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Comparison of blinatumomab and chimeric antigen receptor T cells pre-haploidentical hematopoietic stem cell transplantation for pediatric Philadelphia chromosome negative B-cell acute lymphoblastic leukemia.
Chin Med J (Engl)
January 2025
Peking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Hematopoietic Stem Cell Transplantation, Peking-Tsinghua Center for Life Science, Research Unit of Key Technique for Diagnosis and Treatment of Hematologic Malignancies, Chinese Academic of Medical Sciences, Beijing 100044, China.
Hyper-CVAD and Sequential Blinatumomab Without and With Inotuzumab in Young Adults With Newly Diagnosed Philadelphia Chromosome-Negative B-Cell Acute Lymphoblastic Leukemia.
Am J Hematol
January 2025
Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Adding inotuzumab ozogamicin (InO) to hyper-CVAD and blinatumomab may improve outcomes in newly diagnosed Philadelphia chromosome (Ph)-negative B-cell acute lymphoblastic leukemia (B-ALL). Patients with newly diagnosed B-ALL received up to four cycles of hyper-CVAD followed by four cycles of blinatumomab. Beginning with patient #39, InO 0.
View Article and Find Full Text PDFPhiladelphia Chromosome as a Clinically Favorable Prognostic Factor of B-cell Acute Lymphoblastic Leukemia/Lymphoblastic Lymphoma in Transplant-Ineligible Elderly Patients in the Era of Molecular-Targeted Therapy.
Cureus
November 2024
Department of Hematology, Oita Prefectural Hospital, Oita, JPN.
Background and objective There is scarce data on the treatment outcomes of B-cell acute lymphoblastic leukemia/lymphoblastic lymphoma (B-ALL/LBL) in elderly patients in the era of tyrosine kinase inhibitors (TKIs), blinatumomab, and inotuzumab ozogamicin. In light of this, we aimed to address this gap in data by conducting this retrospective study. Methods Treatment outcomes were retrospectively evaluated by using data from transplant-ineligible patients aged 65 years or older with newly diagnosed B-ALL/LBL (n=29) at two hospitals in Oita, Japan between 2013 and 2023.
View Article and Find Full Text PDFThromboinflammation in ischemic cerebrovascular patients with the JAK2V617F mutation.
Thromb Res
January 2025
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark; Department of Neurology, Zealand University Hospital, Roskilde, Denmark.
Background: The JAK2V617F mutation is a driver of Philadelphia chromosome-negative myeloproliferative neoplasms (MPN) and is also implicated in cardiovascular diseases. Thrombosis in MPN involves JAK2V617F-associated platelet activation and endothelial dysfunction, all potentially influenced by chronic inflammation. Whether the mutation affects thromboinflammatory markers similarly in non-MPN patients remains unclear.
View Article and Find Full Text PDFMolecular profiling in MPN: who should have it and why?
Hematology Am Soc Hematol Educ Program
December 2024
Cancer and Haematology Centre, Department of Clinical Haematology, The Churchill Hospital, Oxford University Hospitals NHS Foundation Trust, Oxford, UK.
Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs) are a group of blood cancers that result from somatic mutations in hematopoietic stem cells, causing constitutive activation of JAK-STAT signaling pathways with consequent overproduction of 1 or more myeloid lineages. The initiating event in MPN pathogenesis is a genetic mutation, and consequently molecular profiling is central to the diagnosis, risk stratification, and, increasingly, monitoring of therapy response in persons with MPN. In this review we summarize current approaches to molecular profiling of classical MPNs (essential thrombocythemia, polycythemia vera, and myelofibrosis), using illustrative clinical case histories to demonstrate how genetic analysis is already fully integrated into MPN diagnostic classification and prognostic risk stratification.
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