Area:
Molecular Biology, Oncology, Cell Biology
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High-probability grants
According to our matching algorithm, Subhamoy Dasgupta is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2017 — 2019 |
Dasgupta, Subhamoy |
K22Activity Code Description: To provide support to outstanding newly trained basic or clinical investigators to develop their independent research skills through a two phase program; an initial period involving and intramural appointment at the NIH and a final period of support at an extramural institution. The award is intended to facilitate the establishment of a record of independent research by the investigator in order to sustain or promote a successful research career. |
Investigating the Role of the Transcriptional Coregulator Src-2 in Castration Resistant Prostate Cancer @ Roswell Park Cancer Institute Corp
Abstract Therapeutic management of metastatic castration-resistant prostate cancer (mCRPC) remains a major clinical challenge. Localized or organ-confined prostate cancer can be cured by surgery, or a combination of androgen deprivation therapy (ADT), radiotherapy and/or chemotherapy. However, tumor recurrence occurs in some men due to the development of ADT-resistant clones which greatly contributes to the lethality of prostate cancer. Aggressive mCRPC frequently metastasizes to distant organs such as bone. As a result treatment becomes challenging and survival rate drops. Hence, there is an urgent need to develop new therapies to cure advanced prostate cancer. Development of aggressive disease is favored by activation of several `escape pathways' among which AR- coactivators such as steroid receptor coactivator-2 (SRC-2/NCOA2) plays a critical role promoting the survival and rapid metastasis of CRPC. SRC-2 promotes a ?metabolic switch? in advanced tumors that predispose them to be dependent on `glutamine' to generate energy and macromolecules required for survival and metastatic growth. Ablation of SRC-2 suppresses prostate tumor survival and metastasis in vivo, indicating this may be a viable approach to treat advanced patients. So our objectives in this proposal are (1) to investigate the mechanisms that promote increased glutamine metabolism in tumors, (2) identify the upstream signaling events that stimulate SRC-2 transcriptional responses to regulate this metabolic reprogramming, and (3) examine the therapeutic benefits of targeting this `metabolic switch' to block cancer progression and metastasis. During the K22 award I expect to identify the molecular links between cellular metabolism and oncogenic events in mCRPC, and examine the potential benefits of targeting this pathway to selectively impair prostate cancer metastasis. The study will make novel insights depicting the altered metabolic pathways and underlying mechanisms promoting the emergence of CRPC, which may lead to the discovery of potential prognostic tools for early detection of clinically significant disease.
|
0.907 |
2020 |
Dasgupta, Subhamoy |
DP2Activity Code Description: To support highly innovative research projects by new investigators in all areas of biomedical and behavioral research. |
Decoding the Nuclear Metabolic Processes Regulating Gene Transcription @ Roswell Park Cancer Institute Corp
In this High Risk High Reward DP2 application I wish to investigate the nuclear functions of mitochondrial metabolic enzymes. It is quite evident from current literature that many of the mitochondrial enzymes are localized to the nucleus, more so in diseased conditions such as cancer. However, there is a significant gap in knowledge about their spatial distribution in the nucleus and biological function. We believe nuclear localization of mitochondrial metabolic enzymes is not random, and there is specific necessity coupled to critical biological functions that regulate this process. In this study we wish to perform a comprehensive functional characterization deciphering the spatial and temporal role of mitochondrial enzymes in the nucleus. Our preliminary findings identified Kreb?s cycle enzymes such as aconitase (ACO2), ?-keto glutarate (AKG), and citrate synthase (CS); and glycolytic enzymes such as pyruvate dehydrogenase (PDH) and ATP-citrate lyase are enriched in the nucleus of cancer cells. We hypothesize these mitochondrial enzymes form complex in the nucleus based which is yet to be characterized. We hypothesize that they function as a large-multi enzyme complex which is recruited to chromatin by transcription factors and coregulators to sustain metabolic stress encountered during gene transcription. Using metabolomics, proteomics, chromatin immunoprecipitation and gene expression analysis, we envision detailing the sequential events driving their recruitment by nuclear factors on chromatin, and their role in reprogramming transcription machinery to drive aggressive cancer. This is a novel concept supported by isolated reports from various groups, yet remains relatively unexplored and a comprehensive mechanistic study is lacking. We envision findings from our study will have a major impact on broad important problems in biomedical research including metabolic disorders and cancer.
|
0.907 |