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Vincent A. Miller

Researcher at Foundation Medicine

Publications -  654
Citations -  76041

Vincent A. Miller is an academic researcher from Foundation Medicine. The author has contributed to research in topics: Lung cancer & Cancer. The author has an hindex of 105, co-authored 647 publications receiving 65822 citations. Previous affiliations of Vincent A. Miller include Vanderbilt University & Memorial Sloan Kettering Cancer Center.

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International Association for the Study of Lung Cancer/American Thoracic Society/European Respiratory Society International Multidisciplinary Classification of Lung Adenocarcinoma

TL;DR: This new adenocarcinoma classification is needed to provide uniform terminology and diagnostic criteria, especially for bronchioloalveolar carcinoma (BAC), the overall approach to small nonresection cancer specimens, and for multidisciplinary strategic management of tissue for molecular and immunohistochemical studies.
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Acquired Resistance of Lung Adenocarcinomas to Gefitinib or Erlotinib Is Associated with a Second Mutation in the EGFR Kinase Domain

TL;DR: Biochemical analyses of transfected cells and growth inhibition studies with lung cancer cell lines demonstrate that the T790M mutation confers resistance to EGFR mutants usually sensitive to either gefitinib or erlotinib, which should help guide the search for more effective therapy against a specific subset of lung cancers.
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Analysis of 100,000 human cancer genomes reveals the landscape of tumor mutational burden

TL;DR: Measurements of TMB from comprehensive genomic profiling are strongly reflective of measurements from whole exome sequencing and model that below 0.5 Mb the variance in measurement increases significantly, demonstrating that many disease types have a substantial portion of patients with high TMB who might benefit from immunotherapy.
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Analysis of Tumor Specimens at the Time of Acquired Resistance to EGFR-TKI Therapy in 155 Patients with EGFR-Mutant Lung Cancers

TL;DR: This is the largest series reporting mechanisms of acquired resistance to EGFR-TKI therapy and identifies EGFR T790M as the most common mechanism of acquired Resistance, whereas MET amplification, HER2 amplification, and small cell histologic transformation occur less frequently.