ArticleJournal of cancer research and clinical oncology2026
Allogeneic CD56
Article in Journal of cancer research and clinical oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Authors and funding
9 authors.
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Abstract
backgroundFanconi anemia (FA) is a rare inherited disorder characterized by genomic instability, bone marrow failure, and a markedly increased risk of developing acute myeloid leukemia (AML). The intrinsic hypersensitivity of FA cells to DNA-damaging agents renders conventional chemotherapy particularly toxic and often ineffective. CASE PRESENTATION: A 31-year-old woman with FA who progressed to AML and failed to achieve remission with standard induction therapy. Bone marrow blasts were initially 10%.
interventionAs part of a clinical trial, she received CD56+ cell-based immunotherapy after FLAG chemotherapy. She subsequently underwent allogeneic hematopoietic stem cell transplantation (HSCT) from a matched sibling donor using a CD3+/CD19-depleted graft. Post-transplant, she received additional infusions of CD56+ cells. OUTCOME: CD56+ immunotherapy reduced bone marrow blasts from 10 to 3%, enabling successful HSCT. Post-transplant, she remained in complete remission with no detectable minimal residual disease (MRD) at both day +30 and day +90.
conclusionCD56+ cell-based immunotherapy can effectively decrease the leukemic burden in FA patients with AML, facilitating successful HSCT. This innovative approach may enhance outcomes for high-risk patients and merits further research.
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