Individualized Dosing Patterns in the Treatment of Older Patients with Gastrointestinal Stromal Tumors: Results of a Registry-Based Observational National Cohort Study Including 871 Patients
ConclusionOlder patients showed higher imatinib trough plasma concentrations compared with younger patients and also had earlier and more often adverse events as the reason for first adjustment of treatment with imatinib followed by dose reduction. However, in a landmark analysis, patients with imatinib dose reductions had no poorer outcomes compared with patients not requiring a dose reduction. (Source: Drugs and Aging)
Source: Drugs and Aging - December 20, 2023 Category: Geriatrics Source Type: research
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Cell Death & Disease, Published online: 18 December 2023; doi:10.1038/s41419-023-06300-2Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination (Source: Cell death and disease)
Source: Cell death and disease - December 18, 2023 Category: Internal Medicine Authors: Xiangfei Sun Qiang Zhang Xiaohan Lin Ping Shu Xiaodong Gao Kuntang Shen Source Type: research
Chemoproteomics Reveals Glaucocalyxin A Induces Mitochondria-Dependent Apoptosis of Leukemia Cells via Covalently Binding to VDAC1
In this study, the effect and molecular mechanism of GLA on imatinib-sensitive and imatinib-resistant CML cells harboring T315I mutation via a combined deconvolution strategy of chemoproteomics and label-free proteomics is investigated. The data demonstrated that GLA restrains proliferation and induces mitochondria-dependent apoptosis in both imatinib-sensitive and resistant CML cells. GLA covalently binds to the cysteine residues of mitochondrial voltage-dependent anion channels (VDACs), resulting in mitochondrial damage and overflow of intracellular apoptotic factors, eventually leading to apoptosis. In addition, the com...
Source: Adv Data - December 17, 2023 Category: Epidemiology Authors: Yehai An Qian Zhang Yu Chen Fei Xia Yin-Kwan Wong Hengkai He Mingjing Hao Jiahang Tian Xiaoyong Zhang Piao Luo Jigang Wang Source Type: research
Chemoproteomics Reveals Glaucocalyxin A Induces Mitochondria-Dependent Apoptosis of Leukemia Cells via Covalently Binding to VDAC1
In this study, the effect and molecular mechanism of GLA on imatinib-sensitive and imatinib-resistant CML cells harboring T315I mutation via a combined deconvolution strategy of chemoproteomics and label-free proteomics is investigated. The data demonstrated that GLA restrains proliferation and induces mitochondria-dependent apoptosis in both imatinib-sensitive and resistant CML cells. GLA covalently binds to the cysteine residues of mitochondrial voltage-dependent anion channels (VDACs), resulting in mitochondrial damage and overflow of intracellular apoptotic factors, eventually leading to apoptosis. In addition, the com...
Source: Adv Data - December 17, 2023 Category: Epidemiology Authors: Yehai An Qian Zhang Yu Chen Fei Xia Yin-Kwan Wong Hengkai He Mingjing Hao Jiahang Tian Xiaoyong Zhang Piao Luo Jigang Wang Source Type: research
miR-181a plays the tumor-suppressor role in chronic myeloid leukemia CD34 < sup > + < /sup > cells partially via SERPINE1
Cell Mol Life Sci. 2023 Dec 16;81(1):10. doi: 10.1007/s00018-023-05036-8.ABSTRACTThe formation of the BCR-ABL fusion gene drives human chronic myeloid leukemia (CML). The last 2 decades have witnessed that specific tyrosine kinase inhibitors (TKIs, e.g., imatinib mesylate, IM) against ABL1 improve disease treatment, although some patients still suffer from relapse and TKI resistance. Therefore, a better understanding of the molecular pathology of CML is still urgently needed. miR-181a-5p (miR-181a) acts as a tumor suppressor in CML; however, the molecular mechanism of miR-181a in CML stem/progenitor cells remains elusive. ...
Source: Cellular and Molecular Life Sciences : CMLS - December 16, 2023 Category: Cytology Authors: Xiuyan Zhang Wenjuan Ma Wen Xue Yu Wang Pan Chen Quanxue Li Yuan-Yuan Li Xiaohui Hu Yun Zhao Haixia Zhou Source Type: research
miR-181a plays the tumor-suppressor role in chronic myeloid leukemia CD34 < sup > + < /sup > cells partially via SERPINE1
Cell Mol Life Sci. 2023 Dec 16;81(1):10. doi: 10.1007/s00018-023-05036-8.ABSTRACTThe formation of the BCR-ABL fusion gene drives human chronic myeloid leukemia (CML). The last 2 decades have witnessed that specific tyrosine kinase inhibitors (TKIs, e.g., imatinib mesylate, IM) against ABL1 improve disease treatment, although some patients still suffer from relapse and TKI resistance. Therefore, a better understanding of the molecular pathology of CML is still urgently needed. miR-181a-5p (miR-181a) acts as a tumor suppressor in CML; however, the molecular mechanism of miR-181a in CML stem/progenitor cells remains elusive. ...
