Objective: To evaluate the effectiveness of ruxolitinib on acute graft-versus-host disease (aGVHD) prophylaxis and its impact on graft-versus-leukemia (GVL) effect in patients after modified donor lymphocyte infusion (mDLI).
Methods: We retrospectively included patients with relapsed leukemia after allogeneic hematopoietic stem cell transplantation (allo-HSCT) who received ruxolitinib prophylaxis between October 2018 and April 2020. The incidence of aGVHD, disease-free survival (DFS), overall survival (OS), and treatment safety were evaluated.
Results: Seventeen patients were followed up for a median time of 8 months (range: 1-26 months). The incidence of aGVHD on Day 30 after mDLI was 41.2% and ranged from Grade 1 to 4; ten of 17 patients (58.8%) achieved a complete response (CR), and two (11.8%) had a partial response (PR). Cytomegalovirus (CMV) reactivation rate was 23.5%, and the median time from mDLI to CMV reactivation was 48.5 days. The mean DFS and OS after mDLI were 1.0 (95% CI 0.0-3.5) and 9.0 (95% CI 1.2-16.8) months, respectively. The causes of death for 10 patients were leukemia relapse (n = 5), aGVHD and septic shock (n = 3), intracranial lesion (n = 1), and COVID-19 (n = 1).
Conclusions: We reported encouraging results of ruxolitinib monotherapy in the prevention of aGVHD and maintenance of GVL for post-transplantation relapsed patients, even though being at high risk with poor initial prognosis.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.trim.2022.101743 | DOI Listing |
Intrachromosomal amplification of chromosome 21 (iAMP21) B-cell precursor acute lymphoblastic leukemia (BCP-ALL) in children is a high-risk subtype for which targeted drugs are lacking. In this study, we determined the frequency of secondary lesions in 28 iAMP21 BCP-ALL patient samples and investigated cellular sensitivity for candidate-targeted drugs. iAMP21 was enriched in aberrations (10.
View Article and Find Full Text PDFJ Infect Dis
January 2025
Peking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Treatment of Hematological Disease, Beijing Key Laboratory of Hematopoietic Stem Cell Transplantation for the Treatment of Hematological Diseases, Beijing, China.
Background: Severe pneumonia after allogeneic hematopoietic stem cell transplantation (allo-HSCT) is associated with high mortality. Given that cytokine, including Interleukin-6 (IL-6), play a critical role in immune-mediated organ injury in patients with severe COVID-19, we hypothesized that cytokines may also contribute to the pathogenesis of severe pneumonia after allo-HSCT. This study aimed to investigate the role of IL-6 in severe pneumonia post-allo-HSCT and explore its underlying mechanism.
View Article and Find Full Text PDFSci Transl Med
January 2025
Knight Cancer Institute, Oregon Health & Science University, Portland, OR 97239, USA.
Familial platelet disorder (FPD) is associated with germline mutations, establishing a preleukemic state and increasing the risk of developing leukemia. Currently, there are no intervention strategies to prevent leukemia progression. Single-cell RNA sequencing ( = 10) combined with functional analysis of samples from patients with -FPD ( > 75) revealed that FPD hematopoietic stem and progenitor cells (HSPCs) displayed increased myeloid differentiation and suppressed megakaryopoiesis because of increased activation of prosurvival and inflammatory pathways.
View Article and Find Full Text PDFINTRODUCTION ETV6::JAK2 is a fusion known to drive Acute Lymphoblastic Leukaemia (ALL) in the presence of other genomic lesions which define the JAK/STAT class of Philadelphia-like Acute Lymphoblastic Leukaemia (Ph-like ALL). Ph-like ALL comprises approximately 15% of ALL. Patients with mutations or gene fusions signaling through the JAK/STAT pathway have particularly poor prognosis.
View Article and Find Full Text PDFPediatr Rheumatol Online J
December 2024
Translational Genetics Research Group, La Fe Health Research Institute (IIS La Fe), Avenida Fernando Abril Martorell nº 106 Tower A, 7th Floor, Valencia, Spain.
Background: Aicardi-Goutières Syndrome is a monogenic type 1 interferonopathy with infantile onset, characterized by a variable degree of neurological damage. Approximately 7% of Aicardi-Goutières Syndrome cases are caused by pathogenic variants in the ADAR gene and are classified as Aicardi-Goutières Syndrome type 6. Here, we present a new homozygous pathogenic variant in the ADAR gene.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!