden of cancer and improve the lives of cancer patients and their families, through research into prevention and cancer biology, the development of new interventions, and the training and mentoring of new researchers. For more information about cancer, please visit the NCI Web site at or call NCI's Cancer Information Service at 1-800-4-CANCER (1-800-422-6237).

The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit .

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U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
National Cancer Institute (NCI)
Embargoed for Release: Tuesday, September 1, 2009, 1 p.m., EDT

CONTACT: NCI Office of Media Relations, 301-496-6641, ncipressofficers@mail.nih.gov>

NIH STUDY REVEALS NEW GENETIC CULPRIT IN DEADLY SKIN CANCER

New information may lead to a new treatment for deadly melanoma. This is why genetic testing is so important. - BRH

NIH STUDY REVEALS NEW GENETIC CULPRIT IN DEADLY SKIN CANCER
Sequencing Work Points to New Target for Melanoma Treatment

Drawing on the power of DNA sequencing, National Institutes of Health researchers have identified a new group of genetic mutations involved in the deadliest form of skin cancer, melanoma. This discovery is particularly encouraging because some of the mutations, which were found in nearly one-fifth of melanoma cases, reside in a gene already targeted by a drug approved for certain types of breast cancer.

In the United States and many other nations, melanoma is becoming increasingly more common. A major cause of melanoma is thought to be sun exposure; the ultraviolet radiation in sunlight can damage DNA and lead to cancer-causing genetic changes within skin cells.

In work published in the September issue of Nature Genetics, a team led by Yardena Samuels, Ph.D., of the National Human Genome Research Institute (NHGRI) sequenced the protein tyrosine kinase (PTK) gene family in tumor and blood samples from people with metastatic melanoma. The samples were collected by the study's coauthor Steven Rosenberg, M.D., Ph.D., a leading expert on melanoma and chief of surgery at the National Cancer Institute (NCI).

The PTK family includes many genes that, when mutated, promote various types of cancer. However, relatively little had been known about roles played by PTK genes in human melanoma. The NIH study was among the first to use large-scale DNA sequencing to systematically analyze all 86 members of the PTK gene family in melanoma samples.

The team's initial survey, which involved samples from 29 melanoma patients, identified mutations in functionally important regions of 19 PTK genes, only three of which had been previously implicated in melanoma. The researchers then conducted more detailed analyses of those 19 genes in samples from a total of 79 melanoma patients.

One of the newly implicated genes stood out from the rest. Researchers detected mutations in the ERBB4 gene (also known as HER4) in 19 percent of patients' tumors, making it by far the most frequently mutated PTK gene in melanoma. In addition, researchers found that many ERBB4 mutations were located in functionally important areas similar to those seen in other PTK oncogenes involved in lung cancer, brain cancer and gastric cancer.

Next, the researchers moved on to laboratory studies of melanoma cells with ERBB4 mutations. They found that these melanoma cells were dependent on the presence of mutant ERBB4 for their growth. What's more, the melanoma cells grew much more slowly when they were exposed to a chemotherapeutic drug known to inhibit ERBB4. The drug, called lapatinib (Tykerb), was approved by the Food and Drug Administration in 2007 for combination use in breast cancer patients already taking the drug capecitabine (Xeloda).

Encouraged by their study results, the researchers are planning a clinical trial using lapatinib in patients with metastatic melanoma harboring ERBB4 mutations. The clinical trial will be conducted under the direction of Dr. Rosenberg at the NIH Clinical Center. "This collaborative study represents an ideal example of how sophisticated genetic analyses can be translated to the benefit of cancer patients," said Dr. Rosenberg.

"We have found what appears to be an Achilles' heel of a sizable share of melanomas," said Dr. Samuels, who is an investigator in the Cancer Genetics Branch of the NHGRI's Division of Intramural Research. "Though additional work is needed to gain a more complete understanding of these genetic mutations and their roles in cancer biology, our findings open the door to pursuing specific therapies that may prove useful for the treatment of melanoma with ERBB4 mutations."

In addition to ERBB4, the researchers identified two additional PTK genes, FLT1 and PTK2B, with a relatively high rate of mutations in melanoma. Each of these genes was mutated in about 10 percent of the tumor samples studied.

