Abstract 5393: Regression of a human T-cell leukemia lacking the methylthioadenosine phosphorylase (MTAP) gene without toxicity of 6-thioguanine (6TG) by pretreatment with methylthioadenosine (MTA)

@article{Bertino2010Abstract5R,
  title={Abstract 5393: Regression of a human T-cell leukemia lacking the methylthioadenosine phosphorylase (MTAP) gene without toxicity of 6-thioguanine (6TG) by pretreatment with methylthioadenosine (MTA)},
  author={Joseph R. Bertino and Nadine N. Johnson-Farley and Raymond P Perez and Adam Lubin and Martin Lubin},
  journal={Cancer Research},
  year={2010},
  volume={70},
  pages={5393-5393}
}
The MTAP gene, at chromosomal locus 9p21, is frequently co-deleted with p16, especially in T-cell acute lymphocytic leukemias, mesotheliomas, gliomas, lung and pancreatic carcinomas, and sarcomas. In normal cells, MTAP cleaves MTA to adenine and 5-methylthioribose-1-phosphate, which are converted to adenine nucleotides and methionine. We previously showed that mice are protected from 6TG toxicity by preadministration of MTA, generating adenine and blocking conversion of 6TG to its nucleotide… 
1 Citations
Targeting tumors that lack methylthioadenosine phosphorylase (MTAP) activity
TLDR
The frequency of MTAP-deficiency is presented and past and recent strategies to target such deficient cells are discussed, including one in which MTA is administered, followed by very high doses of a toxic purine or pyrimidine analog.