These are the fundamental articles surrounding the Hh pathway and maintance and repair.

Tissue repair and stem cell renewal in carcinogenesis

Philip A. Beachy1,4, Sunil S. Karhadkar1,2 and David M. Berman2,3,4

Abstract

Cancer is increasingly being viewed as a stem cell disease, both in its propagation by a minority of cells with stem-cell-like properties and in its possible derivation from normal tissue stem cells. But stem cell activity is tightly controlled, raising the question of how normal regulation might be subverted in carcinogenesis. The long-known association between cancer and chronic tissue injury, and the more recently appreciated roles of Hedgehog and Wnt signalling pathways in tissue regeneration, stem cell renewal and cancer growth together suggest that carcinogenesis proceeds by misappropriating homeostatic mechanisms that govern tissue repair and stem cell self-renewal.
http://www.nature.com/nature/journal/v432/n7015/abs/nature03100.html

HEDGEHOG SIGNALLING IN CANCER FORMATION AND MAINTENANCE

Marina Pasca di Magliano & Matthias Hebrok

The Hedgehog signalling pathway is essential for numerous processes during embryonic development. Members of this family of secreted proteins control cell proliferation, differentiation and tissue patterning in a dose-dependent manner. Although the overall activity of the pathway is diminished after embryogenesis, recent reports show that the pathway remains active in some adult tissues, including adult stem cells in the brain and skin. There is also evidence that uncontrolled activation of the pathway results in specific types of cancer.
Summary

Hedgehog (HH) signalling is required for cell differentiation and organ formation during embryogenesis. In the adult, HH signalling remains active in some organs where it has been implicated in the regulation of stem-cell maintenance and proliferation.

HH signalling targets include genes that are important for cell proliferation — proto-oncogenes — as well as growth factors.

Misregulation of HH signalling has been shown to cause formation of basal-cell carcinoma and medulloblastoma, and mutations of HH pathway components have been found both in familial and sporadic cases. More recently, small-cell lung cancer (SCLC) and pancreatic adenocarcinoma have been linked to HH signalling, providing a molecular mechanism for these aggressive diseases.

Importantly, HH signalling seems to be required not only for cancer initiation but also for tumour growth and survival of medulloblastomas, SCLC and pancreatic adenocarcinoma.

HH inhibitors could provide novel therapeutic approaches for treatment of otherwise hard to cure cancer types. Synthetic compounds have been identified that act as HH inhibitors in a very specific manner.


http://www.nature.com/nrc/journal/v3/n12/abs/nrc1229_fs.html;jsessionid=966BF79E2EE8DAF6705E930098A1BA4D