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Obesity and Malignancies in Women: Searching for New Molecular Links

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Guest Editor
Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, 87036 Arcavacata di Rende, CS, Italy
Interests: cancer; breast cancer; obesity; tumor microenvironment; extracellular vesicles; ESR1 mutations
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Special Issue Information

Dear Colleagues,

Obesity, with its increasing global incidence, poses a significant risk to health, being linked to many debilitating and fatal diseases, including at least 13 unique cancers that can lead to poor patient outcomes across both sexes. Women are more likely to be overweight or obese and thus more susceptible to obesity-related cancers. Although the strong epidemiological link between cancer and obesity has been widely reported, the molecular mechanisms underlying this association are still under investigation. Among the factors thought to be involved in obesity-related malignancies are alterations in the inflammatory status, changes in hormone and adipokine levels, and oxidative stress. However, the complexity of the obese state and the multiple oncogenic modifications that characterize cancer leave considerable room for further understanding. In addition, it is becoming increasingly important to distinguish between the functional roles of visceral and subcutaneous fat, though new molecular mechanisms may emerge from this knowledge.

The aim of this Special Issue is to provide a deeper understanding of the association between obesity and female cancers, mainly focusing on novel pathophysiological implications or additional molecular mechanisms. Therefore, we welcome the submission of original research and review articles that provide insights into the association between obesity and female malignancies.

Dr. Luca Gelsomino
Guest Editor

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Keywords

  • obesity
  • female malignancies
  • adipokines
  • tumor microenvironment

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Published Papers (1 paper)

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Research

14 pages, 2390 KiB  
Article
Sex-Dependent T Cell Dysregulation in Mice with Diet-Induced Obesity
by Christina Brummer, Katrin Singer, Almut Brand, Christina Bruss, Kathrin Renner, Wolfgang Herr, Tobias Pukrop, Christoph Dorn, Claus Hellerbrand, Carina Matos and Marina Kreutz
Int. J. Mol. Sci. 2024, 25(15), 8234; https://doi.org/10.3390/ijms25158234 - 28 Jul 2024
Cited by 2 | Viewed by 1487
Abstract
Obesity is an emerging public health problem. Chronic low-grade inflammation is considered a major promotor of obesity-induced secondary diseases such as cardiovascular and fatty liver disease, type 2 diabetes mellitus, and several cancer entities. Most preliminary studies on obesity-induced immune responses have been [...] Read more.
Obesity is an emerging public health problem. Chronic low-grade inflammation is considered a major promotor of obesity-induced secondary diseases such as cardiovascular and fatty liver disease, type 2 diabetes mellitus, and several cancer entities. Most preliminary studies on obesity-induced immune responses have been conducted in male rodents. Sex-specific differences between men and women in obesity-induced immune dysregulation have not yet been fully outlined but are highly relevant to optimizing prevention strategies for overweight-associated complications. In this study, we fed C57BL/6 female vs. male mice with either standard chow or an obesity-inducing diet (OD). Blood and spleen immune cells were isolated and analyzed by flow cytometry. Lean control mice showed no sex bias in systemic and splenic immune cell composition, whereas the immune responses to obesity were significantly distinct between female and male mice. While immune cell alterations in male OD mice were characterized by a significant reduction in T cells and an increase in myeloid-derived suppressor cells (MDSC), female OD mice displayed preserved T cell numbers. The sex-dependent differences in obesity-induced T cell dysregulation were associated with varying susceptibility to body weight gain and fatty liver disease: Male mice showed significantly more hepatic inflammation and histopathological stigmata of fatty liver in comparison to female OD mice. Our findings indicate that sex impacts susceptibility to obesity-induced T cell dysregulation, which might explain sex-dependent different incidences in the development of obesity-associated secondary diseases. These results provide novel insights into the understanding of obesity-induced chronic inflammation from a sex-specific perspective. Given that most nutrition, exercise, and therapeutic recommendations for the prevention of obesity-associated comorbidities do not differentiate between men and women, the data of this study are clinically relevant and should be taken into consideration in future trials and treatment strategies. Full article
(This article belongs to the Special Issue Obesity and Malignancies in Women: Searching for New Molecular Links)
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