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Nisha Nagarsheth

Researcher at University of Michigan

Publications -  23
Citations -  4343

Nisha Nagarsheth is an academic researcher from University of Michigan. The author has contributed to research in topics: Cancer & T cell. The author has an hindex of 11, co-authored 18 publications receiving 2776 citations. Previous affiliations of Nisha Nagarsheth include National Institutes of Health & Scripps Research Institute.

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Chemokines in the cancer microenvironment and their relevance in cancer immunotherapy

TL;DR: This Review focuses on the main chemokines that are found in the human tumour microenvironment, and elaborate on their patterns of expression, their regulation and their roles in immune cell recruitment and in cancer and stromal cell biology.
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Fusobacterium nucleatum Promotes Chemoresistance to Colorectal Cancer by Modulating Autophagy.

TL;DR: It is found that Fusobacterium (F.) nucleatum was abundant in colorectal cancer tissues in patients with recurrence post chemotherapy, and was associated with patient clinicopathological characterisitcs, and bioinformatic and functional studies demonstrated that F. nucleatum promoted coloreCTal cancer resistance to chemotherapy.
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Epigenetic silencing of TH1-type chemokines shapes tumour immunity and immunotherapy.

TL;DR: Using human ovarian cancers as their model, this paper showed that enhancer of zeste homologue 2 (EZH2)-mediated histone H3 lysine 27 trimethylation (H3K27me3) and DNA methyltransferase 1 (DNMT1)-mediated DNA methylation repress the tumour production of T helper 1 (TH1)-type chemokines CXCL9 and CXCl10, and subsequently determine effector T-cell trafficking to the tumours microenvironment.
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PRC2 epigenetically silences Th1-type chemokines to suppress effector T cell trafficking in colon cancer

TL;DR: Findings reveal that PRC2-mediated epigenetic silencing is not only a crucial oncogenic mechanism, but also a key circuit controlling tumor immunosuppression, and targeting epigenetic programs may have significant implications for improving the efficacy of current cancer immunotherapies relying on effective T-cell-mediated immunity at the tumor site.