Autologous hematopoietic stem cell transplantation is the standard therapy for refractory/relapsed aggressive lymphoma. The initial step of the procedure involves mobilization and collection of hematopoietic stem cells. G-CSF fails to achieve mobilization in 15-25% of lymphoma patients. Plerixafor is a novel CXCR4 antagonist that can promote mobilization. It has been used successfully in patients after the failure of G-CSF. It is reasonable to test whether plerixafor should become the mobilizing agent of choice in patients expected to exhibit difficulties in mobilization. We initiated a study to assess the use of plerixafor as a first-line stem cell mobilizer in 20 elderly or heavily pretreated patients with non-Hodgkin or Hodgkin lymphoma. The minimum defined CD34+ cell dose of ≥2 × 106 cells/kg was achieved by 90% of the patients, and for 83% of them with one apheresis procedure. The target CD34+ dose of ≥5 × 106 cells/kg was achieved by 70% of the patients. The median number of circulating CD34+ cells before and after plerixafor was 14.4 and 42.8 cells/μl, respectively. The post-plerixafor adverse events were mild. All patients promptly engrafted after high-dose chemotherapy treatment. We conclude that plerixafor administration is safe and efficient for upfront mobilization in lymphoma patients predicted to be poor mobilizers.
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http://dx.doi.org/10.1159/000435769 | DOI Listing |
BMC Infect Dis
January 2025
Department of Respiratory Medicine, Faculty of Medicine, Hokkaido University, North 15 West 7, Kita-ku, Sapporo, 060-8638, Japan.
Background: Mycobacterium avium complex (MAC) is a common pathogen causing non-tuberculous mycobacterial infections, primarily affecting the lungs. Disseminated MAC disease occurs mainly in immunocompromised individuals, such as those with acquired immunodeficiency syndrome, hematological malignancies, or those positive for anti-interferon-γ antibodies. However, its occurrence in solid organ transplant recipients is uncommon.
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January 2025
Division of Hematology, Second Xiang-ya Hospital, Central South University, Changsha, China.
Acute B-lymphoblastic leukemia (B-ALL) is a highly heterogeneous hematologic malignancy, characterized by significant molecular differences among patients as the disease progresses. While the PI3K-Akt signaling pathway and metabolic reprogramming are known to play crucial roles in B-ALL, the interactions between lipid metabolism, immune pathways, and drug resistance remain unclear. In this study, we performed multi-omics analysis on different patient cohorts (newly diagnosed, relapsed, standard-risk, and poor-risk) to investigate the molecular characteristics associated with metabolism, signaling pathways, and immune regulation in B-ALL.
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January 2025
Department of Hematology and Oncology, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Pediatric Metabolism and Inflammatory Diseases, Children's Hospital of Chongqing Medical University, No 136 Zhongshan 2 road, YuZhong district, Chongqing, 400014, China.
Genetic alterations play a pivotal role in leukemic clonal transformation, significantly influencing disease pathogenesis and clinical outcomes. Here, we report a novel fusion gene and investigate its pathogenic role in acute lymphoblastic leukemia (ALL). We engineer a transposon transfection system expressing the TOP2B::AFF2 transcript and introduce it into Ba/F3 cells.
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January 2025
Clinical Research Division, Fred Hutchinson Cancer Center, Seattle, WA, USA.
Gut microbiota disruptions after allogeneic hematopoietic cell transplantation (alloHCT) are associated with increased risk of acute graft-versus-host disease (aGVHD). We designed a randomized, double-blind placebo-controlled trial to test whether healthy-donor fecal microbiota transplantation (FMT) early after alloHCT reduces the incidence of severe aGVHD. Here, we report the results from the single-arm run-in phase which identified the best of 3 stool donors for the randomized phase.
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January 2025
Division of Molecular Genetics, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Chronic lymphocytic leukemia is a malignant lymphoproliferative disorder for which primary or acquired drug resistance represents a major challenge. To investigate the underlying molecular mechanisms, we generate a mouse model of ibrutinib resistance, in which, after initial treatment response, relapse under therapy occurrs with an aggressive outgrowth of malignant cells, resembling observations in patients. A comparative analysis of exome, transcriptome and proteome of sorted leukemic murine cells during treatment and after relapse suggests alterations in the proteasome activity as a driver of ibrutinib resistance.
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