{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,18]],"date-time":"2026-03-18T23:50:23Z","timestamp":1773877823710,"version":"3.50.1"},"reference-count":21,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2026,1,22]],"date-time":"2026-01-22T00:00:00Z","timestamp":1769040000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2026,1,22]],"date-time":"2026-01-22T00:00:00Z","timestamp":1769040000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["acsjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cancer"],"published-print":{"date-parts":[[2026,2,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Glucose\u20106\u2010phosphate dehydrogenase (G6PD) deficiency impairs cellular redox balance through reduced NADPH production and is the most common enzymatic disorder\u2010causing anemia. Venetoclax combined with azacitidine (Ven\u2010Aza) targets leukemic stem cells by disrupting oxidative phosphorylation and inducing mitochondrial stress. This study hypothesized that G6PD deficiency may enhance the efficacy of Ven\u2010Aza in acute myeloid leukemia (AML) by reducing leukemic cell metabolic resilience.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      The authors studied 73 consecutive patients with newly diagnosed (ND) AML treated with Ven\u2010Aza. G6PD activity was systematically assessed at diagnosis in all patients and categorized as normal (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a047), borderline (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a011), or deficient (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a015).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Composite complete remission rates were 93% in the G6PD deficient group versus 69% in the normal\/borderline group (\n                      <jats:italic>p<\/jats:italic>\n                      \u00a0=\u00a0.03). Patients with G6PD deficiency had a significantly longer median overall survival (23.8 months; 95% confidence interval [CI], 8.9\u201338.7), as compared to 8.96 months (95% CI, 2.9\u201315.0) in the normal\/borderline group (\n                      <jats:italic>p<\/jats:italic>\n                      \u00a0=\u00a0.034). In multivariate analysis, G6PD\u2010deficiency was associated with improved survival as compared to patients with normal G6PD activity (hazard ratio, 0.417; 95% CI, 0.181\u20130.965,\n                      <jats:italic>p<\/jats:italic>\n                      \u00a0=\u00a0.043). No significant differences were observed across groups in rates of febrile neutropenia, pneumonia, sepsis, or grade 3\u20134 cytopenia.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>G6PD deficiency is associated with higher response rates and improved survival in patients with ND\u2010AML treated with Ven\u2010Aza. These findings support G6PD deficiency as a potential biomarker of therapeutic sensitivity to Ven\u2010AZA and may uncover metabolic vulnerabilities in AML with potential therapeutic implications.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/cncr.70265","type":"journal-article","created":{"date-parts":[[2026,1,22]],"date-time":"2026-01-22T10:34:24Z","timestamp":1769078064000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Glucose\u20106\u2010phosphate dehydrogenase deficiency is associated with improved survival in patients with acute myeloid leukemia treated with venetoclax and azacitidine"],"prefix":"10.1002","volume":"132","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1034-8583","authenticated-orcid":false,"given":"Shira","family":"Buchrits","sequence":"first","affiliation":[{"name":"Institute of Haematology Davidoff Cancer Center Rabin Medical Center Beilinson Hospital  Petah\u2010Tikva Israel"},{"name":"Internal Medicine Department A Rabin Medical Center Beilinson Hospital  Petah\u2010Tikva Israel"},{"name":"Gray Faculty of Medical &amp; Health Sciences Tel Aviv University  Tel\u2010Aviv Israel"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alon","family":"Rozental","sequence":"additional","affiliation":[{"name":"Institute of Haematology Davidoff Cancer Center Rabin Medical Center Beilinson Hospital  Petah\u2010Tikva Israel"},{"name":"Gray Faculty of Medical &amp; Health Sciences Tel Aviv University  Tel\u2010Aviv Israel"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Noa","family":"Korngold","sequence":"additional","affiliation":[{"name":"Gray Faculty of Medical &amp; Health Sciences Tel Aviv University  Tel\u2010Aviv Israel"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ofer","family":"Algor","sequence":"additional","affiliation":[{"name":"Institute of Haematology Davidoff Cancer Center Rabin Medical Center Beilinson Hospital  Petah\u2010Tikva Israel"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shirly","family":"Partouche","sequence":"additional","affiliation":[{"name":"Institute of Haematology Davidoff Cancer Center Rabin Medical Center Beilinson Hospital  Petah\u2010Tikva Israel"},{"name":"Felsenstein Medical Research Center Rabin Medical Center  Petah Tikva Israel"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Galit","family":"Granot","sequence":"additional","affiliation":[{"name":"Gray Faculty of Medical &amp; Health Sciences Tel Aviv University  Tel\u2010Aviv Israel"},{"name":"Felsenstein Medical Research Center Rabin Medical Center  Petah Tikva Israel"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Pia","family":"Raanani","sequence":"additional","affiliation":[{"name":"Institute of Haematology Davidoff Cancer Center Rabin Medical Center Beilinson Hospital  Petah\u2010Tikva Israel"},{"name":"Gray Faculty of Medical &amp; Health Sciences Tel Aviv University  Tel\u2010Aviv Israel"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8662-0707","authenticated-orcid":false,"given":"Ofir","family":"Wolach","sequence":"additional","affiliation":[{"name":"Institute of Haematology Davidoff Cancer Center Rabin Medical Center Beilinson Hospital  Petah\u2010Tikva Israel"},{"name":"Gray Faculty of Medical &amp; Health Sciences Tel Aviv University  Tel\u2010Aviv Israel"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2026,1,22]]},"reference":[{"key":"e_1_2_9_2_1","doi-asserted-by":"publisher","DOI":"10.1182\/blood.2019000944"},{"key":"e_1_2_9_3_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI105786"},{"key":"e_1_2_9_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/s0969\u20102126(00)00104\u20100"},{"key":"e_1_2_9_5_1","doi-asserted-by":"publisher","DOI":"10.3390\/jcm11226689"},{"key":"e_1_2_9_6_1","doi-asserted-by":"publisher","DOI":"10.1080\/15563650.2018.1491984"},{"key":"e_1_2_9_7_1","doi-asserted-by":"publisher","DOI":"10.3322\/caac.21820"},{"key":"e_1_2_9_8_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa2012971"},{"key":"e_1_2_9_9_1","doi-asserted-by":"crossref","unstructured":"WeiAH LooS DaverNG.How I treat patients with AML using azacitidine and venetoclax. 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