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Dissecting mechanisms, novel therapies, and human correlates of metastatic reactivation from dormancy

Award Number: F30CA310469
ORGANIZATION: NATIONAL CANCER INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 07/01/2026
PERIOD OF PERFORMANCE END DATE: 06/30/2029

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Dissecting mechanisms, novel therapies, and human correlates of metastatic reactivation from dormancy - PROJECT SUMMARY Metastatic relapse is a major cause of cancer-related mortality. In patients with a variety of cancers, such as breast cancer or melanoma, relapse may occur years or even decades after curative-intent resection of the primary tumor. These kinetics suggest that disseminated tumor cells (DTCs) enter a phase of dormancy, before reactivating and causing clinically overt metastasis. Mechanisms governing reactivation from dormancy and the required evasion from ensuing immune responses remain poorly understood. Through an integrated approach, leveraging murine models of dormancy and metastasis, in vitro perturbation screens, single-cell and spatial omics, and human data, we identify the innate immune pathway via STING as a critical mediator of immune surveillance upon reawakening from dormancy. We identify a novel mechanism whereby focal adhesion kinase (FAK) disrupts ensuing immune responses, thus promoting reactivation and metastatic progression. Furthermore, to overcome challenges in studying concepts of dormancy and metastasis in patients, we developed a novel analytical framework to infer the duration of dormancy from whole-genome sequencing (WGS) of matched primary tumors and subsequent metastases. Building on this preliminary data, in Aim 1 we will use spatial transcriptomics to characterize the spatiotemporal dynamics of cancer cells and tumor microenvironment (TME) changes during dormancy-to-metastasis transitions in murine models and interrogate immune responses following FAK disruption using a novel proteolysis-targeting chimera. In Aim 2, we have assembled a large cohort of matched primary-metastasis tumors from patients who experienced relapse following variable metastasis-free survival, and have isolated DNA from tumor and normal tissues, as well as tissue sections. We will perform WGS and apply our novel analytical frameworks to estimate the duration of dormancy and employ spatial genomics to identify molecular underpinnings of dormancy and metastasis directly in patients. Together, this work will address mechanistic, pre-clinical, and clinical gaps in our understanding of dormancy, reactivation, and metastasis, and provide a rational strategy for the development of novel treatments to prevent metastatic relapse.


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 = $52,616 )
2026	2026	THE TRUSTEES OF COLUMBIA UNIVERSITY IN THE CITY OF NEW YORK	630 W 168TH ST FL 4	NEW YORK	NY	10032	NEW YORK	USA	Cancer Research Manpower	000	1	5/7/2026	NEW	$52,616
2026	2026	THE TRUSTEES OF COLUMBIA UNIVERSITY IN THE CITY OF NEW YORK	630 W 168TH ST FL 4	NEW YORK	NY	10032	NEW YORK	USA	Cancer Research Manpower	001	1	5/7/2026	NEW	$0
														Subtotal = $52,616

Grand Total All Awards = $52,616

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Dissecting mechanisms, novel therapies, and human correlates of metastatic reactivation from dormancy

Award Number: F30CA310469

ORGANIZATION: NATIONAL CANCER INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 07/01/2026

PERIOD OF PERFORMANCE END DATE: 06/30/2029

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