A5086229141- Lung Cancer Treatments and Mutations
- Lung Cancer Research Studies
- Lung Cancer Diagnosis and Treatment
- Colorectal Cancer Treatments and Studies
- Cancer Immunotherapy and Biomarkers
- Occupational and environmental lung diseases
- Cancer therapeutics and mechanisms
- Cancer Genomics and Diagnostics
- Neuroendocrine Tumor Research Advances
- Medical Imaging and Pathology Studies
- HER2/EGFR in Cancer Research
- Gastric Cancer Management and Outcomes
- Pleural and Pulmonary Diseases
- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Chronic Lymphocytic Leukemia Research
- Cancer-related gene regulation
- Cancer Research and Treatments
- Radiomics and Machine Learning in Medical Imaging
- Cholangiocarcinoma and Gallbladder Cancer Studies
- Peptidase Inhibition and Analysis
- RNA modifications and cancer
- Inflammatory mediators and NSAID effects
- Cancer Treatment and Pharmacology
- Estrogen and related hormone effects
- Neuroblastoma Research and Treatments
Aichi Cancer Center
2016-2025
Saitama International Medical Center
2021-2025
Shanghai Chest Hospital
2023
Peking University
2021-2022
Peking University Cancer Hospital
2021-2022
Fujian Medical University
2021
Union Hospital
2021
First Affiliated Hospital Zhejiang University
2020
Nanfang Hospital
2020
National Cancer Center Hospital East
2007-2017
Purpose To evaluate the relationship between mutations of epidermal growth factor receptor (EGFR) gene and effectiveness gefitinib treatment in patients with recurrent lung cancer after pulmonary resection. Patients Methods We sequenced exons 18-21 EGFR using total RNA extracted from 59 who were treated for cancer. Gefitinib was evaluated by both imaging studies change serum carcinoembryonic antigen (CEA) levels. Results found 33 (56%). Of these mutations, 17 deletions around codons 746-750...
Among patients with non–small-cell lung cancer (NSCLC), MET exon 14 skipping mutations occur in 3 to 4% and amplifications 1 6%. Capmatinib, a selective inhibitor of the receptor, has shown activity models various types activation.
Abstract Purpose: Non–small cell lung cancers carrying activating mutations in the gene for epidermal growth factor receptor (EGFR) are highly sensitive to EGFR-specific tyrosine kinase inhibitors. However, most patients who initially respond subsequently experience disease progression while still on treatment. Part of this “acquired resistance” is attributable a secondary mutation resulting threonine methionine at codon 790 (T790M) EGFR. Experimental Design: We sequenced exons 18 21 EGFR...
Phase I data (ASCEND-1) showed ceritinib efficacy in patients with ALK-rearranged non-small-cell lung cancer (NSCLC), regardless of brain metastases status and or without prior therapy an inhibitor the ALK protein. Data are presented from a phase II trial (ASCEND-2) which safety were evaluated who had NSCLC previously treated at least one platinum-based chemotherapy experienced progression during crizotinib treatment as their last therapy.Patients advanced NSCLC, including those asymptomatic...
New molecular targeted agents are needed for patients with non-small-cell lung cancer (NSCLC) who progress while receiving erlotinib, gefitinib, or both. Afatinib, an oral irreversible ErbB family blocker, has preclinical activity in epidermal growth factor receptor (EGFR [ErbB1]) mutant models EGFR-activating mutations, including T790M.This was a Japanese single-arm phase II trial conducted stage IIIB to IV pulmonary adenocarcinoma progressed after ≥ 12 weeks of prior erlotinib and/or...
This phase III trial of concurrent thoracic radiotherapy (TRT) was conducted to compare third-generation chemotherapy with second-generation in patients unresectable stage non-small-cell lung cancer (NSCLC).Eligible received the following treatments: A (control), four cycles mitomycin (8 mg/m(2) on day 1)/vindesine (3 days 1, 8)/cisplatin (80 1) plus TRT 60 Gy (treatment break for 1 week); B, weekly irinotecan (20 mg/m(2))/carboplatin (area under plasma concentration-time curve [AUC] 2) 6...
Anaplastic lymphoma kinase (ALK) rearrangement-positive non-small-cell lung cancers can be effectively treated with an ALK tyrosine inhibitor (TKI) such as crizotinib, but the response magnitude and duration are heterogeneous. Several variants have been identified, few studies focused on effects of different efficacy crizotinib.Among 55 patients crizotinib initial ALK-TKI between January 2007 December 2014, we identified 35 tumor specimens that could evaluated for by reverse transcription...
Malignant mesothelioma (MM) is an aggressive neoplasm associated with asbestos exposure. We carried out genome-wide array-based comparative genomic hybridization analysis 14 MM cell lines. Three lines showed overlapping homozygous deletion at chromosome 13q12, which harbored the LATS2 (large tumor suppressor homolog 2) gene. With 6 other and 25 tumors, we found 10 inactivating deletions or mutations of among 45 MMs. encodes a serine/threonine kinase, component Hippo tumor-suppressive...
•Nivolumab with carboplatin, paclitaxel, and bevacizumab was evaluated as first-line therapy for nonsquamous NSCLC.•The nivolumab combination provided superior PFS across all patients any PD-L1 expression levels.•The median of 12.1 months is the longest among phase III studies NSCLC without driver mutations.•No new safety signals were observed. BackgroundThis international, randomized, double-blind study (ONO-4538-52/TASUKI-52) cytotoxic chemotherapy treatment non-small-cell lung cancer...
The prognosis of patients with bone metastasis from lung cancer has not been well documented. We assessed the survival rates after and prognostic factors in 118 metastases cancer. cumulative were 59.9% at 6 months, 31.6% 1 year, 11.3% 2 years. mean was 9.7 months (median, 7.2 months; range, 0.1-74.5 months). A favorable more likely women adenocarcinoma, solitary metastasis, no to appendicular bone, pathologic fractures, performance status or less, use systemic chemotherapy, an epithelial...
Malignant mesothelioma (MM) is an incurable malignancy that caused by exposure to asbestos and accompanied severe fibrosis. Because MM usually diagnosed at advanced stage clinical identification of early lesions difficult, its molecular pathogenesis has not been completely elucidated. Nearly 75% cases have inactivating mutations in the NF2 (neurofibromatosis type 2; Merlin) gene or downstream signaling molecules Hippo cascade, which negatively regulates transcription factor Yes-associated...