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Biotech / Medical : CRIS, Curis (formerly CBMI) -- Ignore unavailable to you. Want to Upgrade?


To: tuck who wrote (446)3/13/2003 2:28:12 PM
From: tuck  Read Replies (1) | Respond to of 668
 
>>CAMBRIDGE, Mass.--(BUSINESS WIRE)--March 13, 2003--CURIS, Inc. (NASDAQ:CRIS - News) - The current issue of Nature reports that a significant subset of small-cell lung cancers requires activation of a biological pathway called Hedgehog to maintain their malignant growth.
According to this study conducted by scientists at the Johns Hopkins University School of Medicine, cyclopamine, a specific inhibitor of the Hedgehog pathway, can block growth of these small-cell lung tumors in a model of the disease.

Cyclopamine is a compound that was originally isolated from an extract of a plant found in the western United States. A patent application, describing the use of cyclopamine to selectively block the Hedgehog pathway for therapeutic purposes, was filed by the Johns Hopkins University School of Medicine and subsequently licensed to CURIS. CURIS has a long-standing interest in developing drugs that either promote or inhibit signaling activity in the Hedgehog pathway.

Inappropriate Hedgehog signaling has also been demonstrated in several other types of cancers, including basal cell carcinoma, medulloblastoma, and other cancers. CURIS believes that inhibition of Hedgehog signaling constitutes a significant new approach to the treatment of certain cancers.

"In addition to pursuing the cyclopamine lead, CURIS also has several other drug candidates that can block the Hedgehog pathway. These are conventional drug-like small molecules that are very specific and available for oral administration," stated Dr. Lee Rubin, CURIS' Chief Scientific Officer. "Our goal is to develop the best possible drug candidate for Hedgehog-dependent cancers."

"Cyclopamine is one of several promising drug candidates presently under development at Curis," said Daniel Passeri, CURIS' President and Chief Executive Officer. "We are encouraged by this promising data which adds to our growing portfolio of cancer drug development opportunities." <<

snip

All I could find was this letter in last week's issue:

>>Nature AOP, published online 5 March 2003; doi:10.1038/nature01493

Hedgehog signalling within airway epithelial progenitors and in small-cell lung cancer

D. NEIL WATKINS*, DAVID M. BERMAN†‡, SCOTT G. BURKHOLDER*, BAOLIN WANG‡, PHILIP A. BEACHY‡ & STEPHEN B. BAYLIN*

* Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA
† Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA
‡ Department of Molecular Biology and Genetics, and Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA

Correspondence and requests for materials should be addressed to D.N.W. (e-mail: nwatkins@jhmi.edu).

Embryonic signalling pathways regulate progenitor cell fates in mammalian epithelial development and cancer. Prompted by the requirement for sonic hedgehog (Shh) signalling in lung development, we investigated a role for this pathway in regeneration and carcinogenesis of airway epithelium. Here we demonstrate extensive activation of the hedgehog (Hh) pathway within the airway epithelium during repair of acute airway injury. This mode of Hh signalling is characterized by the elaboration and reception of the Shh signal within the epithelial compartment, and immediately precedes neuroendocrine differentiation. We reveal a similar pattern of Hh signalling in airway development during normal differentiation of pulmonary neuroendocrine precursor cells, and in a subset of small-cell lung cancer (SCLC), a highly aggressive and frequently lethal human tumour with primitive neuroendocrine features. These tumours maintain their malignant phenotype in vitro and in vivo through ligand-dependent Hh pathway activation. We propose that some types of SCLC might recapitulate a critical, Hh-regulated event in airway epithelial differentiation. This requirement for Hh pathway activation identifies a common lethal malignancy that may respond to pharmacological blockade of the Hh signalling pathway.<<

It turned up from a search on cyclopamine, so it's at least related.

Cheers, Tuck