{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T09:35:47Z","timestamp":1785404147680,"version":"3.56.0"},"posted":{"date-parts":[[2026,5,19]]},"group-title":"Cancer Biology","reference-count":79,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T00:00:00Z","timestamp":1779148800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.biorxiv.org\/about\/FAQ#license"}],"funder":[{"id":[{"id":"https:\/\/ror.org\/04twxam07","id-type":"ROR","asserted-by":"publisher"}]},{"DOI":"10.13039\/100020487","name":"Break Through Cancer","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100020487","id-type":"DOI","asserted-by":"crossref"}]},{"name":"National Institute of Health"},{"name":"National Cancer Institute"},{"name":"Cancer Prevention Reserch Institute of Texas"},{"DOI":"10.13039\/100007449","name":"Takeda Science Foundation","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100007449","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,5,19]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                <jats:p>\n                  Measurable (or minimal) residual disease (MRD) predicts relapse in patients with acute myeloid leukemia (AML). However, the biological and spatial characteristics of the AML bone marrow (BM) microenvironment (BMME) in which MRD cells survive remain largely unexplored; in particular, little is known of the BMME in\n                  <jats:italic>TP53<\/jats:italic>\n                  mutant (\n                  <jats:italic>TP53<\/jats:italic>\n                  <jats:sup>mut<\/jats:sup>\n                  ) AML. Here, we applied sequential immunofluorescence to whole BM biopsy specimens obtained from patients with\n                  <jats:italic>TP53<\/jats:italic>\n                  wild-type (\n                  <jats:italic>TP53<\/jats:italic>\n                  <jats:sup>WT<\/jats:sup>\n                  ) AML and\n                  <jats:italic>TP53<\/jats:italic>\n                  <jats:sup>mut<\/jats:sup>\n                  AML at diagnosis and in morphological complete remission (CR) to generate a comprehensive spatial map of the hematopoietic and BMME components. We identified\n                  <jats:italic>TP53<\/jats:italic>\n                  <jats:sup>mut<\/jats:sup>\n                  leukemia cells based on high p53 expression and delineated their spatial organization relative to stromal and immune niches. Biopsy-based cell composition analysis revealed marked B-cell depletion and an increased abundance of regulatory T-cells (Tregs) in\n                  <jats:italic>TP53<\/jats:italic>\n                  <jats:sup>mut<\/jats:sup>\n                  BM at CR. Unlike\n                  <jats:italic>TP53<\/jats:italic>\n                  <jats:sup>WT<\/jats:sup>\n                  BM,\n                  <jats:italic>TP53<\/jats:italic>\n                  <jats:sup>mut<\/jats:sup>\n                  BM at CR exhibited persistent\n                  <jats:italic>TP53<\/jats:italic>\n                  <jats:sup>mut<\/jats:sup>\n                  erythroid and immature leukemia cell clusters, spatially segregated from T-cell clusters, in perisinusoidal niches, suggesting niche-level immune evasion. Spatial profiling further revealed that Tregs characterized by FOXP3 upregulation were enriched near\n                  <jats:italic>TP53<\/jats:italic>\n                  <jats:sup>mut<\/jats:sup>\n                  MRD cells, indicating a locally enhanced immunosuppressive activity. Single-cell RNA sequencing\u2013based cell-cell communication analysis identified erythroid\u2013T-cell interactions mediated by the GDF15-CD48 axis as a potential mechanism of T-cell suppression, suggesting that the erythroid differentiation of\n                  <jats:italic>TP53<\/jats:italic>\n                  <jats:sup>mut<\/jats:sup>\n                  AML cells enhances local immunosuppression. Collectively, our results show a spatially organized immunosuppressive BMME in\n                  <jats:italic>TP53<\/jats:italic>\n                  <jats:sup>mut<\/jats:sup>\n                  AML and highlight the potential of spatial proteomics to identify actionable MRD niches in leukemias.\n                <\/jats:p>\n                <jats:sec>\n                  <jats:title>Key points<\/jats:title>\n                  <jats:list list-type=\"bullet\">\n                    <jats:list-item>\n                      <jats:p>\n                        <jats:italic>TP53<\/jats:italic>\n                        mutant erythroid and immature leukemia cells form spatial clusters segregated from T-cells in complete remission.\n                      <\/jats:p>\n                    <\/jats:list-item>\n                    <jats:list-item>\n                      <jats:p>\n                        An erythroblast-centered immunosuppressive niche characterizes\n                        <jats:italic>TP53<\/jats:italic>\n                        mutant leukemia cells.\n                      <\/jats:p>\n                    <\/jats:list-item>\n                  <\/jats:list>\n                <\/jats:sec>","DOI":"10.64898\/2026.05.15.725421","type":"posted-content","created":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T16:40:16Z","timestamp":1779208816000},"source":"Crossref","is-referenced-by-count":0,"title":["Niche-level immune evasion in\n                  <i>TP53<\/i>\n                  mutant AML residual disease revealed by spatial proteomics"],"prefix":"10.64898","author":[{"given":"Hideaki","family":"Mizuno","sequence":"first","affiliation":[{"name":"Section of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuki","family":"Nishida","sequence":"additional","affiliation":[{"name":"Section of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrea","family":"Bedoy","sequence":"additional","affiliation":[{"name":"Section of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Edward","family":"Ayoub","sequence":"additional","affiliation":[{"name":"Section of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoonkyu","family":"Lee","sequence":"additional","affiliation":[{"name":"Section of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akshay","family":"Basi","sequence":"additional","affiliation":[{"name":"Department of Hematopoietic Biology & Malignancy, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Koji","family":"Sasaki","sequence":"additional","affiliation":[{"name":"Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guillermo","family":"Garcia-Manero","sequence":"additional","affiliation":[{"name":"Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jared","family":"Burks","sequence":"additional","affiliation":[{"name":"Department of Hematopoietic Biology & Malignancy, Division of Cancer Medicine, The University of 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