NHGRI Scientific Director Eric D. Green, M.D., Ph.D., pointed out how such research is helping to lay the groundwork for the era of personalized medicine. "We envision a day when each cancer patient will have therapies tailored to the specific genetic profile of his or her tumor. Ultimately, this should lead to more effective and less toxic approaches to cancer care," said Dr. Green, who directs the NIH Intramural Sequencing Center, which generated the DNA sequence data for the melanoma study.

In addition to NIH scientists, the team included a researcher from the Johns Hopkins Kimmel Cancer Center in Baltimore.

In May 2009, Dr. Samuel's group reported in Nature Genetics another large-scale DNA sequencing study of a different group of genes involved in melanoma, the matrix metalloproteinase (MMP) gene family. This earlier study found that one gene, MMP-8, thought to spur cancerous growth actually served to inhibit it. Those findings are now helping to shape melanoma treatment strategies aimed at MMP genes.

For high resolution micrographs of metastatic melanoma, go to and .

NCI leads the National Cancer Program and the NIH effort to dramatically reduce the burden of cancer and improve the lives of cancer patients and their families, through research into prevention and cancer biology, the development of new interventions, and the training and mentoring of new researchers. For more information about cancer, please visit the NCI Web site at or call NCI's Cancer Information Service at 1-800-4-CANCER (1-800-422-6237).



NHGRI is one of the 27 institutes and centers at the NIH, an agency of the Department of Health and Human Services. The NHGRI Division of Intramural Research develops and implements technology to understand, diagnose and treat genomic and genetic diseases. Additional information about NHGRI can be found at its Web site, .

The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit .

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RISK OF PANCREATIC CANCER LINKED TO VARIATION IN GENE THAT DETERMINES BLOOD TYPE

A gene variation or gene defect has been found that increases the risk of pancreatic cancer, which is one of the deadliest of all cancers. - BRH

RISK OF PANCREATIC CANCER LINKED TO VARIATION IN GENE THAT DETERMINES BLOOD TYPE
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U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
National Cancer Institute (NCI)
Embargoed for Release: Sunday, August 2, 2009, 1 p.m., EDT

CONTACT: NCI Office of Media Relations, 301-496-6641,

RISK OF PANCREATIC CANCER LINKED TO VARIATION IN GENE THAT DETERMINES BLOOD TYPE

Common variants of the gene that determines human blood type are associated with an increased risk of pancreatic cancer, according to a study by scientists at the National Cancer Institute (NCI), part of the National Institutes of Health, and colleagues from many universities and research institutions. The study, published online Aug. 2, 2009, in Nature Genetics, is consistent with an observation first made more than 50 years ago.

In the study, the researchers discovered that genetic variation in a region of chromosome 9 that contains the gene for ABO blood type was associated with pancreatic cancer risk. Individuals with the variant that results in blood types A, B, or AB were at an increased risk of pancreatic cancer, compared to those with the variant for blood type O. This finding is consistent with previous research, some of it dating back to the 1950s and 1960s, that had shown increased risks of gastric and pancreatic cancer among individuals of the A and B blood groups (i.e., blood types A, B, and AB). The latest results provide a genetic basis for those earlier observations.

A person's blood type depends on which form or forms of the ABO gene they inherit from their parents. The protein produced by the ABO gene determines the type of carbohydrates (complex sugars) that are present on the surface of red blood cells and other cells, including cells of the pancreas. The proteins encoded by the A and B forms of the gene transfer different carbohydrates onto the cell surfaces to make A and B blood types. The O form encodes a protein that is unable to transfer carbohydrates. Studies by other researchers have shown that ABO protein encoding in pancreatic tumor cells is different than in normal pancreatic cells.

To discover genetic variations that contribute to pancreatic cancer risk, the research team conducted a genome-wide association study (GWAS). In a GWAS, researchers analyze common variants, called single-nucleotide polymorphisms (SNPs), in the genomes of people with a disease and people without the disease. Initially, the research team studied the genomes of 1,896 patients with pancreatic cancer and 1,939 control subjects to identify SNPs with a strong association with pancreatic cancer. The team then verified its findings by studying the genomes of another 2,457 people with pancreatic cancer and 2,654 people without the disease. In the end, they identified several SNPs on the long arm of chromosome 9 that were associated with pancreatic cancer risk and mapped to the ABO gene.

