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Targeting FGFR4 to overcome chemoresistance in ovarian cancer

Award Number: R21CA280020
ORGANIZATION: NATIONAL CANCER INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 12/05/2023
PERIOD OF PERFORMANCE END DATE: 06/30/2024

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Targeting FGFR4 to overcome chemoresistance in ovarian cancer - Abstract Many anti-tubulin agents, such as paclitaxel (Taxol), have been used extensively for treatment of several types of cancer, including ovarian, lung, and breast cancers. Despite their wide use in cancer treatment, however, patient response is highly variable and drug resistance remains a major clinical issue. It is therefore essential to identify prognostic markers to predict the patient response and to enhance drug sensitivity. Protein tyrosine kinases (PTKs) play significant roles in cancer development, and many PTK inhibitors have been widely used for treatment of malignancies and in clinical trials. We conducted Phos-tag-based biochemical screenings to determine the regulation and function of PTKs during Taxol chemotherapeutics. In response to Taxol treatment, one of the most significant changes in the PTK family is the marked protein degradation of fibroblast growth factor receptor 4 (FGFR4). In addition, FGFR4 controls Taxol chemosensitivity in ovarian cancer cells. Importantly, FGFR4 expression levels are elevated in recurrent post-chemotherapy ovarian cancer patients. These preliminary results provide a strong premise in support of our hypothesis that the FGFR4 signaling functions as a therapeutic target for paclitaxel-based chemotherapeutics in treatment of drug-resistant and/or recurrent patients. We will test our central hypothesis by two specific aims. Aim 1: Determine how FGFR4 is regulated during Taxol treatment; Aim 2: Targeting FGFR4 to overcome paclitaxel chemoresistance in ovarian cancer. The identification of new regulators and/or signaling pathways triggered by anti-tubulin drugs will shed light on the mechanisms underlying chemoresistance. Our study identifies the FGFR4 signaling as a potential therapeutic target in recurrent ovarian cancer and suggests that combining selective inhibitors of FGFR4 (in clinical development) with Taxol will have enhanced efficacy in the treatment of chemo-resistant and/or recurrent patients.


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 = -$153,539 )
2025	2024	BOARD OF REGENTS OF THE UNIVERSITY OF NEBRASKA	987835 NEBRASKA MEDICAL CENTER	OMAHA	NE	68198	DOUGLAS	USA	Cancer Treatment Research	000	1	11/5/2024	NEW	-$153,539
														Subtotal = -$153,539

Issue Date FY: 2024 ( Subtotal = $215,284 )
2024	2024	BOARD OF REGENTS OF THE UNIVERSITY OF NEBRASKA	987835 NEBRASKA MEDICAL CENTER	OMAHA	NE	68198	DOUGLAS	USA	Cancer Treatment Research	001	1	7/3/2024	NEW	$0
2024	2024	BOARD OF REGENTS OF THE UNIVERSITY OF NEBRASKA	987835 NEBRASKA MEDICAL CENTER	OMAHA	NE	68198	DOUGLAS	USA	Cancer Treatment Research	000	1	12/5/2023	NEW	$215,284
														Subtotal = $215,284

Grand Total All Awards = $61,745

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Targeting FGFR4 to overcome chemoresistance in ovarian cancer

Award Number: R21CA280020

ORGANIZATION: NATIONAL CANCER INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

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

PERIOD OF PERFORMANCE START DATE: 12/05/2023

PERIOD OF PERFORMANCE END DATE: 06/30/2024

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