{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T22:10:19Z","timestamp":1791583819229,"version":"4.3.4"},"reference-count":56,"publisher":"BMJ","issue":"1","license":[{"start":{"date-parts":[[2026,1,28]],"date-time":"2026-01-28T00:00:00Z","timestamp":1769558400000},"content-version":"unspecified","delay-in-days":27,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"name":"Sichuan Science and Technology Program","award":["2024NSFSC1943"],"award-info":[{"award-number":["2024NSFSC1943"]}]},{"name":"Postdoctoral Fellowship Program of China Postdoctoral Science Foundation","award":["GZC20241157"],"award-info":[{"award-number":["GZC20241157"]}]},{"name":"Postdoctor Research Fund of West China Hospital, Sichuan University","award":["2024HXBH178"],"award-info":[{"award-number":["2024HXBH178"]}]}],"content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":["J Immunother Cancer"],"accepted":{"date-parts":[[2026,1,8]]},"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Non-small cell lung cancer (NSCLC) is the most common type of lung cancer and the leading cause of cancer-related deaths. Immune checkpoint inhibitors (ICIs) of programmed death-1 (PD-1)\/programmed death ligand-1 signaling induce tumor regression in some patients with NSCLC, but most patients with NSCLC exhibit resistance to ICIs therapy. NSCLC shapes the potent tumor immunosuppressive microenvironment (TIME) that underlies tumor immune tolerance and acquired resistance. Therefore, elucidating the cellular and molecular mechanisms by which NSCLC establishes and sustains the TIME is essential for developing novel strategies to overcome immune resistance and enhance the clinical benefit of ICIs.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>The correlation between sterile alpha motif domain and histidine-aspartate domain-containing protein 1 (SAMHD1) expression and ICIs was analyzed via immunohistochemistry. Cell migration assay was performed to assess the effect of SAMHD1 on macrophage recruitment. Multicolor flow cytometry was performed to analyze the effect of SAMHD1 knockdown on the tumor microenvironment. SAMHD1 regulation of the dual specificity phosphatase 6-extracellular regulated protein kinases 1\/2 (DUSP6-ERK1\/2) pathway was verified by RNA sequencing and western blotting.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Here, we identify the SAMHD1 as a potential therapeutic target and a major determinant of poor response to ICIs in patients with NSCLC. Tumors with high SAMHD1 expression show resistance to anti-PD-1 antibody (\u03b1PD-1) treatment, whereas tumors with low SAMHD1 expression are highly sensitive. SAMHD1-dependent resistance to \u03b1PD-1 is characterized by increased tumor-associated macrophages (TAMs) infiltration and reduced CD8+T\u2009cell numbers. Mechanistically, SAMHD1 regulates the expression of macrophage-associated chemokines by influencing the activation of the DUSP6-ERK1\/2 pathway, which contributes to TAMs aggregation within NSCLC tumors to shape an immunosuppressive microenvironment. The HIV accessory protein viral protein-x (VPX) specifically degrades SAMHD1 to promote HIV replication. Similarly, the vpx-engineered oncolytic adenovirus (oAd-vpx) targets SAMDH1 degradation to enhance oncolytic adenovirus replication and weaken the hostile immune microenvironment shaped by TAMs, thereby triggering a CD8+T-cell-dependent antitumor immune response. The combination of oAd-vpx and \u03b1PD-1 inhibits tumor growth and enhances sensitivity to ICIs in both mouse and human NSCLC.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>This research identifies a key mechanism of SAMHD1-driven immunosuppression and highlights its important role in oncolytic adenovirus therapy. This study provides a theoretical basis for targeting SAMHD1 as a drug therapy strategy in patients with NSCLC.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/jitc-2025-013550","type":"journal-article","created":{"date-parts":[[2026,1,29]],"date-time":"2026-01-29T05:20:23Z","timestamp":1769664023000},"page":"e013550","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":3,"title":["SAMHD1 drives immunosuppression in non-small cell lung cancer by promoting macrophage infiltration and restricting oncolytic adenovirus replication"],"prefix":"10.1136","volume":"14","author":[{"given":"Shichuan","family":"Hu","sequence":"first","affiliation":[{"name":"Department of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jian","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Oncology & Department of Pathology, The Second People's Hospital of Neijiang, Sichuan, China"},{"name":"Lung Cancer Center\/Lung Cancer Institute, West China Hospital, Sichuan University, Chengdu, Sichuan, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhiwu","family":"Wang","sequence":"additional","affiliation":[{"name":"Hebei Key Laboratory of Molecular Oncology & Department of Chemoradiotherapy, Tangshan People\u2019s Hospital, Hebei, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yong","family":"Zhang","sequence":"additional","affiliation":[{"name":"Peking University Cancer Hospital (Inner Mongolia Campus) & Affiliated Cancer Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia Autonomous Region, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chang","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Oncology & Department of Pathology, The Second People's Hospital of Neijiang, Sichuan, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Oncology & Department of Pathology, The Second People's Hospital of Neijiang, Sichuan, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Feng","family":"Luo","sequence":"additional","affiliation":[{"name":"Lung Cancer Center\/Lung Cancer Institute, West China Hospital, Sichuan University, Chengdu, Sichuan, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5440-5941","authenticated-orcid":false,"given":"Ping","family":"Cheng","sequence":"additional","affiliation":[{"name":"Department of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6397-9429","authenticated-orcid":false,"given":"Jiantao","family":"Wang","sequence":"additional","affiliation":[{"name":"Lung Cancer Center\/Lung Cancer Institute, West China Hospital, Sichuan University, Chengdu, Sichuan, China"},{"name":"Department of Radiation Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, Sichuan, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-8886-1073","authenticated-orcid":false,"given":"Jing","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"239","published-online":{"date-parts":[[2026,1,28]]},"reference":[{"key":"2026012821201406000_14.1.e013550.1","doi-asserted-by":"publisher","DOI":"10.3322\/caac.21820"},{"key":"2026012821201406000_14.1.e013550.2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jtho.2015.09.009"},{"key":"2026012821201406000_14.1.e013550.3","doi-asserted-by":"crossref","first-page":"127","DOI":"10.1016\/j.lungcan.2019.05.029","article-title":"Immune checkpoint inhibitors, alone or in combination with chemotherapy, as first-line treatment for advanced non-small cell lung cancer. 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