"Only by working across disciplines and with more than a dozen research groups were we able to make this important discovery of the potential role of the ABO gene in pancreatic cancer risk," said co-author Patricia Hartge, Sc.D., of NCI's Division of Cancer Epidemiology and Genetics (DCEG). "Although it will take much more work, this finding may lead to improved diagnostic and therapeutic interventions that are so desperately needed."


Pancreatic cancer is the fourth leading cause of cancer death in the United States. It is difficult to detect, and in many people it is not diagnosed until after the disease has spread to other parts of the body. Less than five percent of Americans with pancreatic cancer survive five years past diagnosis. Risk factors include smoking, diabetes, race, and a family history of the disease.

"Pancreatic cancer is the newest beneficiary of so-called high-throughput genotyping that, over the past two years, has yielded scores of genetic hot-spots linked to risk for cancer and other diseases," said co-author Stephen J. Chanock, M.D., chief of NCI's Laboratory of Translational Genomics in DCEG. "As more variants are discovered and follow-up studies are conducted to examine the biological effects of these variants, a better understanding will emerge of the inherited risk factors and mechanisms that lead to the development of pancreatic cancer."

The study was part of PanScan, a GWAS of pancreatic cancer conducted by the Pancreatic Cancer Cohort Consortium, composed of 14 academic centers. The investigators are conducting whole-genome scans to identify common genetic variants that may be markers of susceptibility to pancreatic cancer.

Analyses and data from PanScan will be available through NCI's caBIG (Cancer Biomedical Informatics Grid). The summary results for similar data on breast and prostate cancer are already freely available to other researchers at this Web site.

For more information on Dr. Hartge's research, please go to .

For more information on Dr. Chanock's research, please go to .

For more information about PanScan, please go to .

NCI leads the National Cancer Program and the NIH effort to dramatically reduce the burden of cancer and improve the lives of cancer patients and their families, through research into prevention and cancer biology, the development of new interventions, and the training and mentoring of new researchers. For more information about cancer, please visit the NCI Web site at or call NCI's Cancer Information Service at 1-800-4-CANCER (1-800-422-6237).

The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit .
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REFERENCE: Amundadottir L., et al. Genome-wide association study identifies ABO Blood Group Susceptibility Variants for Pancreatic Cancer. "Nature Genetics." Online August 2, 2009.

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Keywords: National Institute of Health, United States, National Cancer Institute, Genome-wide association study, United States Department of Health and Human Services, National Cancer Program, Single-nucleotide polymorphism

NIH AND VA ANNOUNCE $7 MILLION PARTNERSHIP FOR SUBSTANCE ABUSE RESEARCH AMONG MILITARY PERSONNEL, VETERANS AND THEIR FAMILIES

More research for Dr. Drew.... and everyone needing to know more about substance abuse.

NIH AND VA ANNOUNCE $7 MILLION PARTNERSHIP FOR SUBSTANCE ABUSE RESEARCH AMONG MILITARY PERSONNEL, VETERANS AND THEIR FAMILIES

U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
National Institute on Drug Abuse (NIDA)
For Immediate Release: Thursday, July 30, 2009

MEDIA CONTACT: Stephanie Older, 301-443-6245,

NIH AND VA ANNOUNCE $7 MILLION PARTNERSHIP FOR SUBSTANCE ABUSE RESEARCH AMONG MILITARY PERSONNEL, VETERANS AND THEIR FAMILIES
Research will focus on war efforts in Iraq and Afghanistan

Washington, D.C. - Two federal departments have joined forces to create a first-time collaborative funding project to support research on substance abuse and associated problems among U.S. military personnel, veterans and their families. The National Institute on Drug Abuse (NIDA), part of the National Institutes of Health, in partnership with two other NIH Institutes -- the National Institute on Alcohol Abuse and Alcoholism (NIAAA), and the National Cancer Institute (NCI) -- are jointly collaborating with the Department of Veterans Affairs (VA), on a seven million dollar funding opportunity announcement for research in this area. NIH is the leading scientific agency within the U.S. Department of Health and Human Services.

