Feb-2010 Hedgehog Pathway Articles
Posted: Sat Feb 27, 2010 11:53 amHuman Invasive Prostate Cancer Cells
origin of basal cell carcinoma
Increased expression of the hedgehog signaling pathway in pediatric solid malignancies
human Indian Hedgehog pathway in human chondrosarcoma cells
Multiple Myeloma: A Paradigm for Translation of the Cancer Stem Cell Hypothesis.
Novel Therapeutic Agents Against Cancer Stem Cells of Chronic Myeloid Leukemia
- Altogether, these observations suggest that EGFR and sonic hedgehog cascades may represent the potential therapeutic targets of great clinical interest to eradicate the total prostate cancer cell mass and improve the current docetaxel-based therapies against locally advanced and invasive prostate cancers, and thereby prevent metastases and disease relapse.
http://www.ncbi.nlm.nih.gov/pubmed/20179163
origin of basal cell carcinoma
- http://www.ncbi.nlm.nih.gov/pubmed/20154679
Increased expression of the hedgehog signaling pathway in pediatric solid malignancies
- RESULTS: In neuroblastoma, 96%, 100%, and 68%; in rhabdomyosarcoma, 78%, 100%, and 78%; in Wilms' tumor, 71%, 100%, and 43%; and in hepatoblastoma, 100%, 100%, and 73% of the specimens stained positive for Shh, Ptch, and Gli1, respectively. Differentiated neuroblastoma cells showed more intense Gli1 expression than in immature neuroblastoma cells. In rhabdomyosarcoma, the expression of Gli1 was higher in alveolar type than in embryonal type. CONCLUSIONS: These findings suggest that the Shh-Ptch1-Gli1 signaling pathways are frequently activated in most pediatric malignant tumors. The Hh signaling pathway may therefore play an important role in the differentiation and malignant potential of pediatric malignancies.
http://www.ncbi.nlm.nih.gov/pubmed/20152358
human Indian Hedgehog pathway in human chondrosarcoma cells
- EGCG inhibited the human Indian Hedgehog pathway, down-regulated PTCH and Gli-1 levels, and induced apoptosis as confirmed by DAPI staining followed by flow cytometry. Protein expression levels of caspase-3 were unchanged in response to EGCG treatment in chondrosarcoma cells; however, the expression levels of Bcl-2 were significantly decreased and the levels of Bax were significantly increased. CONCLUSIONS: Our findings demonstrate that EGCG is effective for growth inhibition of a chondrosarcoma cell lines in vitro, and suggest that EGCG may be a new therapeutic option for patients with chondrosarcoma.
http://www.ncbi.nlm.nih.gov/pubmed/20127255
Multiple Myeloma: A Paradigm for Translation of the Cancer Stem Cell Hypothesis.
- However, it is common that the signaling pathway components regulating normal stem cell self-renewal are aberrantly activated in human cancers and may serve as potential therapeutic targets. One class of shared regulatory pathways are those active during normal embryonic patterning and organ formation such as Hedgehog (Hh), Notch and Wingless (Wnt), and emerging data suggest that these may play a role in CSCs. Here we review the identification and characterization of MM CSCs, the role of Hh in MM, and issues to be considered during the early clinical testing of CSC targeting agents.
http://www.ncbi.nlm.nih.gov/pubmed/20184542
Novel Therapeutic Agents Against Cancer Stem Cells of Chronic Myeloid Leukemia
- Chronic myeloid leukemia (CML) is induced by the BCR-ABL oncogene, a product of Philadelphia (Ph) chromosome. The BCR-ABL kinase inhibitor imatinib is a standard treatment for Ph(+) leukemia, and has been shown to induce a complete hematologic and cytogenetic response in most chronic phrase CML patients. However, imatinib does not cure CML, and one of the reasons is that imatinib does not kill leukemia stem cells (LSCs) in CML both in vitro and in vivo. Recently, several new targets or drugs have been reported to inhibit LSCs in cultured human CD34(+) CML cells or in mouse model of BCR-ABL induced CML, including an Alox5 pathway inhibitor, Hsp90 inhibitors, omacetaxine, hedgehog inhibitor and BMS-214662. Specific targeting of LSCs but not normal stem cell is a correct strategy for developing new anti-cancer therapies in the future.
http://www.ncbi.nlm.nih.gov/pubmed/20184539