A 49-year-old man was admitted to our hospital with a 1-month history of dysphagia. An upper endoscopy revealed a lower esophageal submucosal tumor. Immunohistochemical staining of the biopsy specimen revealed KIT positivity. Thus, the tumor was diagnosed as a gastrointestinal stromal tumor (GIST). After 6 months of imatinib treatment, the tumor decreased from 92 mm × 55 mm × 80 mm to 65 mm × 35 mm × 55 mm in diameter, and surgery was performed. The tumor was completely resected without rupture, by partial esophagogastric resection through a thoracotomy incision, using an abdominal laparoscopic approach. Immunohistochemical staining revealed that the tumor was negative for c-kit but positive for CD34. Genetic examination showed that the tumor had a mutation in exon 11. The patient experienced minor leakage but recovered conservatively. Adjuvant imatinib was initiated 64 days after surgery. We report this rare case to show the potential of preoperative imatinib treatment in patients with large esophageal GISTs, to achieve complete resection without rupture.
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http://dx.doi.org/10.1186/1477-7819-12-47 | DOI Listing |
J Cardiovasc Pharmacol
January 2025
Department of Respiratory and Critical Care Medicine, Affiliated Hospital of Nantong University, Nantong 226001, China.
Pulmonary vascular remodeling and arterial hypertension (PAH) correlate to increased platelet-derived growth factor (PDGF) activity and elevated KIT expression. Imatinib has emerged as a potential therapeutic agent for PAH. The purpose of this systematic review and meta-analysis was to assess the effectiveness of imatinib in treatment of PAH.
View Article and Find Full Text PDFZhongguo Shi Yan Xue Ye Xue Za Zhi
December 2024
Blood Diseases Institute, Xuzhou Medical University, Department of Hematology, The Affiliated Hospital of Xuzhou Medical University.
Objective: To explore whether Ph acute lymphoblastic leukemia (ALL) cell line SUP-B15 treated with imatinib occurs a tolerant status charactered by cell proliferation suppression but apoptotic resistance, then evaluate whether IGF1-R inhibitor AEW541 can break this tolerance, and further explain its mechanisms.
Methods: SUP-B15 cells were treated with different concentrations of imatinib or AEW541. Cell proliferation was assayed by Deep Blue, and apoptotic cells were determined by Annexin V/7-AAD staining.
Zhongguo Shi Yan Xue Ye Xue Za Zhi
December 2024
Department of Hematology, The Affiliated Hospital of North Sichuan Medical College, Nanchong 637000, Sichuan Province, China.
Objective: To compare the efficacy and safety of flumatinib (FM) and imatinib (IM) as first-line treatment in newly-diagnosed patients with chronic myeloid leukemia in chronic phase (CML-CP) in real world.
Methods: A total of 84 newly-diagnosed CP-CML patients in our center from December 2019 to December 2022 were retrospectively analyzed. Among them, 32 cases received FM as first-line treatment, and 52 cases received IM.
In Vivo
December 2024
Department of Medical Oncology, Hyogo Cancer Center, Akashi, Japan.
Background/aim: Gastrointestinal stromal tumors (GISTs) are rare cancers originating from Cajal's stromal cells in the gastrointestinal tract. The most common driver mutation in these cancers is the KIT mutation. This report presents a case of response to low-dose imatinib in a patient with GIST harboring KIT exon 11 W557_K558 deletion.
View Article and Find Full Text PDFBr J Clin Pharmacol
December 2024
Novartis Pharma AG, Basel, Switzerland.
Aims: This study aims to evaluate the exposure-efficacy relationship of nilotinib and longitudinal BCR::ABL1 levels in patients with newly diagnosed Philadelphia chromosome-positive chronic myeloid leukaemia in chronic phase (CML-CP) and those who are imatinib-resistant or intolerant using a semimechanistic disease model.
Methods: The analysis included 489 CML-CP patients from 3 nilotinib trials (NCT00109707; NCT00471497; NCT01043874) with duration of follow-up ranging from 2 to 9 years. The semimechanistic disease model of CML-CP consisted of quiescent leukaemic stem cells, proliferating drug-susceptible and -resistant bone marrow cells.
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