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Defining Inflammatory Triggers that Induce Diverse Subtypes of Gastric Metaplasia

Award Number: F30DK134124
ORGANIZATION: NATIONAL INSTITUTE OF DIABETES & DIGESTIVE & KIDNEY DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 01/01/2023
PERIOD OF PERFORMANCE END DATE: 12/31/2026

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Defining Inflammatory Triggers that Induce Diverse Subtypes of Gastric Metaplasia - PROJECT SUMMARY Chronic gastritis initiates a pathological progression of disease which in some individuals culminates in gastric cancer, the fourth leading cause of cancer related mortality worldwide. Helicobacter pylori infection is the most common cause of gastritis and responsible for most gastric cancer cases worldwide. Autoimmune gastritis is another prominent cause of gastritis increasing the risk of gastric cancer development. Persistent gastric inflammation initiates the transformation of healthy epithelial cells into pre-cancerous metaplastic cells which transform into adenocarcinoma in a subset of individuals. Recent transcriptomic analyses of gastric adenocarcinoma have led to the identification of four distinct molecular subtypes. This discovery has improved targeted treatment and surveillance strategies for each distinct gastric cancer subtype. Currently, there is a need for an in-depth molecular analysis of pre-cancerous gastric metaplasia. We recently discovered that gastric metaplasia can also take on distinct molecular phenotypes in the autoimmune setting. It needs to be determined whether metaplasia arising out of H. pylori infection, known to inject cytotoxins that can interfere with cell- signaling pathways possibly promoting oncogenic transformation, is phenotypically distinct from metaplasia arising out of autoimmune gastritis. If metaplastic subtypes are conserved, then chronic inflammatory signals, independent of etiology, likely contribute to cancer progression; however, if metaplastic subtypes in infection are distinct from autoimmunity, then factors unique to the bacterial infection likely drive an alternative trajectory of oncogenic transformation. Furthermore, how certain inflammatory cytokines (e.g., IL-4/IL-13) impact the development of gastric metaplasia and specific molecular subtypes of metaplasia needs to be established. Identifying molecular phenotypes of pre-cancerous metaplastic cells, in distinct disease settings, that may carry differential oncogenic potentials, will contribute to the discovery of novel screening targets to decrease the gastric cancer burden in highly susceptible individuals. Identifying the inflammatory signals that promote the development of potentially high-risk metaplastic cells will aid in discovery of new therapeutic strategies for inhibiting gastric cancer. In this proposal, metaplasia arising out of two common etiologies of gastritis, H. pylori infection and autoimmune gastritis, will be molecularly defined and compared. Gastric metaplasia from human gastritis patients will be transcriptionally profiled to determine the phenotypes of metaplasia induced by human disease. The impact of inflammatory cytokines, IL-4 and IL-13, on inducing/expanding phenotypically distinct subtypes of gastric metaplasia will also be determined. This work will improve the mechanistic understanding of gastric carcinogenesis in the settings of H. pylori infection and autoimmune gastritis. This knowledge can then be used to improve medical prevention strategies and identify novel targets for therapeutic intervention of gastric cancer.


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: 2025 ( Subtotal = $54,538 )
2025	2025	SAINT LOUIS UNIVERSITY	221 N GRAND BLVD	SAINT LOUIS	MO	63103	SAINT LOUIS CITY	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	000	3	12/6/2024	NON-COMPETING CONTINUATION	$53,974
2025	2025	SAINT LOUIS UNIVERSITY	221 N GRAND BLVD	SAINT LOUIS	MO	63103	SAINT LOUIS CITY	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	001	3	5/29/2025	NON-COMPETING CONTINUATION	$564
														Subtotal = $54,538

Issue Date FY: 2024 ( Subtotal = $53,974 )
2024	2024	SAINT LOUIS UNIVERSITY	221 N GRAND BLVD	SAINT LOUIS	MO	63103	SAINT LOUIS CITY	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	000	2	12/7/2023	NON-COMPETING CONTINUATION	$52,694
2024	2024	SAINT LOUIS UNIVERSITY	221 N GRAND BLVD	SAINT LOUIS	MO	63103	SAINT LOUIS CITY	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	001	2	4/29/2024	NON-COMPETING CONTINUATION	$1,280
														Subtotal = $53,974

Issue Date FY: 2023 ( Subtotal = $52,694 )
2023	2023	SAINT LOUIS UNIVERSITY	221 N GRAND BLVD	SAINT LOUIS	MO	63103	SAINT LOUIS CITY	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	000	1	12/15/2022	NEW	$51,752
2023	2023	SAINT LOUIS UNIVERSITY	221 N GRAND BLVD	SAINT LOUIS	MO	63103	SAINT LOUIS CITY	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	002	1	2/17/2023	NEW	$942
2023	2023	SAINT LOUIS UNIVERSITY	221 N GRAND BLVD	SAINT LOUIS	MO	63103	SAINT LOUIS CITY	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	001	1	12/15/2022	NEW	$0
														Subtotal = $52,694

Grand Total All Awards = $161,206

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Defining Inflammatory Triggers that Induce Diverse Subtypes of Gastric Metaplasia

Award Number: F30DK134124

ORGANIZATION: NATIONAL INSTITUTE OF DIABETES & DIGESTIVE & KIDNEY DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 01/01/2023

PERIOD OF PERFORMANCE END DATE: 12/31/2026

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