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Joao Victor Machado Alessi

Researcher at Harvard University

Publications -  67
Citations -  574

Joao Victor Machado Alessi is an academic researcher from Harvard University. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 5, co-authored 22 publications receiving 134 citations. Previous affiliations of Joao Victor Machado Alessi include Adma & University of São Paulo.

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Acquired resistance to pd-(l)1 blockade in patients with non-small cell lung cancer

TL;DR: In this article , the authors compared pre and post PD-(L)1 blockade, chemotherapy (control cohort #1) and targeted therapy (EGFR inhibitors, control cohort #2) tumor biopsies.
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Letter to the Editor: Reply to Zhao, Wu, and Ma.

TL;DR: Zhao et al. as discussed by the authors identified that better patient performance status, low derived neutrophil-to-lymphocyte ratio in the blood, increasing programmed death-ligand 1 expression, and STK11/KEAP1/SMARCA4 wild-type status are associated with improved clinical outcomes to first-line chemoimmunotherapy (CIT) in NSCLC.
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Abstract 4117: Clinicopathologic and molecular characterization of KRASG12D lung cancers

TL;DR: Patients with advanced KRASmut NSCLC and adequate baseline tissue for multiplex-immunofluorescence harbored KRASG12D, which had lower PD-L1 tumor proportion score (TPS) and lower tumor mutation burden (TMB) compared to patients with KRASnon-G 12D,high-sm, and there was no difference in clinical outcomes to chemo-IMmunotherapy.
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512 Time-of-day of pembrolizumab infusion and clinical outcomes of patients with NSCLC: too soon to promote morning infusions

TL;DR: In this paper , the authors evaluated the association between time-of-day patterns of pembrolizumab infusion and outcomes in a cohort of patients with treatment-naïve metastatic lung cancer with PD-L1 expression.
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Abstract 2143: Clinicopathologic, genomic and immunophenotypic landscape of ATM mutations in non-small cell lung cancer

TL;DR: Deleterious ATM mutations defined a subset of NSCLC with unique clinicopathologic, genomic, and immunophenotypic features and had similar outcomes to PD-(L)1 inhibition +/- chemotherapy, compared to ATMWT cases, and similar immune cell subsets infiltration.