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Dissecting mechanisms of tumor initiation via immunomodulation

Award Number: SC1GM140907
ORGANIZATION: NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 03/17/2021
PERIOD OF PERFORMANCE END DATE: 02/28/2025

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Dissecting mechanisms of tumor initiation via immunomodulation - Project Summary/Abstract Since the year 2000, pancreatic cancer diagnosis has been on the rise with future projections considering it to be the 2nd leading cause of cancer death by 2030. Furthermore, the majority of patients die within 1 year of diagnosis due to a lack of early detection and early intervention, both of which limit therapy options. Pancreatic ductal adenocarcinoma (PDAC) is the major form of pancreatic cancer and a disorder of oncogenic Kras. Turning off Kras mutants, including KrasG12D or KrasG12V is the key to curing PDAC. However, there are no known inhibitors which directly target these two mutants. PDAC originates from acinar cells through the acinar-to-ductal metaplasia (ADM) process. Upon acquisition of oncogenic Kras mutation, it converts acinar cells to duct-like cells, which subsequently develop into cancer cells. Because 1) activating Kras mutations are required for PDAC growth and maintenance; 2) ADM is the initial step of PDAC development; 3) KrasG12D and KrasG12V in PDAC are undruggable; and 4) PDAC patients are diagnosed too late, it is important to understand how KrasG12D regulates ADM and precancerous lesion formation. Acquiring information pertaining to the ADM process and its regulation will provide groundwork for the identification of biomarkers used for early detection, and drug targets for early intervention successfully reducing the death toll of PDAC. We identified CCL9 as a new downstream target of KrasG12D in pancreas acini of ADM and subsequent PanIN development. So far, little is known about CCL9 in physiological and pathological settings. Gene amplification of CCL15, a human orthologue of CCL9, is present in human PDAC and is a predictor of shorter survival. The goal of this proposal is to dissect the mechanisms and functions of KrasG12D/CCL9 axis on PDAC initiation and tumor development. We will accomplish this goal with the following specific aims. 1. To delineate the mechanisms of CCL9-induced PDAC initiation through ADM; 2. To evaluate the in vivo function of CCL9 in KrasG12D-mediated PDAC initiation. Successful completion of these aims will reveal new functions of CCL9 in PDAC initiation and growth, add new mechanistic insights into the early event of PDAC development, and establish the essential groundwork for CCL15, the human orthologue of CCL9, as one of the biomarkers for early detection and the new treatment strategies for early intervention in the clinic to fight PDAC death.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2024 ( Subtotal = $308,000 )
2024	2024	CLARK ATLANTA UNIVERSITY, INC.	223 JAMES P BRAWLEY DR SW	ATLANTA	GA	30314	FULTON	USA	Biomedical Research and Research Training	000	4	2/16/2024	NON-COMPETING CONTINUATION	$277,200
2024	2024	CLARK ATLANTA UNIVERSITY, INC.	223 JAMES P BRAWLEY DR SW	ATLANTA	GA	30314	FULTON	USA	Biomedical Research and Research Training	001	4	6/18/2024	NON-COMPETING CONTINUATION	$30,800
														Subtotal = $308,000

Issue Date FY: 2023 ( Subtotal = $346,500 )
2023	2023	CLARK ATLANTA UNIVERSITY, INC.	223 JAMES P BRAWLEY DR SW	ATLANTA	GA	30314	FULTON	USA	Biomedical Research and Research Training	000	3	2/13/2023	NON-COMPETING CONTINUATION	$346,500
														Subtotal = $346,500

Issue Date FY: 2022 ( Subtotal = $269,500 )
2022	2022	CLARK ATLANTA UNIVERSITY, INC.	223 JAMES P BRAWLEY DR SW	ATLANTA	GA	30314	FULTON	USA	Biomedical Research and Research Training	001	2	6/14/2022	NON-COMPETING CONTINUATION	$26,950
2022	2022	CLARK ATLANTA UNIVERSITY, INC.	223 JAMES P BRAWLEY DR SW	ATLANTA	GA	30314	FULTON	USA	Biomedical Research and Research Training	000	2	2/9/2022	NON-COMPETING CONTINUATION	$242,550
														Subtotal = $269,500

Issue Date FY: 2021 ( Subtotal = $346,500 )
2021	2021	CLARK ATLANTA UNIVERSITY, INC.	223 JAMES P BRAWLEY DR SW	ATLANTA	GA	30314	FULTON	USA	Biomedical Research and Research Training	000	1	3/17/2021	NEW	$346,500
														Subtotal = $346,500

Grand Total All Awards = $1,270,500

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Dissecting mechanisms of tumor initiation via immunomodulation

Award Number: SC1GM140907

ORGANIZATION: NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 03/17/2021

PERIOD OF PERFORMANCE END DATE: 02/28/2025

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