Abstract
Sonic Hedgehog in SCLC.
Highlights
The Hedgehog (Hh) signal transduction pathway has been discovered as a central regulator of embryonic development, tissue maintenance and repair [1]
The ligand-dependent activation of Hh signaling can occur in an autocrine manner, where cancer cells express both the ligand and the receptor, or in a paracrine manner, where ligand produced from cancer cells is activating Hh signaling in tumor stroma or vice versa
To characterize Hh function in Small cell lung carcinoma (SCLC) and to evaluate the therapeutic potential of Hh inhibitors in this cancer, we have investigated the possibility of a direct interaction between Hh and BN/G protein coupled receptor (GRPR) signaling pathways
Summary
The Hedgehog (Hh) signal transduction pathway has been discovered as a central regulator of embryonic development, tissue maintenance and repair [1]. Clinical trials using molecular inhibitors targeting Hh pathway components, in particular the Smo receptor, have often yielded limited clinical benefits unless they are used for the treatment of tumors harboring defined genetic mutations inactivating tumor suppressors (e.g. Ptch receptor) or activating oncogenes (e.g. Smo receptor, Gli transcription factor, Shh ligand) within the Hh pathway.
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