ATX restricts anti-tumor eosinophil responses

Sharon Grisaru-Tal; Ariel Munitz

doi:10.1038/s43018-023-00718-5

ATX restricts anti-tumor eosinophil responses

Sharon Grisaru-Tal, Ariel Munitz^*

^*Corresponding author for this work

Clinical Microbiology and Immunology

Research output: Contribution to journal › Comment/debate

1 Scopus citations

Abstract

Autotaxin (ATX) produces lysophosphatidic acid (LPA), which directly promotes pancreatic ductal adenocarcinoma (PDAC) growth, but the role of the tumor microenvironment (TME) in ATX-driven tumor growth is unclear. ATX–LPA signaling in PDAC is now shown to shape the TME by inhibiting eosinophil recruitment, resulting in increased tumor growth.

Original language	English
Pages (from-to)	221-223
Number of pages	3
Journal	Nature Cancer
Volume	5
Issue number	2
DOIs	https://doi.org/10.1038/s43018-023-00718-5
State	Published - Feb 2024

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10.1038/s43018-023-00718-5

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title = "ATX restricts anti-tumor eosinophil responses",

abstract = "Autotaxin (ATX) produces lysophosphatidic acid (LPA), which directly promotes pancreatic ductal adenocarcinoma (PDAC) growth, but the role of the tumor microenvironment (TME) in ATX-driven tumor growth is unclear. ATX–LPA signaling in PDAC is now shown to shape the TME by inhibiting eosinophil recruitment, resulting in increased tumor growth.",

author = "Sharon Grisaru-Tal and Ariel Munitz",

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AB - Autotaxin (ATX) produces lysophosphatidic acid (LPA), which directly promotes pancreatic ductal adenocarcinoma (PDAC) growth, but the role of the tumor microenvironment (TME) in ATX-driven tumor growth is unclear. ATX–LPA signaling in PDAC is now shown to shape the TME by inhibiting eosinophil recruitment, resulting in increased tumor growth.

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ATX restricts anti-tumor eosinophil responses

Abstract

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