z-logo
open-access-imgOpen Access
Epidermal activation of Hedgehog signaling establishes an immunosuppressive microenvironment in basal cell carcinoma by modulating skin immunity
Author(s) -
GrundGröschke Sandra,
Ortner Daniela,
SzenesNagy Antal B.,
Zaborsky Nadja,
Weiss Richard,
Neureiter Daniel,
Wipplinger Martin,
Risch Angela,
Hammerl Peter,
Greil Richard,
Sibilia Maria,
Gratz Iris K.,
Stoitzner Patrizia,
Aberger Fritz
Publication year - 2020
Publication title -
molecular oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.332
H-Index - 88
eISSN - 1878-0261
pISSN - 1574-7891
DOI - 10.1002/1878-0261.12758
Subject(s) - smoothened , basal cell carcinoma , biology , cancer research , skin cancer , hedgehog , hedgehog signaling pathway , immune system , immunotherapy , innate immune system , acquired immune system , immunology , microbiology and biotechnology , signal transduction , cancer , medicine , pathology , genetics , basal cell
Activation of hedgehog/glioma‐associated oncogene homolog (HH/GLI) signaling induces basal cell carcinoma (BCC) and establishes an immunosuppressive tumor microenvironment. HH/GLI signaling inhibits the activity of antitumoral T cells via programmed death ligand 1/programmed death‐1 immune checkpoint signaling and the recruitment of immunosuppressive regulatory T cells. BCCs also show strong infiltration with antitumoral neutrophils. The data support the evaluation of combination treatments with HH inhibitors and immune checkpoint blockers.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here
Accelerating Research

Address

John Eccles House
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom