Journal
CANCER INVESTIGATION
Volume 29, Issue 10, Pages 683-691Publisher
TAYLOR & FRANCIS INC
DOI: 10.3109/07357907.2011.626475
Keywords
Tumor suppressor gene; SCLC; FHIT; p53
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Funding
- National Cancer Institute, National Institutes of Health [SPORE P50CA70907, R01CA116322]
- A. P. Moeller Foundation for the Advancement of Medical Science
- Novo Nordisk Foundation
- Danish Cancer Society
- Danish Medical Research Council
- Aase and Ejnar Danielsen Foundation
- Kathrine and Vigo Skovgaards foundation
- VFK Krebsforschung gGmbH in Germany
- Fulbright Commission
- Dagmar Marshall foundation
- Lundbeck foundation
- University of Copenhagen
- NATIONAL CANCER INSTITUTE [P50CA070907, R01CA116322] Funding Source: NIH RePORTER
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The candidate tumor suppressor fragile histidine traid (FHIT) is frequently inactivated in small cell lung cancer (SCLC). Mutations in the p53 gene also occur in the majority of SCLC leading to the accumulation of the mutant protein. Here we evaluated the effect of FHIT gene therapy alone or in combination with the mutant p53-reactivating molecule, PRIMA-1(Met)/APR-246, in SCLC. Overexpression of FHIT by recombinant adenoviral vector (Ad-FHIT)-mediated gene transfer in SCLC cells inhibited their growth by inducing apoptosis and when combined with PRIMA-1(Met)/APR-246, a synergistic cell growth inhibition was achieved.
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