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Nissi Varki

Researcher at University of California, San Diego

Publications -  193
Citations -  18035

Nissi Varki is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Sialic acid & Antibody. The author has an hindex of 75, co-authored 188 publications receiving 16502 citations. Previous affiliations of Nissi Varki include University of California, Berkeley & University of Chicago.

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Journal ArticleDOI

Evidence for a human-specific mechanism for diet and antibody-mediated inflammation in carcinoma progression

TL;DR: It is shown here that human tumors accumulate Neu5Gc that is covalently attached to multiple classes of glycans, and that the human propensity to develop diet-related carcinomas is contributed to by local chronic inflammation, resulting from interaction of metabolically-accumulated dietary Neu 5Gc with circulating anti-Neu5gc antibodies.
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alpha 2-6-Linked sialic acids on N-glycans modulate carcinoma differentiation in vivo.

TL;DR: First in vivo evidence for a role of ST6Gal-I in tumor progression was confirmed using a novel approach, which conditionally restored St6gal1 in cell lines derived from the null tumors.
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Human-specific Regulation of α2–6-linked Sialic Acids

TL;DR: Since the last common ancestor with apes, humans underwent a concerted bidirectional switch in α2–6-linked Sia expression between airway epithelial cell surfaces and secreted mucins, showing that Sia linkage expression patterns can be conserved during millions of years of evolution within some vertebrate taxa while undergoing sudden major changes in other closely related ones.
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Loss of N-Glycolylneuraminic Acid in Human Evolution IMPLICATIONS FOR SIALIC ACID RECOGNITION BY SIGLECS

TL;DR: The human loss of Neu5Gc may alter biological processes involving siglec-1, and possibly, sigleC-4a or -5, the myelin-associated glycoprotein, which may have some preference for Neu 5Gc.
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L-selectin facilitation of metastasis involves temporal induction of Fut7-dependent ligands at sites of tumor cell arrest.

TL;DR: Hematogenous carcinoma metastasis is supported by aggregated platelets and leukocytes, forming tumor cell emboli, and L-selectin facilitation of metastasis progression involves leukocyte-endothelial interactions at sites of intravascular arrest supported by local induction of L- selectin ligands via fucosyltransferase-7.