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Elevated collagen I and fibronectin in the ovarian cancer pre-metastatic niche

Award Number: R01CA290693
ORGANIZATION: NATIONAL CANCER INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 12/11/2024
PERIOD OF PERFORMANCE END DATE: 11/30/2029

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Elevated collagen I and fibronectin in the ovarian cancer pre-metastatic niche - High-grade serous ovarian cancer (HGSOC) has a five-year survival rate of <50% due to the rapid and extensive metastasis observed in patients. Metastasis in HGSOC can occur through transcoelomic spread, in which tumor cells detach, float through the peritoneal fluid, attach to the peritoneal cavity-facing surfaces of tissues, and establish new tumors. Rapid metastasis is supported when the primary tumor sends signals that convert healthy tissues to a site that is more hospitable for metastasizing tumor cells; the altered tissue is called a premetastatic niche (PMN). Determining what is different in the PMN, how this difference supports metastasis, and the mechanisms responsible for these alterations could lead to therapeutic approaches that slow or stop metastasis. The most common site of distal metastasis in HGSOC is the omentum, a visceral fat deposit. We examined the omentum from healthy females and patients with early-stage HGSOC (prior to metastasis to the omentum). Our preliminary data demonstrated that collagen type I (Col I) density, cellular fibronectin (cFN) density, transglutaminase-2 (TGM2) cross-links, and collagen fiber thickness were all significantly increased in the omentum of patients with early-stage HGSOC. We hypothesize that these changes in the ECM of the omentum result in a PMN that supports tumor progression through direct effects on tumor cell adhesion, invasion, migration, proliferation, and apoptosis, and that the observed ECM changes result from preconditioning of this niche by factors in the peritoneal fluid. We will test this hypothesis across three Aims: 1) Examine the direct effect of ECM alterations observed in the HGSOC PMN on tumor cells. 2) Determine the impact of ECM alterations in the PMN on HSGOC metastatic seeding and expansion. 3) Elucidate mechanisms by which the ECM of the omentum is converted to that of the PMN. These studies will be conducted by an inter-disciplinary team with expertise in ovarian cancer from basic science and clinical perspectives, in vitro culture system development, in vivo mouse models, ECM, biomaterials, and exosomes. Completion of these Aims will determine how changes in the ECM that precede tumor cell arrival influence metastasis. Additionally, we will determine which factors in the peritoneal fluid regulate these changes in the ECM to identify future therapeutic strategies or biomarkers for patients at high risk.


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 = $550,340 )
2026	2026	UNIVERSITY OF WISCONSIN SYSTEM	21 N PARK ST STE 6301	MADISON	WI	53715	DANE	USA	Cancer Biology Research	000	2	12/22/2025	NON-COMPETING CONTINUATION	$550,340
														Subtotal = $550,340

Issue Date FY: 2025 ( Subtotal = $612,288 )
2025	2025	UNIVERSITY OF WISCONSIN SYSTEM	21 N PARK ST STE 6301	MADISON	WI	53715	DANE	USA	Cancer Biology Research	000	1	12/11/2024	NEW	$612,288
														Subtotal = $612,288

Grand Total All Awards = $1,162,628

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Elevated collagen I and fibronectin in the ovarian cancer pre-metastatic niche

Award Number: R01CA290693

ORGANIZATION: NATIONAL CANCER INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

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

PERIOD OF PERFORMANCE START DATE: 12/11/2024

PERIOD OF PERFORMANCE END DATE: 11/30/2029

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