{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T15:52:00Z","timestamp":1789487520339,"version":"build-2803163510"},"reference-count":55,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2026,7,26]],"date-time":"2026-07-26T00:00:00Z","timestamp":1785024000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,7,26]],"date-time":"2026-07-26T00:00:00Z","timestamp":1785024000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Molecular Carcinogenesis"],"published-print":{"date-parts":[[2026,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Hepatocellular carcinoma (HCC) develops within an immunologically complex tumor microenvironment that is heavily shaped by infiltrating myeloid cells. Immune\u2010based treatment strategies such as atezolizumab plus bevacizumab have shown promising therapeutic benefits, but patients do not experience durable responses. This shortfall motivates current efforts to elucidate signaling programs that sustain pro\u2010tumor myeloid states. Focal adhesion kinase (FAK, encoded by\n                    <jats:italic>PTK2<\/jats:italic>\n                    ) integrates adhesion, growth factor, proliferative, and inflammatory signaling, but the contribution of FAK in myeloid cells to HCC has not been tested. In this study, we used human HCC transcriptomic analyses and a myeloid\u2010specific FAK knockout mouse model to investigate the role of myeloid\u2010intrinsic FAK in HCC progression. Analysis of the PRHCCdb single\u2010cell database showed\n                    <jats:italic>PTK2<\/jats:italic>\n                    expression was detectable in myeloid populations. Higher\n                    <jats:italic>PTK2<\/jats:italic>\n                    expression in myeloid\u2010rich TCGA\u2010LIHC tumors was associated with a significantly worse overall survival. Further analysis of the NCI\u2010CLARITY single\u2010cell data set localized the strongest FAK\u2010associated transcriptional programs to a monocyte\u2010derived macrophage state marked by\n                    <jats:italic>VCAN<\/jats:italic>\n                    and\n                    <jats:italic>COLEC12<\/jats:italic>\n                    . Specifically, this population demonstrated hypoxia\u2010associated and inflammatory signatures. To test the functional role of FAK in myeloid cells, we generated myeloid\u2010specific FAK knockout (LysMCre;FAK\n                    <jats:sup>f\/f<\/jats:sup>\n                    ) mice. Deletion of FAK did not alter baseline liver morphology, liver\u2010to\u2010body weight ratio, or proliferation. When challenged with the MET\/\u03b2\u2010catenin\u2010driven HCC model via hydrodynamic tail vein injection, myeloid\u2010specific FAK deletion did not significantly affect survival, gross tumor burden, or tumor proliferation. However, tumors from the LysMCre;FAK\n                    <jats:sup>f\/f<\/jats:sup>\n                    mice showed significantly reduced F4\/80\n                    <jats:sup>+<\/jats:sup>\n                    macrophage accumulation compared with FAK\n                    <jats:sup>f\/f<\/jats:sup>\n                    controls. These findings indicate that myeloid\u2010specific FAK promotes macrophage accumulation, but its loss alone is insufficient to alter tumor burden, proliferation, or survival in this oncogene\u2010driven HCC model.\n                  <\/jats:p>","DOI":"10.1002\/mc.70156","type":"journal-article","created":{"date-parts":[[2026,7,26]],"date-time":"2026-07-26T19:22:27Z","timestamp":1785093747000},"page":"1209-1225","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Myeloid Focal Adhesion Kinase Promotes Macrophage Accumulation but Does Not Alter Tumor Progression in Hepatocellular Carcinoma"],"prefix":"10.1002","volume":"65","author":[{"ORCID":"https:\/\/orcid.org\/0009-0007-1917-5205","authenticated-orcid":false,"given":"Eugene","family":"Ham","sequence":"first","affiliation":[{"name":"Department of Surgery Loyola University Chicago Stritch School of Medicine Maywood Illinois USA"},{"name":"Department of Cancer Biology Loyola University Chicago Stritch School of Medicine Maywood Illinois USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1851-6676","authenticated-orcid":false,"given":"Kyle","family":"Boedeker","sequence":"additional","affiliation":[{"name":"Department of Surgery Loyola University Chicago Stritch School of Medicine Maywood Illinois USA"},{"name":"Department of Cancer Biology Loyola University Chicago Stritch School of Medicine Maywood Illinois USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0009-7303","authenticated-orcid":false,"given":"Claudia Rose","family":"Keating","sequence":"additional","affiliation":[{"name":"Department of Surgery Loyola University Chicago Stritch School of Medicine Maywood Illinois USA"},{"name":"Department of Cancer Biology Loyola University Chicago Stritch School of Medicine Maywood Illinois USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruisong","family":"Ye","sequence":"additional","affiliation":[{"name":"Department of Surgery Loyola University Chicago Stritch School of Medicine Maywood Illinois USA"},{"name":"Department of Cancer Biology Loyola University Chicago Stritch School of Medicine Maywood Illinois USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frankie","family":"Montalbano","sequence":"additional","affiliation":[{"name":"Department of Surgery Loyola University Chicago Stritch School of Medicine Maywood Illinois USA"},{"name":"Department of Cancer Biology Loyola University Chicago Stritch School of Medicine Maywood Illinois USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0008-1280-8273","authenticated-orcid":false,"given":"Sophia","family":"Mankaruse","sequence":"additional","affiliation":[{"name":"Department of Surgery Loyola University Chicago Stritch School of Medicine Maywood Illinois USA"},{"name":"Department of Cancer Biology Loyola University Chicago Stritch School of Medicine Maywood Illinois USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xianzhong","family":"Ding","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine Loyola University Chicago Stritch School of Medicine Maywood Illinois USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jonathan P.","family":"Rennhack","sequence":"additional","affiliation":[{"name":"Department of Cancer Biology Loyola University Chicago Stritch School of Medicine Maywood Illinois USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8093-3094","authenticated-orcid":false,"given":"Wei","family":"Qiu","sequence":"additional","affiliation":[{"name":"Department of Surgery Loyola University Chicago Stritch School of Medicine Maywood Illinois USA"},{"name":"Department of Cancer Biology Loyola 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