The FMS proto-oncogene encodes a polypeptide growth factor receptor expressed on the cell surface of monocytes and B lymphocytes within the haematological system. Mutations of the FMS gene at codons 301 and 969 have been detected in a number of haematological disorders. Mutations at these codons are thought to be important in the pathogenesis of leukaemia in cells expressing a mutant receptor. Following our finding that the colony stimulating factor-1 receptor (CSF-1R) was expressed on B cells, we have assessed DNA from 17 patients with B-cell chronic lymphocytic leukaemia (CLL), 15 with acute lymphoblastic leukaemias (ALL), two samples from patients with B-cell non-Hodgkin's lymphoma (B-NHL), and 20 haematologically normal individuals for the presence of C-terminal mutations of the FMS gene. Using single stranded conformational polymorphism analysis (SSCP), a single band shift was detected resulting from a nucleotide insertion at codon 965 in the DNA isolated from a patient with B-NHL. These results indicate that mutations of the FMS gene in this region are rare in B-cell malignancy but may contribute to the pathogenesis of leukaemias and lymphomas in a small subset of patients. However, the presence of other mutations not detected using this type of analysis cannot be excluded.
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Oncologist
January 2025
Netherlands Cancer Institute-Antoni van Leeuwenhoek Hospital, Thoracic Oncology, 1066 CX Amsterdam, The Netherlands.
Introduction: We describe the safety of sotorasib monotherapy in patients with KRAS G12C-mutated advanced non-small cell lung cancer (NSCLC) and discuss practical recommendations for managing key risks.
Methods: Incidence rates of treatment-related adverse events (TRAEs) were pooled from 4 clinical trials: CodeBreaK 100 (NCT03600883), CodeBreaK 101 (NCT04185883), CodeBreaK 105 (NCT04380753), and CodeBreaK 200 (NCT04303780) and graded according to CTCAE v5.0.
Sci Rep
January 2025
Department of General Surgery, Qilu Hospital, Shandong University, Jinan, 250012, Shandong Province, China.
The crosstalk between cancers and the immune microenvironment plays a critical role in malignant progression. FMS-like tyrosine kinase 3 (FLT3) is a frequently mutated gene in acute myeloid leukemia (AML). However, its role in solid cancers remains poorly understood.
View Article and Find Full Text PDFTransl Oncol
February 2025
The First Clinical Medical College of Lanzhou University, Lanzhou 730000, China; Department of Hematology, The First Hospital of Lanzhou University, Lanzhou 730000, China. Electronic address:
Gilteritinib treats acute myeloid leukemia (AML) with the FMS-like receptor tyrosine kinase-3 (FLT3) internal tandem duplication (ITD) mutation. Dysregulation of histone modification affects the genesis and progression of AML. Strategies targeting key histone regulators have not been applied to the treatment of AML.
View Article and Find Full Text PDFBiomark 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 PDFZhonghua Xue Ye Xue Za Zhi
December 2024
Department of Hematology, Jiangsu Province Hospital, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
This study aimed to assess the efficacy and safety of gilteritinib combined with chemotherapy in treating newly diagnosed FLT3-mutated acute myeloid leukemia (AML). We retrospectively collected clinical data from 16 patients newly diagnosed with FLT3-mutated AML at Jiangsu Province Hospital. Patients received induction therapy with the classic "3 + 7" regimen or the VA regimen, and all patients were immediately supplied with gilteritinib after detecting FLT3-ITD/TKD mutations.
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