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ArfGAP with the SH3 Domain, Ankyrin Repeat and PH Domain 1 Inversely Regulates Programmed Death-Ligand 1 Through Negative Feedback of Phosphorylated Epithelial Growth Factor Receptor and Activation of Nuclear Factor-Kappa B in Non-Small Cell Lung Cancer.
Cancer Manag Res
January 2025
Department of Thoracic Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Background: Signaling pathways centered on the G-protein ADP-ribosylation factor 6 (Arf6) and its downstream effector ArfGAP with the SH3 Domain, Ankyrin Repeat and PH Domain 1 (AMAP1) drive cancer invasion, metastasis, and therapy resistance. The Arf6-AMAP1 pathway has been reported to promote receptor recycling leading to programmed cell death-ligand 1 (PD-L1) overexpression in pancreatic ductal carcinoma. Moreover, AMAP1 regulates of nuclear factor-kappa B (NF-κB), which is an important molecule in inflammation and immune activation, including tumor immune interaction through PD-L1 regulation.
View Article and Find Full Text PDFPulmonary Arterial Hypertension in a Patient With a Lung Mass: Any Link?
Cureus
December 2024
Pulmonology, King Abdulaziz Medical City, Jeddah, SAU.
A 52-year-old female patient with a history of atrial septal defect repair presented with progressive dyspnea and echocardiographic findings suggestive of pulmonary hypertension (PH). Incidentally, a lung mass was discovered on computed tomography (CT). Initial evaluation revealed World Health Organization functional class III symptoms and significant weight loss.
View Article and Find Full Text PDFTransformation of lung adenocarcinoma to small cell lung cancer following osimertinib treatment: a case report and literature review.
Anticancer Drugs
January 2025
Department of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) effectively treat EGFR-mutant lung adenocarcinoma, demonstrating initial efficacy but eventually leading to acquired resistance. Small cell transformation is a rare resistance mechanism to EGFR-TKIs in lung adenocarcinoma, which can complicate clinical diagnosis and treatment. We present a patient with lung adenocarcinoma who underwent a prior pneumonectomy and adjuvant chemotherapy and was treated with osimertinib after the recurrence of lung cancer.
View Article and Find Full Text PDFA cohort-based multi-omics identifies nuclear translocation of eIF5B /PD-L1/CD44 complex as the target to overcome Osimertinib resistance of ARID1A-deficient lung adenocarcinoma.
Exp Hematol Oncol
January 2025
Department of Medical Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.
Background: Osimertinib has emerged as a critical element in the treatment landscape following recent clinical trials. Further investigation into the mechanisms driving resistance to Osimertinib is necessary to address the restricted treatment options and survival advantages that are compromised by resistance in patients with EGFR-mutated lung adenocarcinoma (LUAD).
Methods: Spatial transcriptomic and proteomic analyses were utilized to investigate the mechanisms of Osimertinib resistance.
A Prospective Phase II Trial of First-Line Osimertinib for Patients With EGFR Mutation-Positive NSCLC and Poor Performance Status (OPEN/TORG2040).
J Thorac Oncol
January 2025
Department of Respiratory Medicine and Medical Oncology, Yokohama Municipal Citizen's Hospital, Yokohama, Japan.
Introduction: Osimertinib is the first-line treatment for patients with NSCLC who have EGFR mutations and favorable performance status (PS). Despite the increasing clinical data on osimertinib, evidence for its use in patients with impaired PS remains limited. Therefore, a multicenter phase II trial (OPEN/TORG2040) was conducted to evaluate the efficacy and safety of first-line osimertinib treatment in patients with EGFR mutation-positive NSCLC and a poor PS.
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