There is a growing awareness that returning military personnel -- whatever their overseas role -- need help confronting a variety of war related problems including traumatic brain injury, post traumatic stress disorder, depression, anxiety, sleep disturbances, and substance abuse, including tobacco, alcohol and other drugs. Many of these problems are interconnected, and contribute to individual health and family relationship crises, yet there has been little research on how to prevent and treat the unique characteristics of wartime related substance abuse issues. The funding opportunity announcement will focus on the causes, screening and identification, prevention and treatment of substance use and abuse--including alcohol, tobacco and other drugs--and associated problems, including post-traumatic stress disorder.

"Active duty military personnel and the community of veterans have sacrificed so much for our country that we owe them nothing less than the best that research can offer," said Acting NIH Director Raynard S. Kington, M.D., Ph.D.

This funding opportunity announcement was prompted by a meeting held in January to gain a better understanding of the substance abuse intervention needs of military personnel, veterans, and their families and develop recommendations for prevention and treatment research priorities in this area. This is the first post-meeting announcement and is specific to those serving, or who have served, in Operation Enduring Freedom (Afghanistan) and/or Operation Iraqi Freedom.


"Working in collaboration with key federal agencies, we hope to learn more about how to address the array of social and emotional problems caused by the trauma of war that bring so much pain to soldiers and their families," said NIDA Director Nora D. Volkow. "Even though they are no longer in combat, many of these brave men and women are now fighting substance addiction -- another dangerous enemy."

"The transition period as soldiers withdraw from battlefield stress and face the rigors of re-adjusting to life at home can be a critical turning point," said NIAAA Acting Director Kenneth Warren. "This partnership will enhance our efforts to find solutions to the complex alcohol and substance abuse problems that plague our soldiers and their families."

The grant applications submitted will be reviewed by an NIH review panel that includes scientific expertise regarding substance abuse and associated conditions. Each agency will fund grants relevant to its mission. NIDA will fund $2 million, NIAAA $2 million, NCI $1 million and the VA $2 million.

As the research evolves, the VA will look for new tools to confront a complex cascade of problems which increasingly threaten the medical and physical health of its patients.

Dr. Joel Kupersmith, the VA's chief research and development officer, comments, "VA has long supported a strong research program for veterans, and this request for applications provides the opportunity to clearly focus on essential issues encountered by the newest generation of veterans in conjunction with federal partners."

Research questions related to all phases of the deployment cycle (i.e., pre-deployment, deployment, re-integration, and separation) and all branches of the military (e.g., Army, Navy, Marines, Air Force, Coast Guard, U.S. Military Reserves, National Guard) and veterans are of interest. The deadline for grant applications is December 22, 2009.

The Department of Veterans Affairs (VA) -- VA's Office of Research and Development (ORD) aspires to discover knowledge, develop VA researchers and health care leaders, and create innovations that advance health care for our veterans and the nation. For more information about VA Research: .

The National Institute on Alcohol Abuse and Alcoholism, part of the NIH, is the primary U.S. agency for conducting and supporting research on the causes, consequences, prevention, and treatment of alcohol abuse, alcoholism, and alcohol problems, and disseminates research findings to general, professional, and academic audiences. Additional alcohol research information and publications are available at .

NCI leads the National Cancer Program and the NIH effort to dramatically reduce the burden of cancer and improve the lives of cancer patients and their families, through research into prevention and cancer biology, the development of new interventions, and the training and mentoring of new researchers. For more information about cancer, please visit the NCI Web site at or call NCI's Cancer Information Service at 1-800-4-CANCER (1-800-422-6237).

The National Institute on Drug Abuse is a component of the National Institutes of Health, U.S. Department of Health and Human Services. NIDA supports most of the world's research on the health aspects of drug abuse and addiction. The Institute carries out a large variety of programs to inform policy and improve practice. Fact sheets on the health effects of drugs of abuse and information on NIDA research and other activities can be found on the NIDA home page at . To order publications in English or Spanish, call NIDA's new DrugPubs research dissemination center at 1-877-NIDA-NIH or 240-645-0228 (TDD) or fax or email requests to 240-645-0227 or drugpubs@nida.nih.gov. Online ordering is available at .

The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit .

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