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Research
| Technology Name (St. Jude Reference #) |
Caspase 8 Acts as a Tumor Suppressor (SJ-98-0024) |
| Description | This technology is useful in the diagnosis and prognosis of neuroblastoma and other cancers by determining the methylation state of the CASP 8 promoter region. Caspase 8 is a tumor suppressor that is frequently deleted or inactivated in neuroblastoma. It is inactivated by MYC and has been found to be inactive in 90 percent of the neuroblastomas analyzed in which MYCN is amplified. Furthermore, such neuroblastomas have a very poor prognosis. |
| Keywords | Tumor suppressor, cancer, neuroblastoma, diagnostic, gene therapy, methylation, apoptosis |
| Granted Patents or Published Applications | US Patent No. 7,052,834 |
| Related Scientific References | Teitz, Tal, et al., "Caspase 8 is deleted or silenced preferentially in childhood neuroblastomas with amplification of MYCN" Nature Medicine 6: 529-535 (2000);
Juin, et al., "Caspase 8: The killer you can't live without" News and Views article Nature Medicine 6: 498-500 (2000); Engels IH, et al., "Caspase-8/FLICE functions as an executioner caspase in anticancer drug-induced apoptosis" Oncogene 19:4563-4573 (2000); Belka C, et al., "Differential role of caspase-8 and BID activation during radiation- and CD95-induced apoptosis" Oncogene 19:1181-1190 (2000); Hopkins-Donaldson S, et al., "Loss of caspase-8 expression in highly malignant human neuroblastoma cells correlates with resistance to tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis" Cancer Res. 60:4315-4319 (2000); Takita J, et al., "Allelic imbalance on chromosome 2q and alterations of the caspase 8 gene in neuroblastoma" Oncogene 20:4424-4432 (2001); Han Z, et al., "A Fas-associated Death Domain Protein-dependent Mechanism Mediates the Apoptotic Action of Non-steroidal Anti-inflammatory Drugs in the Human Leukemic Jurkat Cell Line" J. Biol. Chem. 276:38748-38754 (2001); Igney FH, and Krammer PH, "Death and anti-death: tumour resistance to apoptosis" Nature Reviews Cancer 2:1-12 (2002) |
| Licensing Opportunities | We are seeking licensees in all fields for the development of this technology. |
Contact the Office of Technology Licensing (Phone: 901-595-2342, Fax: 901-595-3148) for more information.
Last update: June 2006
