Fatty Acid Metabolism, Oxidative phosphorylation, and cholesterol homeostasis pathways in endometrial cancer organoids

Lead Investigator: Shujie Yang, University of Iowa
Title of Proposal Research: Fatty Acid Metabolism, Oxidative phosphorylation, and cholesterol homeostasis pathways in endometrial cancer organoids
Vivli Data Request: 9141
Funding Source: None
Potential Conflicts of Interest: None

Summary of the Proposed Research:

Obesity is a risk factor for many diseases, including at least 20 types of cancer. It is well known that obesity increases endometrial cancer (EC) risk more than any other cancer. American cancer society studies revealed that 70% of endometrial cancers are attributable to excess body weight. EC is the most common gynecologic cancer with incidence (~66,570 new cases/year) and deaths (~12,940 deaths/year) on the rise. Cancer survival has improved since the mid-1970s for all of the most common cancers except cervical and EC, which calls for major treatment advancements. The mechanisms of how obesity promote EC progression was not well understood and urgently needed. We wish to know the published data in this paper and understand Fatty Acid Metabolism, Oxidative phosphorylation, and cholesterol homeostasis pathways in EC organoids. The outstanding genes in those pathways will not only explain the mechanism of obesity driven EC, but also might serves as potential targets to prevent or inhibit obestiy driven EC, eventually leading to future treatments strategy to benefit EC patients.

Requested Studies:

Genomic, Transcriptomic, and Drug Screening Data from a Pan-cancer Organoid Cohort with Source Tumor Samples
Data Contributor: Tempus Labs, Inc.
Study ID: T21.01
Sponsor ID: T21.01