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Define the molecular mechanisms in and identify biomarkers for FAK-driven hepatocellular carcinoma

Award Number: F30CA287907
ORGANIZATION: NATIONAL CANCER INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 04/01/2024
PERIOD OF PERFORMANCE END DATE: 03/31/2028

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Define the molecular mechanisms in and identify biomarkers for FAK-driven hepatocellular carcinoma - Abstract Hepatocellular carcinoma (HCC) is a deadly cancer with poor prognosis and limited therapeutic options. Biopsies are contraindicated in HCC, restricting our ability to identify unique tumor drivers and subsequent therapeutic targets. Innovative target identification for HCC treatment is thus a critical research gap. Our lab has previously established focal adhesion kinase (FAK) as a driver of HCC, with 16% of HCC patients presenting with an amplification of the PTK2 gene that encodes FAK. However, the mechanism of FAK in HCC tumor promotion remains unknown. After treatment with a proteolysis-targeting chimera for FAK in HCC cell lines, unbiased RNA-sequencing showed that connective tissue growth factor (CTGF) was significantly downregulated following the pharmacological degradation of FAK. CTGF has recently been established as a tumor promoter across several cancer types, but its role in HCC remains elusive. CTGF is secreted from cells and can be detected in conditioned media in vitro and serum in vivo. Preliminary work in HCC cell lines has confirmed a relationship between FAK expression and CTGF expression under several different conditions. CTGF expression and secretion is decreased following the degradation of FAK; CTGF expression and secretion is increased following FAK overexpression; and basal expression levels of FAK and CTGF show high correlation across a panel of HCC cell lines. Furthermore, the knockdown of CTGF was found to significantly inhibit cell growth both in vitro and in vivo. Given this preliminary data, we hypothesize that FAK promotes CTGF expression, and CTGF in turn promotes HCC. Furthermore, we hypothesize that serum CTGF levels can be used as a surrogate marker for FAK expression and/or activity in HCC, indicating the utility of a FAK-targeting treatment in the clinic. We will address these hypotheses by (1) determining the mechanism through which FAK promotes CTGF expression in HCC, (2) evaluating the contribution of CTGF to HCC growth, and (3) determining if CTGF serum levels are correlated to tumor FAK protein and FAK Y397 phosphorylation levels in HCC mouse models and patient samples. This study will utilize a combination of in vitro and in vivo models as well as patient samples obtained from clinical collaborators. Overall, this study will characterize a novel tumor-promotion pathway and elucidate a unique predictive biomarker in HCC.


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: 2026 ( Subtotal = $54,538 )
2026	2026	LOYOLA UNIVERSITY OF CHICAGO	2160 S 1ST AVE	MAYWOOD	IL	60153	COOK	USA	Cancer Research Manpower	000	3	3/4/2026	NON-COMPETING CONTINUATION	$54,538
														Subtotal = $54,538

Issue Date FY: 2025 ( Subtotal = $47,015 )
2025	2025	LOYOLA UNIVERSITY OF CHICAGO	2160 S 1ST AVE	MAYWOOD	IL	60153	COOK	USA	Cancer Research Manpower	000	2	5/14/2025	NON-COMPETING CONTINUATION	$47,015
														Subtotal = $47,015

Issue Date FY: 2024 ( Subtotal = $47,015 )
2024	2024	LOYOLA UNIVERSITY OF CHICAGO	2160 S 1ST AVE	MAYWOOD	IL	60153	COOK	USA	Cancer Research Manpower	001	1	3/27/2024	NEW	$0
2024	2024	LOYOLA UNIVERSITY OF CHICAGO	2160 S 1ST AVE	MAYWOOD	IL	60153	COOK	USA	Cancer Research Manpower	002	1	5/8/2024	NEW	$1,280
2024	2024	LOYOLA UNIVERSITY OF CHICAGO	2160 S 1ST AVE	MAYWOOD	IL	60153	COOK	USA	Cancer Research Manpower	000	1	3/27/2024	NEW	$45,735
														Subtotal = $47,015

Grand Total All Awards = $148,568

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Define the molecular mechanisms in and identify biomarkers for FAK-driven hepatocellular carcinoma

Award Number: F30CA287907

ORGANIZATION: NATIONAL CANCER INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 04/01/2024

PERIOD OF PERFORMANCE END DATE: 03/31/2028

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