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However, their role in medulloblastoma (MB) progression and chemoresistance remains elusive.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We utilized the CD11b-diphtheria toxin receptor (DTR)\/Ptch1-deficient MB model to genetically delete TAMs. NeuroD2-SmoA1 MB mice were treated with CSF1R inhibitor PLX3397, PI3K inhibitor buparlisib, and a combination of PLX3397 with chemotherapy to examine the functional significance of TAMs in MB. Tumor tissues and cell co-culture system were analyzed using RNA sequencing (RNA-seq), Western blotting, flow cytometry, immunohistochemistry, quantitative polymerase chain reaction, and EdU assay to delineate mechanistic interactions.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Myeloid-derived TAMs were abundant in MB tissues and primarily exhibited M2-like polarization. We demonstrated that TAM depletion, achieved either genetically via diphtheria toxin or pharmacologically via PLX3397-mediated preferential targeting of M2-like TAMs, markedly downregulates Zic1 expression and impedes MB growth. Mechanistically, M2-like TAMs secreted high levels of IGF1 to activate the PI3K\/mTOR\/Zic1 axis in MB cells, whereas the PI3K inhibitor buparlisib effectively reduced the population of Zic1-expressing cells and restricted MB growth. Notably, the PI3K\/mTOR\/Zic1 axis was demonstrated to confer chemoresistance. While chemotherapy exacerbates M2-like TAM accumulation within MB, combining PLX3397 with chemotherapy abrogates this infiltration and attenuates IGF1\/PI3K\/Zic1 signaling axis. This combination strategy synergistically inhibits tumor growth and extends survival in mice.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our findings demonstrate that inhibiting the TAM-induced IGF1\/PI3K\/Zic1 signaling axis results in MB regression and chemosensitization. These results underscore the therapeutic potential of combining a clinical CSF1R inhibitor with standard chemotherapy as an effective treatment strategy for SHH-MB.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/neuonc\/noag058","type":"journal-article","created":{"date-parts":[[2026,3,20]],"date-time":"2026-03-20T04:40:33Z","timestamp":1773981633000},"page":"1556-1570","source":"Crossref","is-referenced-by-count":0,"title":["Targeting tumor-associated macrophage-induced IGF1\/PI3K\/Zic1 axis triggers SHH medulloblastoma regression and chemosensitization"],"prefix":"10.1093","volume":"28","author":[{"given":"Yan-Chun","family":"Pang","sequence":"first","affiliation":[{"name":"Key Laboratory of Chinese Medicinal Resource from Lingnan, Ministry of Education, School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine , 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