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High-probability grants
According to our matching algorithm, Geoffrey D. Girnun is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2001 — 2002 |
Girnun, Geoffrey D |
F32Activity Code Description: To provide postdoctoral research training to individuals to broaden their scientific background and extend their potential for research in specified health-related areas. |
The Role of Ppargamma in Colon Cancer and Development @ Dana-Farber Cancer Institute
In recent years the peroxisome proliferator-activated receptor gamma (PPAR gama) has been shown to play a role in cancer. Several groups have shown that PPAR gama plays an anticancer role in several tissues including breast, prostate and relevent to this proposal, colon. However two groups have shown a procancer role for PPAR gama in the colon. Therefore understanding the role of PPAR gama in preventing or promoting colon cancer is important especially considering the use of ligands for PPAR gama in the treatment of type II diabetes. In addition, PPAR gama is expressed at high levels in the colon, implying a role for PPAR gama colonic growth, function, and development. Therefore the goal of this research proposal is to determine the role of PPAR gamain colon carcingenesis and colon function. The specific aims involve: 1) Critically examining the role of PPAR gama in colon carcinogenesis and 2) Examining the role of PPAR gama as a regulator of colonic epithelial cell growth, differentiation and development in vivo using PPAR gama colon specific knock-out mice.
|
0.903 |
2003 — 2007 |
Girnun, Geoffrey D |
K01Activity Code Description: For support of a scientist, committed to research, in need of both advanced research training and additional experience. |
Covalent Modifaction of Ppar Gamma in Colon Cancer @ Dana-Farber Cancer Institute
DESCRIPTION (provided by applicant): The nuclear hormone receptor peroxisome proliferator-activated receptor gamma (PPARgamma) has been shown to play a crucial role in adipogenesis. In recent years, there has been an interest in the role of PPARgamma in cancer. Colon cancer represents one of the leading causes of death in the United States. PPARgamma is expressed at high levels in normal and malignant colonic tissue. Therefore, we have been interested in understanding the role of this receptor in the colon.. Interestingly, the role of PPARgamma in the colon has been controversial with studies indicating both anti- and pro-cancer effects. Recently we have demonstrated in mice heterozygous at the PPAR? locus, that PPARgamma is playing a tumor suppressor role in the colon. Since PPARgamma is a tumor suppressor, the presence of PPARgamma in colonic tumors and cells suggests a disconnect between PPARgamma function and expression. Several studies have shown that PPARgamma is inactivated following MAPKinase-mediated phosphorylation of a conserved serine residue. Several pathways that lead to activation of the MAPKinase pathway have been shown have increased activity in colon cancer. This suggests that one possible reason for the presence of PPARgamma in colon cancer, and discrepancy in response to PPARgamma ligands could be due to PPARgamma phosphorylation. This proposal describes several experiments to critically evaluate the role of PPARgamma phosphorylation in colon cancer. Using pharmacological and eventually genetic approaches we will examine the role phosphorylation of PPARgamma on colon cancer cell growth and gene expression both in vitro and in vivo. A crucial aspect of these studies will be to determine possible mechanisms for the loss of PPARgamma activity due to phosphorylation. This will entail examining the ability of cofactors, both known and potentially novel, to interact in a phospho-dependent manner. Understanding the mechanism of phosphorylation-mediated inactivation of PPARgamma will not only provide insight in to the role of PPARgamma phosphorylation in colon cancer, but also other diseases where PPARgamma has been shown to play a role such as atherosclerosis and diabetes.
|
0.976 |
2012 — 2016 |
Girnun, Geoffrey D |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Metabolic Control of Hepatocellular Carcinoma by Pgc1alpha @ University of Maryland Baltimore
DESCRIPTION (provided by applicant): Hepatocellular carcinoma (HCC) is the fifth most common cancer and the fourth leading cause of cancer death worldwide. For late state stage HCC, five year survival is less than 2%. Therefore prevention of HCC represents the most promising approach to reduce incidence and mortality from this cancer. Altered tumor metabolism has become appreciated as an early and important driver of many cancers including HCC. Increased lipogenesis is commonly found in patients with HCC, and is considered an early event. However, the mechanisms driving some of these metabolic changes/programs is not well understood. We recently showed that loss of the transcriptional coactivator PGC1 greatly reduced chemically induced hepatocellular carcinogenesis. PGC1? is a critical regulator of metabolism, playing a key role in control of oxidative metabolism. However, PGC1 has recently also been shown to regulate lipogenesis. Indeed, we also show that loss of PGC1 is associated with a reduction in the expression of genes driving fatty acid synthesis in the liver. Furthermore, we show that PGC1 promoted increased de novo fatty acid synthesis. Finally using established tumor xenografts, we show that inhibition of fatty acid synthesis blocks the ability of PGC1 to promote tumor growth. Based on this recent work as well as additional preliminary studies we hypothesize that control of energy and lipogenic pathways by PGC1 mediates its effects on HCC. In addition, diabetes, which is linked to an increased risk of HCC, displays many of these metabolic alterations even prior to tumor formation. This is significant since PGC1? is elevated in the livers of diabetic mice and humans, conditions associated with increased hepatic fatty acid synthesis and increased risk of HCC. Therefore we also hypothesize that PGC1 is an important player in the developed of HCC associated with diabetes. We will test these hypotheses in the following independent specific aims. Specific Aim 1) To test the hypothesis that PGC1 promotes hepatocellular carcinogenesis via increasing fatty acid synthesis, Specific Aim 2) Determine whether regulation of AMPK activity by PGC1 is responsible for the effects of PGC1 on carcinogenesis, and Specific Aim 3) Determine whether PGC1? is responsible for the HCC associated with diabetes. Understanding how PGC1? controls metabolic alterations driving HCC and identifying a potentially relevant patient population to target for intervention with therapies directed against PGC1 would greatly reduce the incidence and hence mortality from this challenging cancer. PUBLIC HEALTH RELEVANCE: Identifying how metabolic pathways control tumor development will lead to effective cancer therapies. PGC1 regulates key metabolic pathways implicated in cancer biology and is linked to metabolic diseases in the liver. Therefore, PGC1 represents a promising cancer prevention target. PGC1 is also associated with diabetes, a significant risk factor for hepatocellular carcinoma. Therefore these studies offer the promise of elucidating the mechanisms by which diabetes increases liver cancer risk and identification of a relevant patient population.
|
0.976 |