{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T10:44:20Z","timestamp":1790765060369,"version":"4.1.0"},"reference-count":149,"publisher":"MDPI AG","issue":"10","license":[{"start":{"date-parts":[[2023,5,11]],"date-time":"2023-05-11T00:00:00Z","timestamp":1683763200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cancers"],"abstract":"<jats:p>Despite exhaustive studies, researchers have made little progress in the field of adoptive cellular therapies for relapsed\/refractory acute myeloid leukemia (AML), unlike the notable uptake for B cell malignancies. Various single antigen-targeting chimeric antigen receptor (CAR) T cell Phase I trials have been established worldwide and have recruited approximately 100 patients. The high heterogeneity at the genetic and molecular levels within and between AML patients resembles a black hole: a great gravitational field that sucks in everything. One must consider the fact that only around 30% of patients show a response; there are, however, consequential off-tumor effects. It is obvious that a new point of view is needed to achieve more promising results. This review first introduces the unique therapeutic challenges of not only CAR T cells but also other adoptive cellular therapies in AML. Next, recent single-cell sequencing data for AML to assess somatically acquired alterations at the DNA, epigenetic, RNA, and protein levels are discussed to give a perspective on cellular heterogeneity, intercellular hierarchies, and the cellular ecosystem. Finally, promising novel strategies are summarized, including more sophisticated next-generation CAR T, TCR-T, and CAR NK therapies; the approaches with which to tailor the microenvironment and target neoantigens; and allogeneic approaches.<\/jats:p>","DOI":"10.3390\/cancers15102713","type":"journal-article","created":{"date-parts":[[2023,5,11]],"date-time":"2023-05-11T04:29:01Z","timestamp":1683779341000},"page":"2713","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":55,"title":["The Black Hole: CAR T Cell Therapy in AML"],"prefix":"10.3390","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8613-2105","authenticated-orcid":false,"given":"Erden","family":"Atilla","sequence":"first","affiliation":[{"name":"Fred Hutchinson Cancer Research Center, Clinical Research Division, 1100 Fairview Ave N, Seattle, WA 98109, USA"},{"name":"GENYO Centre for Genomics and Oncological Research, Genomic Medicine Department, Pfizer\/University of Granada\/Andalusian Regional Government, Health Sciences Technology Park, 18016 Granada, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4673-2111","authenticated-orcid":false,"given":"Karim","family":"Benabdellah","sequence":"additional","affiliation":[{"name":"GENYO Centre for Genomics and Oncological Research, Genomic Medicine Department, Pfizer\/University of Granada\/Andalusian Regional Government, Health Sciences Technology Park, 18016 Granada, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2023,5,11]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","unstructured":"Vishwasrao, P., Li, G., Boucher, J.C., Smith, D.L., and Hui, S.K. 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