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Cansu Cimen Bozkus

Researcher at Icahn School of Medicine at Mount Sinai

Publications -  24
Citations -  1718

Cansu Cimen Bozkus is an academic researcher from Icahn School of Medicine at Mount Sinai. The author has contributed to research in topics: Cancer & Biology. The author has an hindex of 6, co-authored 16 publications receiving 1110 citations. Previous affiliations of Cansu Cimen Bozkus include Purdue University.

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Journal ArticleDOI

Immunology of COVID-19: Current State of the Science.

Nicolas Vabret, +87 more
- 16 Jun 2020 - 
TL;DR: The current state of knowledge of innate and adaptive immune responses elicited by SARS-CoV-2 infection and the immunological pathways that likely contribute to disease severity and death are summarized.
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Shared Immunogenic Poly-Epitope Frameshift Mutations in Microsatellite Unstable Tumors.

TL;DR: This study uncovers the widespread occurrence and strong immunogenicity of tumor-specific antigens derived from shared frameshift mutations in MSI-H cancer and Lynch syndrome patients, suitable for the design of common "off-the-shelf" cancer vaccines.
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Expression of Cationic Amino Acid Transporter 2 Is Required for Myeloid-Derived Suppressor Cell-Mediated Control of T Cell Immunity.

TL;DR: It is demonstrated that cationic amino acid transporter 2 (Cat2), coordinately with Arg1 and Nos2, contributes to the transport of l-Arg in MDSCs and is an important regulator of MDSC suppressive function.
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Profiling SARS-CoV-2 HLA-I peptidome reveals T cell epitopes from out-of-frame ORFs.

TL;DR: This article reported the first HLA-I immunopeptidome of SARS-CoV-2 in two cell lines at different times post infection using mass spectrometry and found HLAI peptides derived not only from canonical open reading frames (ORFs) but also from internal out-of-frame ORFs in spike and nucleocapsid not captured by current vaccines.
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Immune Checkpoint Blockade Enhances Shared Neoantigen-Induced T Cell Immunity Directed against Mutated Calreticulin in Myeloproliferative Neoplasms

TL;DR: It is demonstrated that while a subset of CALR+ MPN patients develops specific T cell responses against mut-CALR C-terminus, programmed cell death protein 1 (PD-1) or cytotoxic T lymphocyte antigen 4 (CTLA-4) expression abrogates the full complement of responses.