{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T09:13:16Z","timestamp":1788513196138,"version":"build-2803163510"},"reference-count":45,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2026,5,27]],"date-time":"2026-05-27T00:00:00Z","timestamp":1779840000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2026,5,27]],"date-time":"2026-05-27T00:00:00Z","timestamp":1779840000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100020174","name":"Health Research Charities Ireland","doi-asserted-by":"publisher","award":["HRCI\u2010HRB\u20102022\u2010020"],"award-info":[{"award-number":["HRCI\u2010HRB\u20102022\u2010020"]}],"id":[{"id":"10.13039\/100020174","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100010414","name":"Health Research Board","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100010414","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100022542","name":"Breakthrough Cancer Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100022542","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["European J of Haematology"],"published-print":{"date-parts":[[2026,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Multiple myeloma (MM) is an incurable malignancy of terminally\u2010differentiated plasma cells that represents a major clinical challenge despite unprecedented therapeutic advances, particularly for patients with cytogenetically\u2010defined high\u2010risk MM (HR\u2010MM). Updated in 2025, the evolving cytogenetic classification of HR\u2010MM includes gains or amplifications in chromosome 1q. One gene of emerging interest on chromosome 1q is\n                    <jats:italic>F11R,<\/jats:italic>\n                    which codes for a protein called Junctional Adhesion Molecule\u2010A (JAM\u2010A). Upregulation of JAM\u2010A has been linked with the development of several aggressive malignancies, most recently MM. In the current study,\n                    <jats:italic>F11R<\/jats:italic>\n                    gene expression was found to be significantly higher in gain\/amp(1q) MM patients from the CoMMpass database, and to correlate with poorer overall survival in MM patients. Furthermore, elevated\n                    <jats:italic>F11R<\/jats:italic>\n                    expression was accompanied by an increased burden of circulating CD138\n                    <jats:sup>+<\/jats:sup>\n                    cells, potentially an early hallmark of extramedullary disease (EMD). As JAM\u2010A signalling putatively promotes tumorigenic behaviour through\n                    <jats:italic>cis\u2010<\/jats:italic>\n                    dimerization\u2010dependent adhesion signalling, structure\u2010based rational design principles were utilised to design novel peptide inhibitors that selectively disrupt JAM\u2010A\n                    <jats:italic>cis<\/jats:italic>\n                    \u2010dimerization. In\u00a0vitro testing of novel peptides across a panel of MM cell lines and primary CD138+ cells from MM patients demonstrated anti\u2010proliferative and pro\u2010senescence properties of the novel peptides. Moreover, candidate peptide P4 significantly inhibited the growth of CD138+ plasmacytoma\u2010like tumours in an in\u00a0vivo xenograft model involving implantation onto the chick chorioallantoic membrane. Collectively, these findings support the validity of JAM\u2010A as an emerging druggable target and provide a strong rationale for further preclinical investigations of JAM\u2010A inhibitors in MM.\n                  <\/jats:p>","DOI":"10.1111\/ejh.70225","type":"journal-article","created":{"date-parts":[[2026,5,28]],"date-time":"2026-05-28T03:49:53Z","timestamp":1779940193000},"page":"995-1006","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Junctional Adhesion Molecule\u2010A (\n                    <scp>JAM<\/scp>\n                    \u2010A) Associates With High\u2010Risk Disease in Multiple Myeloma Patients and a Structure\u2010Based Rationally\u2010Designed Peptide Inhibitor Attenuates Tumorigenic Features In\u00a0Vitro and In\u00a0Vivo"],"prefix":"10.1111","volume":"117","author":[{"given":"Niamh","family":"McAuley","sequence":"first","affiliation":[{"name":"Department of Surgery RCSI University of Medicine 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