<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>26</volume><submitter>Aquino-Acevedo AN</submitter><pubmed_abstract>Mounting evidence suggests that chronic stress and subsequent distress can promote ovarian cancer progression. These altered psychological states have been linked to sustained release of stress hormones, activation of the β-adrenergic receptors in ovarian cancer cells, and induction of pro-tumoral signaling pathways. In addition, data suggest that chronic stress promotes an inflammatory landscape highlighted by increased infiltration of tumor-associated macrophages into the ovarian tumor microenvironment (TME). In ovarian cancer, ascites is a unique TME comprised of tumor, and immune cells, which secrete pro-tumoral cytokines and chemokines that modulate tumor-associated immunity. However, our knowledge about how stress hormones impact the ascites TME remains limited. We hypothesized that </pubmed_abstract><journal>Brain, behavior, &amp; immunity - health</journal><pagination>100558</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9694096</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Stress hormones are associated with inflammatory cytokines and attenuation of T-cell function in the ascites from patients with high grade serous ovarian cancer.</pubmed_title><pmcid>PMC9694096</pmcid><pubmed_authors>Previs RA</pubmed_authors><pubmed_authors>Armaiz-Pena GN</pubmed_authors><pubmed_authors>Ortiz-Leon M</pubmed_authors><pubmed_authors>Whitaker R</pubmed_authors><pubmed_authors>Yi JS</pubmed_authors><pubmed_authors>Cruz-Robles ME</pubmed_authors><pubmed_authors>Aquino-Acevedo AN</pubmed_authors><pubmed_authors>Dutil J</pubmed_authors><pubmed_authors>Knochenhauer H</pubmed_authors><pubmed_authors>Castillo-Ocampo Y</pubmed_authors><pubmed_authors>Russell S</pubmed_authors><pubmed_authors>Morales-Lopez C</pubmed_authors><pubmed_authors>Bonilla-Claudio M</pubmed_authors><pubmed_authors>Gaillard SL</pubmed_authors><pubmed_authors>Hernandez-Cordero ER</pubmed_authors><pubmed_authors>Chen DT</pubmed_authors><pubmed_authors>Rivera-Lopez YA</pubmed_authors></additional><is_claimable>false</is_claimable><name>Stress hormones are associated with inflammatory cytokines and attenuation of T-cell function in the ascites from patients with high grade serous ovarian cancer.</name><description>Mounting evidence suggests that chronic stress and subsequent distress can promote ovarian cancer progression. These altered psychological states have been linked to sustained release of stress hormones, activation of the β-adrenergic receptors in ovarian cancer cells, and induction of pro-tumoral signaling pathways. In addition, data suggest that chronic stress promotes an inflammatory landscape highlighted by increased infiltration of tumor-associated macrophages into the ovarian tumor microenvironment (TME). In ovarian cancer, ascites is a unique TME comprised of tumor, and immune cells, which secrete pro-tumoral cytokines and chemokines that modulate tumor-associated immunity. However, our knowledge about how stress hormones impact the ascites TME remains limited. We hypothesized that </description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Dec</publication><modification>2025-04-04T19:51:14.348Z</modification><creation>2025-04-04T19:51:14.348Z</creation></dates><accession>S-EPMC9694096</accession><cross_references><pubmed>36439058</pubmed><doi>10.1016/j.bbih.2022.100558</doi></cross_references></HashMap>