A5032896791- Lung Cancer Treatments and Mutations
- Colorectal Cancer Treatments and Studies
- Lung Cancer Research Studies
- Cancer therapeutics and mechanisms
- Cancer Mechanisms and Therapy
- Gastric Cancer Management and Outcomes
- HER2/EGFR in Cancer Research
- PI3K/AKT/mTOR signaling in cancer
- Cytokine Signaling Pathways and Interactions
- Hepatocellular Carcinoma Treatment and Prognosis
- RNA modifications and cancer
- Epigenetics and DNA Methylation
- Chronic Lymphocytic Leukemia Research
- Cancer Genomics and Diagnostics
- Cancer, Hypoxia, and Metabolism
- Lung Cancer Diagnosis and Treatment
- Cancer-related gene regulation
- Lymphoma Diagnosis and Treatment
- Cancer Treatment and Pharmacology
- Glutathione Transferases and Polymorphisms
- Pancreatic and Hepatic Oncology Research
- Metastasis and carcinoma case studies
- Synthesis and biological activity
- Cancer Research and Treatments
- Cancer Immunotherapy and Biomarkers
Okayama University Hospital
2012-2024
Massachusetts General Hospital
2018-2024
Harvard University
2021-2024
Kawasaki Medical School
2014-2024
Global Cancer Institute
2022
Okayama University
2014-2017
Okayama Shoka University
2013-2016
We present a cohort of 41 patients with osimertinib resistance biopsies, including 2 an acquired CCDC6-RET fusion. Although RET fusions have been identified in resistant EGFR-mutant non-small cell lung cancer (NSCLC), their role to EGFR inhibitors is not well described. To assess the biological implications cancer, we expressed PC9 (EGFR del19) and MGH134 L858R/T790M) cells found that was sufficient confer tyrosine kinase (TKI). The selective BLU-667 cabozantinib resensitized...
Crizotinib is the standard of care for advanced non-small cell lung cancer (NSCLC) patients harboring anaplastic lymphoma kinase (ALK) fusion gene, but resistance invariably develops. Unlike crizotinib, alectinib a selective ALK tyrosine inhibitor (TKI) with more potent antitumor effects and favorable toxicity profile, even in crizotinib-resistant cases. However, acquired to alectinib, as other TKIs, remains limitation its efficacy. Therefore, we investigated mechanisms by which human NSCLC...
IntroductionOsimertinib is an irreversible EGFR tyrosine kinase inhibitor approved for the first-line treatment of patients with metastatic NSCLC harboring exon 19 deletions or L858R mutations. Patients treated osimertinib invariably develop acquired resistance by mechanisms involving additional mutations, MET amplification, and other pathways. There no known involvement oncogenic MUC1-C protein in resistance.MethodsH1975/EGFR (L858R/T790M) patient-derived cells were investigated dependence...
Introduction: Widespread use of generic drugs is considered to be indispensable if reductions in total health care costs are achieved, but the market share such remains low. In general, have same active ingredients as brand-name drugs, this not always case. Thus, toxicity profiles may vary when and compared. We retrospectively investigated incidence hyponatremia patients receiving cisplatin (CDDP) a counterpart thereof. Methods: reviewed medical records treated with CDDP (n=53) formulation...
Abstract Acquired drug resistance to even the most effective anti-cancer targeted therapies remains an unsolved clinical problem. Although many drivers of acquired have been identified 1‒6 , underlying molecular mechanisms shaping tumor evolution during treatment are incompletely understood. The extent which therapy actively drives by promoting mutagenic processes 7 or simply provides selective pressure necessary for outgrowth drug-resistant clones 8 open question. Here, we report that lung...
Malignant mesothelioma is an aggressive and therapy-resistant neoplasm arising from mesothelial cells. Evidence suggests that the major pathology associated with asbestos-induced local iron overload. In present study, we induced iron-induced in rats based on previous reports. Ten Wistar were given ferric saccharate nitrilotriacetate i.p. for 5 days a week. Five of ten exhibited widespread mesotheliomas peritoneum tunica vaginalis. The tumor cells showed positive immunostaining calretinin,...
