The Metabolic Landscape of Gynecological Cancer: Identifying Targets for Therapeutic Intervention

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: closed (28 April 2025) | Viewed by 3485

Special Issue Editor


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Guest Editor
Department of Obstetrics & Gynecology, The University of Chicago, Chicago, IL, USA
Interests: cancer metabolism; tumor microenvironment

Special Issue Information

Dear Colleagues,

Gynecological cancer (comprised of ovarian/fallopian tube, primary peritoneal, endometrial, cervical, vulvar, and vaginal cancers) are distinct in their origin and etiology. Nonetheless, surgery coupled with chemo/radiation therapy has long been the standard of care and has yielded little patient benefit. Therefore, there is a need to understand these diseases better and identify novel approaches to targeting gynecological cancer.

While biologicals targeting angiogenesis, DNA repair and immunotherapy have shown promise in clinical studies, the metabolic targeting of gynecological cancer remains less explored. The aim of this Special Issue is to showcase original research articles, reviews, perspectives, clinical trials, and short communications highlighting metabolic features of gynecological cancer, with the objective to identify potential approaches that would lead to therapeutic interventions.

This Special Issue will help generate interest and provide insights into the metabolic targeting of gynecological cancers.

Dr. Abir Mukherjee
Guest Editor

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Published Papers (1 paper)

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Review

26 pages, 2045 KiB  
Review
Biological Functions and Therapeutic Potential of NAD+ Metabolism in Gynecological Cancers
by Subin Myong, Anh Quynh Nguyen and Sridevi Challa
Cancers 2024, 16(17), 3085; https://doi.org/10.3390/cancers16173085 - 5 Sep 2024
Cited by 1 | Viewed by 2765
Abstract
Nicotinamide adenine dinucleotide (NAD+) is an important cofactor for both metabolic and signaling pathways, with the dysregulation of NAD+ levels acting as a driver for diseases such as neurodegeneration, cancers, and metabolic diseases. NAD+ plays an essential role in [...] Read more.
Nicotinamide adenine dinucleotide (NAD+) is an important cofactor for both metabolic and signaling pathways, with the dysregulation of NAD+ levels acting as a driver for diseases such as neurodegeneration, cancers, and metabolic diseases. NAD+ plays an essential role in regulating the growth and progression of cancers by controlling important cellular processes including metabolism, transcription, and translation. NAD+ regulates several metabolic pathways such as glycolysis, the citric acid (TCA) cycle, oxidative phosphorylation, and fatty acid oxidation by acting as a cofactor for redox reactions. Additionally, NAD+ acts as a cofactor for ADP-ribosyl transferases and sirtuins, as well as regulating cellular ADP-ribosylation and deacetylation levels, respectively. The cleavage of NAD+ by CD38—an NAD+ hydrolase expressed on immune cells—produces the immunosuppressive metabolite adenosine. As a result, metabolizing and maintaining NAD+ levels remain crucial for the function of various cells found in the tumor microenvironment, hence its critical role in tissue homeostasis. The NAD+ levels in cells are maintained by a balance between NAD+ biosynthesis and consumption, with synthesis being controlled by the Preiss–Handler, de novo, and NAD+ salvage pathways. The primary source of NAD+ synthesis in a variety of cell types is directed by the expression of the enzymes central to the three biosynthesis pathways. In this review, we describe the role of NAD+ metabolism and its synthesizing and consuming enzymes’ control of cancer cell growth and immune responses in gynecologic cancers. Additionally, we review the ongoing efforts to therapeutically target the enzymes critical for NAD+ homeostasis in gynecologic cancers. Full article
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