Source: Cellular and Molecular Life Sciences : CMLS - December 16, 2023 Category: Cytology Authors: Xiuyan Zhang Wenjuan Ma Wen Xue Yu Wang Pan Chen Quanxue Li Yuan-Yuan Li Xiaohui Hu Yun Zhao Haixia Zhou Source Type: research
miR-181a plays the tumor-suppressor role in chronic myeloid leukemia CD34 < sup > + < /sup > cells partially via SERPINE1
Cell Mol Life Sci. 2023 Dec 16;81(1):10. doi: 10.1007/s00018-023-05036-8.ABSTRACTThe formation of the BCR-ABL fusion gene drives human chronic myeloid leukemia (CML). The last 2 decades have witnessed that specific tyrosine kinase inhibitors (TKIs, e.g., imatinib mesylate, IM) against ABL1 improve disease treatment, although some patients still suffer from relapse and TKI resistance. Therefore, a better understanding of the molecular pathology of CML is still urgently needed. miR-181a-5p (miR-181a) acts as a tumor suppressor in CML; however, the molecular mechanism of miR-181a in CML stem/progenitor cells remains elusive. ...
Source: Cellular and Molecular Life Sciences : CMLS - December 16, 2023 Category: Cytology Authors: Xiuyan Zhang Wenjuan Ma Wen Xue Yu Wang Pan Chen Quanxue Li Yuan-Yuan Li Xiaohui Hu Yun Zhao Haixia Zhou Source Type: research
miR-181a plays the tumor-suppressor role in chronic myeloid leukemia CD34 < sup > + < /sup > cells partially via SERPINE1
Cell Mol Life Sci. 2023 Dec 16;81(1):10. doi: 10.1007/s00018-023-05036-8.ABSTRACTThe formation of the BCR-ABL fusion gene drives human chronic myeloid leukemia (CML). The last 2 decades have witnessed that specific tyrosine kinase inhibitors (TKIs, e.g., imatinib mesylate, IM) against ABL1 improve disease treatment, although some patients still suffer from relapse and TKI resistance. Therefore, a better understanding of the molecular pathology of CML is still urgently needed. miR-181a-5p (miR-181a) acts as a tumor suppressor in CML; however, the molecular mechanism of miR-181a in CML stem/progenitor cells remains elusive. ...
Source: Cellular and Molecular Life Sciences : CMLS - December 16, 2023 Category: Cytology Authors: Xiuyan Zhang Wenjuan Ma Wen Xue Yu Wang Pan Chen Quanxue Li Yuan-Yuan Li Xiaohui Hu Yun Zhao Haixia Zhou Source Type: research
Cancers, Vol. 15, Pages 5854: Diagnostics and Treatment of Extrameningeal Solitary Fibrous Tumors
Anna M. Czarnecka
Solitary fibrous tumors (SFT) are rare mesenchymal neoplasms that account for less than 2% of all soft tissue masses. In the latest WHO 2020 Classification of Soft Tissue Tumors, extrameningeal SFT was listed as intermediate (rarely metastasizing) or malignant neoplasms. Due to the lack of characteristic clinical features, their diagnosis and treatment remain challenging. The pathogenesis of SFT is often associated with the presence of fusions of the NAB2-STAT6 gene on the 12q13 chromosome. Cytoplasmic CD34 positive staining is considerably characteristic for most SFTs; less frequently, factor XII, v...
Source: Cancers - December 15, 2023 Category: Cancer & Oncology Authors: Anna Maria Janik Anna Terlecka Mateusz J. Spa łek Kjetil Boye Bart łomiej Szostakowski Paulina Chmiel Anna Szumera-Cie ćkiewicz Klaudia Bobak Tomasz Świtaj Piotr Rutkowski Anna M. Czarnecka Tags: Review Source Type: research
Resistance mutations in CML and how we approach them
Hematology Am Soc Hematol Educ Program. 2023 Dec 8;2023(1):469-475. doi: 10.1182/hematology.2023000447.ABSTRACTAmong the variety of resistance mechanisms that may underlie a non-optimal response to tyrosine kinase inhibitor (TKI) therapy in chronic myeloid leukemia patients, secondary point mutations in the BCR::ABL1 kinase domain (KD) represent the only actionable one. Each of the 5 ATP-competitive inhibitors (imatinib, dasatinib, nilotinib, bosutinib, ponatinib) has a well-defined spectrum of resistance mutations. Growing clinical experience will soon allow to also elucidate the full spectrum of mutations conferring resi...
Source: Hematology ASH Education Program - December 9, 2023 Category: Hematology Authors: Simona Soverini Source Type: research
