FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4313816265> ?p ?o ?g. }

• W4313816265 endingPage "C035" @default.
• W4313816265 startingPage "C035" @default.
• W4313816265 abstract "Abstract Triple-negative breast cancer (TNBC), a highly aggressive and metastatic subtype of breast cancer, lacks expression of the estrogen and progesterone receptors and amplification of HER2 and comprises 15-20% of all breast cancer. Incidence and mortality of TNBC are higher in Black Americans than in other racial/ethnic groups. Conversely, Black patients are underrepresented in clinical breast cancer drug trials, limiting our understanding of differential treatment responses. Leukocyte infiltration is a key modulator of TNBC outcome, and Black patients show immunological differences that may contribute to differential outcomes in TNBC. About 60-80% of Black Americans are homozygous for a polymorphism in the Atypical Chemokine Receptor 1 (ACKR1) promoter region that causes loss of ACKR1 expression on red blood cells, also known as the “Duffy-null” serotype. ACKR1 is expressed on tumor cells, red blood cells, and endothelial cells, and can act as a chemokine sink or chemokine concentrator, depending on the context. Whole-tumor RNA analysis shows that overall loss of ACKR1 expression in TNBC tumors correlates strongly with decreased survival, but it is unclear which ACKR1-expressing cell type(s) contribute to this effect. Under inflammatory conditions, ACKR1 expression in endothelial cells localizes chemotactic cytokines at the endothelial junction, and loss of endothelial ACKR1 blocks the ability of leukocytes to extravasate through the endothelial barrier into surrounding tissues. We hypothesized that loss of endothelial/stromal ACKR1 reduces immune infiltration and activation in TNBC and racial/ethnic differences in ACKR1 expression may contribute to health disparities. To determine the role of ACKR1 in tumor immune infiltration, we chose a syngeneic immunocompetent mouse model to incorporate species-matched stromal-tumor interactions. We orthotopically inoculated E0771.LMB cells, a C57BL6/J syngeneic TNBC cell line, into ACKR1null and ACKR1het female mice. Tumor growth was measured triweekly, and tumor mass was measured at the 28-day endpoint. To measure immune infiltration, we fluorescently stained representative tumor cryosections with CD45 to detect all classes of infiltrating hematopoietic cells involved in immune response. There was no significant difference in tumor volume and mass among the ACKR1null and ACKR1het controls. Tumors implanted in ACKR1het controls showed broadly infiltrated leukocytes clusters, while tumors in ACKR1nullhosts showed sparse and infrequent leukocyte infiltration. Conclusion: Stromal ACKR1 does not have a strong effect on primary tumor growth. Loss of stromal ACKR1 reduces infiltration of leukocytes into the tumor microenvironment even when ACKR1 is not manipulated in the tumor cells, suggesting that ACKR1 in endothelial or other stromal cells regulates immune response in TNBC. Impact: Understanding the immunogenic functions of ACKR1 allelic variation will elucidate mechanisms of racially distinct therapeutic response in TNBC, enhance precision oncology, and promote cancer health equity. Citation Format: Chinwe Obianuju Ewenighi-Amankwah, Tanner Roach, Joseph Dufraine, Naiche Adler, Jan Kitajewski. ACKR1 expression in stromal cells regulates immune infiltration in triple negative breast cancer [abstract]. In: Proceedings of the 15th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2022 Sep 16-19; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2022;31(1 Suppl):Abstract nr C035." @default.
• W4313816265 created "2023-01-09" @default.
• W4313816265 creator A5011080058 @default.
• W4313816265 creator A5018317129 @default.
• W4313816265 creator A5048121977 @default.
• W4313816265 creator A5058264933 @default.
• W4313816265 creator A5082730558 @default.
• W4313816265 date "2023-01-01" @default.
• W4313816265 modified "2023-09-27" @default.
• W4313816265 title "Abstract C035: ACKR1 expression in stromal cells regulates immune infiltration in triple negative breast cancer" @default.
• W4313816265 doi "https://doi.org/10.1158/1538-7755.disp22-c035" @default.
• W4313816265 hasPublicationYear "2023" @default.
• W4313816265 type Work @default.
• W4313816265 citedByCount "0" @default.
• W4313816265 crossrefType "journal-article" @default.
• W4313816265 hasAuthorship W4313816265A5011080058 @default.
• W4313816265 hasAuthorship W4313816265A5018317129 @default.
• W4313816265 hasAuthorship W4313816265A5048121977 @default.
• W4313816265 hasAuthorship W4313816265A5058264933 @default.
• W4313816265 hasAuthorship W4313816265A5082730558 @default.
• W4313816265 hasConcept C121608353 @default.
• W4313816265 hasConcept C126322002 @default.
• W4313816265 hasConcept C12823836 @default.
• W4313816265 hasConcept C13373296 @default.
• W4313816265 hasConcept C16930146 @default.
• W4313816265 hasConcept C203014093 @default.
• W4313816265 hasConcept C2780110267 @default.
• W4313816265 hasConcept C45635710 @default.
• W4313816265 hasConcept C502942594 @default.
• W4313816265 hasConcept C530470458 @default.
• W4313816265 hasConcept C71924100 @default.
• W4313816265 hasConcept C86803240 @default.
• W4313816265 hasConcept C8891405 @default.
• W4313816265 hasConceptScore W4313816265C121608353 @default.
• W4313816265 hasConceptScore W4313816265C126322002 @default.
• W4313816265 hasConceptScore W4313816265C12823836 @default.
• W4313816265 hasConceptScore W4313816265C13373296 @default.
• W4313816265 hasConceptScore W4313816265C16930146 @default.
• W4313816265 hasConceptScore W4313816265C203014093 @default.
• W4313816265 hasConceptScore W4313816265C2780110267 @default.
• W4313816265 hasConceptScore W4313816265C45635710 @default.
• W4313816265 hasConceptScore W4313816265C502942594 @default.
• W4313816265 hasConceptScore W4313816265C530470458 @default.
• W4313816265 hasConceptScore W4313816265C71924100 @default.
• W4313816265 hasConceptScore W4313816265C86803240 @default.
• W4313816265 hasConceptScore W4313816265C8891405 @default.
• W4313816265 hasIssue "1_Supplement" @default.
• W4313816265 hasLocation W43138162651 @default.
• W4313816265 hasOpenAccess W4313816265 @default.
• W4313816265 hasPrimaryLocation W43138162651 @default.
• W4313816265 hasRelatedWork W1966181922 @default.
• W4313816265 hasRelatedWork W2005666125 @default.
• W4313816265 hasRelatedWork W2050374169 @default.
• W4313816265 hasRelatedWork W2075500674 @default.
• W4313816265 hasRelatedWork W2105242530 @default.
• W4313816265 hasRelatedWork W2157754339 @default.
• W4313816265 hasRelatedWork W2194913163 @default.
• W4313816265 hasRelatedWork W3177574928 @default.
• W4313816265 hasRelatedWork W4220923253 @default.
• W4313816265 hasRelatedWork W4313816265 @default.
• W4313816265 hasVolume "32" @default.
• W4313816265 isParatext "false" @default.
• W4313816265 isRetracted "false" @default.
• W4313816265 workType "article" @default.