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JAK2 V617F Mutation Leading to Portal Vein Thrombosis in a Young Patient: A Case Report.
Cureus
December 2024
Radiodiagnosis, Malla Reddy Medical College for Women, Hyderabad, IND.
Myeloproliferative neoplasms (MPNs) are clonal hematopoietic stem cell disorders commonly characterized by excessive production of blood cell lineages. The JAK2 V617F mutation plays a crucial role in the pathogenesis of these conditions, often leading to thrombotic complications. Here, we present the case of a 21-year-old man who presented with acute abdominal pain and was found to have portal vein thrombosis with splenomegaly.
View Article and Find Full Text PDFIntroduction: Recent Rift Valley fever (RVF) epidemiology in eastern Africa region is characterized by widening geographic range and increasing frequency of small disease clusters. Here we conducted studies in southwestern (SW) Uganda region that has since 2016 reported increasing RVF activities.
Methods: A 22-month long hospital-based study in three districts of SW Uganda targeting patients with acute febrile illness (AFI) or unexplained bleeding was followed by a cross-sectional population-based human-animal survey.
An exploration of unusual antimicrobial resistance phenotypes in Salmonella Typhi from Blantyre, Malawi reveals the ongoing role of IncHI1 plasmids.
Gates Open Res
January 2025
Liverpool School of Tropical Medicine, Liverpool, England, UK.
Typhoid fever is a significant public health problem endemic in Southeast Asia and Sub-Saharan Africa. Antimicrobial treatment of typhoid is however threatened by the increasing prevalence of antimicrobial resistant (AMR) Typhi, especially in the globally successful lineage (4.3.
View Article and Find Full Text PDFA germline FLT3 variant in aplastic anemia.
Biomark Res
January 2025
Department of Oncology, Montefiore Medical Center and Albert Einstein College of Medicine, Bronx, NY, USA.
FMS-like tyrosine kinase 3 (FLT3) genetic variants are commonly seen in high-grade myeloid neoplasms and are typically gain-of-function mutations associated with a proliferative disease phenotype. Inactivating FLT3 variants have been less frequently described in non-malignant, autoimmune disorders and are uncommon in aplastic anemia (AA). Herein, we report the first to our knowledge, and unusual case of a germline, gain-of-function, FLT3 variant in a patient with severe AA treated successfully with immunosuppressive therapy.
View Article and Find Full Text PDFWhile the genetic paradigm of cancer etiology has proven powerful, it remains incomplete as evidenced by the widening spectrum of non-cancer cell-autonomous "hallmarks" of cancer. Studies have demonstrated the commonplace presence of high oncogenic mutational burdens in homeostatically-stable epithelia. Hence, the presence of driver mutations alone does not result in cancer.
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