The prognosis of patients who relapse with acute myeloid leukemia (AML) after undergoing stem cell transplantation (SCT) is poor. There exist some treatments for relapsed AML; however, almost all treatments are associated with a high level of regimen-related toxicities (RRTs). The RRT of donor lymphocyte infusion is lower than that of other treatments; however, the efficacy of this treatment in treating patients with relapsed AML is lower than that observed in patients with chronic myelomonocytic leukemia. We herein report a case of relapsed AML after SCT in a 65-year-old man. We performed donor lymphocyte infusion; however, it was not effective. We then administered chemotherapy with cytosine arabinoside and macrophage colony-stimulating factor/granulocyte colony-stimulating factor and complete remission was achieved. Since graft-versus-host disease occurred after the administration of low-dose chemotherapy in this case, we speculated that the chemotherapy induced a graft-versus-leukemia effect.
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http://dx.doi.org/10.2169/internalmedicine.51.7933 | DOI Listing |
Inversion of chromosome 16 [inv(16)] is one of the most common chromosomal rearrangements in Acute Myeloid Leukemia (AML) and generates the fusion gene , which initiates leukemogenesis. Patients with inv(16) at diagnosis invariably have the rearrangement at relapse, leading to the assumption that is required after leukemic transformation. However, this has yet to be shown experimentally.
View Article and Find Full Text PDFAnn Pharmacother
January 2025
Department of Hematologic Malignancies, Fred Hutchinson Cancer Center, Seattle, WA, USA.
Background: Addition of midostaurin to standard "7+3" (cytarabine and anthracycline) significantly prolongs overall and event-free survival. At University of Washington/Fred Hutchinson Cancer Center (UW/FHCC), the standard regimen for newly diagnosed (ND) and relapsed/refractory (R/R) AML is cladribine, high-dose cytarabine, GCSF, and mitoxantrone (CLAG-M); midostaurin is added if FLT3-mutated. There is limited data on the use of FLT3-inhibitors with high-dose cytarabine regimens in AML.
View Article and Find Full Text PDFCancer Genet
January 2025
PhD of Hematology, Assistant Professor, Department of Medical Laboratory Sciences, School of Paramedical Sciences, Hamadan University of Medical Sciences, Hamadan, Iran. Electronic address:
Cancers (Basel)
January 2025
Department of Clinical and Experimental Medicine, Brighton and Sussex Medical School, Falmer, Brighton BN1 9PX, UK.
Background/objectives: Acute myeloid leukemia (AML) is an aggressive neoplasm. Although most patients respond to induction therapy, they commonly relapse due to recurrent disease in the bone marrow microenvironment (BMME). So, the disruption of the BMME, releasing tumor cells into the peripheral circulation, has therapeutic potential.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, CA 92350, USA.
Acute myeloid leukemia (AML) is an aggressive malignancy that poses significant challenges due to high rates of relapse and resistance to treatment, particularly in older populations. While therapeutic advances have been made, survival outcomes remain suboptimal. The evolution of DNA and RNA sequencing technologies, including whole-genome sequencing (WGS), whole-exome sequencing (WES), and RNA sequencing (RNA-Seq), has significantly enhanced our understanding of AML at the molecular level.
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