Biology:Tumor reversion
Tumor reversion history started in the early 1960s with the flat revertant cells when researchers used the NIH3T3 cells to assay the transforming potential of oncoviruses and oncogenes. Robert Pollack, later in 1968, made the observation that some of the cells infected with SV40 or polyoma viruses no longer showed the typical oncogenic phenotype, but instead, acquired a flat morphology (Pollack et al., 1968). These cells had also lost their oncogenic potential, and were therefore named "flat revertants".
New approaches, using different biological systems, led to the identification of more than 300 genes,[1][2][3] implicated in the tumor reversion process (Telerman et al., 2009). Targeting genes of tumor reversion to suppress the malignant phenotype led to the identification of a series of drugs able to inhibit intra-cellular levels of TCTP, a key gene in tumor reversion.[citation needed]
References
- ↑ "Biological models and genes of tumor reversion: cellular reprogramming through tpt1/TCTP and SIAH-1". Proc Natl Acad Sci U S A 99 (23): 14976–81. Oct 2002. doi:10.1073/pnas.222470799. PMID 12399545.
- ↑ "Translationally controlled tumor protein is a target of tumor reversion". Proc Natl Acad Sci U S A 101 (43): 15364–9. Oct 2004. doi:10.1073/pnas.0406776101. PMID 15489264.
- ↑ "TCTP protects from apoptotic cell death by antagonizing bax function". Cell Death Differ. 15: 1211–20. Aug 2008. doi:10.1038/cdd.2008.18. PMID 18274553.
- Pollack RE, Green H, Todaro GJ (1968). "Growth control in cultured cells: selection of sublines with increased sensitivity to contact inhibition and decreased tumor-producing ability". Proc Natl Acad Sci U S A 60: 126–133. doi:10.1073/pnas.60.1.126.
- Telerman A, Amson R (2009). "The molecular programme of tumour reversion: the steps beyond malignant transformation". Nat Rev Cancer 9: 206–216. doi:10.1038/nrc2589.
- http://www.tumor-reversion.org/
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