The echinoderm microtubule associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) fusion gene was identified in patients with non-small cell lung cancer. To the best of our knowledge, there are only three lines harboring EML4-ALK gene, which have contributed to development therapeutic strategies. Therefore, we tried establish a new cancer line EML4-ALK. A 61-year-old Japanese female presented chest discomfort. She diagnosed left adenocarcinoma T4N3M1 Stage IV. Although she treated...
Abstract Background The efficacy of crizotinib treatment for recurring EML4‐ALK ‐positive non‐small cell lung cancer (NSCLC) previously treated with alectinib is unclear. Based on our preclinical findings regarding hepatocyte growth factor/mesenchymal epithelial transition (MET) pathway activation as a potential mechanism acquired resistance to alectinib, we conducted phase II trial the anaplastic lymphoma kinase/MET inhibitor, crizotinib, in patients alectinib‐refractory, NSCLC. Methods...
The Thoratec (Vectra) polyurethane vascular access graft (TPVA) is among the most recent additions to list of materials used construct prosthetic grafts for during hemodialysis. We give TPVA very high marks, and recognize utility such a use in However, strong elasticity this can lead unexpected complications after suturing. devised new surgical method using TPVA-ePTFE (expanded polytetrafluoroethylene) composite graft, substituting anastomosis section with portion ePTFE material, have been...
Abstract Background: Osimertinib is an irreversible EGFR tyrosine kinase inhibitor approved for the first-line treatment of patients with metastatic NSCLC harboring exon 19 deletions or L858R mutations. Patients treated osimertinib invariably develop acquired resistance by mechanisms involving additional mutations, MET amplification and other pathways. There no known involvement oncogenic MUC1-C protein in resistance. Methods: H1975/EGFR(L858R/T790M) patient-derived cells (EMT, amplified,...
Abstract Background: Programmed cell death protein-1 (PD-1) and programmed ligand-1 (PD-L1) play a major role in suppressing the immune system by forming PD-1/PD-L1 complex, which transmits an inhibitory signal to reduce T-cell activity. PD-L1 is often expressed various malignant tumors. On other hand, PD-1 generally observed activated lymphocytes myeloid-derived dendritic cells. Of cells, only Jurkat cells (under special conditions) angioimmunoblastic lymphoma tissue express on their...
Abstract Background. The combination of afatinib and cetuximab induced an unprecedented response in lung tumors harboring EGFR T790M clinical trials (Cancer Discov. 2014). However, up to 20% patients discontinued treatment due adverse events, including skin rashes diarrhea, the median progression-free survival therapy was 4.7 months. There is clearly still room for improvement therapy. Bevacizumab, a key drug cancer treatment, thought have wide variety effects, anti-vascularization,...
e19140 Background: Crizotinib, which is capable of blocking MET, ALK and ROS1, has been demonstrated the superior efficacy on first second line therapy for advanced/metastatic patients with NSCLC harboring EML4-ALK fusion gene compared chemotherapy. Alectinib, selective inhibitor also showed dramatic response rate, long duration acceptable toxic profile (Lancet Oncol 14, 2013: 590-98). Two randomized clinical trials comparing alectinib crizotinib in a first-line setting are ongoing....
<p>Supplementary Data and Methods</p>
Abstract Acquired drug resistance to even the most effective anti-cancer targeted therapies remains an unsolved clinical problem. Although many drivers of acquired have been identified, underlying molecular mechanisms shaping tumor evolution during treatment are incompletely understood. We recently demonstrated that lung cancer commonly used in clinic induce expression cytidine deaminase APOBEC3A (A3A), leading sustained mutagenesis tolerant cells persisting therapy. Preventing...