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The selenium-containing protein SELENOF has been implicated in breast carcinogenesis by cell culture and animal studies. SELENOF translation is highly regulated in part by the RNA helicase eIF4a3, which binds to the key regulatory regions in the SELENOF mRNA and suppress its translation. In addition, SELENOP, the primary selenium transporter, plays a critical role in selenium delivery to tissues and may influence selenoprotein synthesis. This study aimed to examine the levels of SELENOF and eIF4a3, along with SELENOF and SELENOP genotypes, in breast cancer tissues from African American and Caucasian women<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      To study their roles in breast cancer outcome and racial disparity, human tissues were assessed by multiplex immunofluorescence staining with antibodies directed against SELENOF and eIF4a3 and DNA from these tissues were genotyped for previously studied variations in\n                      <jats:italic>SELENOF<\/jats:italic>\n                      and the selenium transporter protein\n                      <jats:italic>SELENOP<\/jats:italic>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Elevated levels of both SELENOF and eIF4a3 were observed in breast cancer tissues. SELENOF expression and genotype varied by HER2 status, while\n                      <jats:italic>SELENOP<\/jats:italic>\n                      genotypes were associated with breast cancer and showed age-related differences. SELENOF and eIF4a3 were also higher in tissues derived from African American women, who also exhibited higher frequency of a\n                      <jats:italic>SELENOP<\/jats:italic>\n                      polymorphism in the non-coding region of the gene\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>These findings suggest that SELENOF, eIF4a3, and SELENOP may contribute to breast cancer progression and racial disparities in outcomes. Their differential expression and genetic variation highlight potential molecular mechanisms underlying these disparities and may inform future therapeutic or diagnostic strategies.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s10552-025-02123-y","type":"journal-article","created":{"date-parts":[[2026,1,21]],"date-time":"2026-01-21T08:18:26Z","timestamp":1768983506000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Contributions of selenoproteins to breast cancer etiology and racial disparity"],"prefix":"10.1007","volume":"37","author":[{"given":"Soumen","family":"Bera","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Li","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Weiwei","family":"Ma","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ziqiao","family":"Xu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria","family":"Sverdlov","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ryan","family":"Deaton","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Virgilia","family":"Macias","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Klara","family":"Valyi-Nagy","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andre","family":"Kajdacsy-Balla","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kent","family":"Hoskins","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth L.","family":"Wiley","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Irida","family":"Kastrati","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alan M.","family":"Diamond","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,1,21]]},"reference":[{"key":"2123_CR1","first-page":"290","volume":"66","author":"CE DeSantis","year":"2016","unstructured":"DeSantis CE, Siegel RL, Sauer AG et al (2016) Cancer statistics for African Americans, 2016: progress and opportunities in reducing racial disparities. 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All genetic data analyzed were derived from previously collected samples. The research complies with institutional and national guidelines for the use of human biological materials in biomedical research. The UIC Office for the Protection of Research Subjects determined that use of the TMA does not meet the definition of human subject research as defined by 45 CFR 46.102(e)\/ 21 CFR 50.3(g) and 21 CFR 56.102(e).","order":3,"name":"Ethics","group":{"name":"EthicsHeading","label":"Ethical approval"}}],"article-number":"35"}}