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Abstract
[...]the results from this report indicate that the inhibitory effects of acidosis on c-myc oncogene expression are partially due to TDAG8-mediated G? Overall, it is hypothesized in this report that extracellular acidosis provides a selective pressure against cancer cells, which modulates clonal cell evolution. [...]TDAG8 is a proton sensor that plays an important role in this process, which has important implications for blood cancer progression as well as cancer cell clonal evolution parallel to extracellular acidosis found within the tumor microenvironment. [...]it is unclear whether the over-expression of TDAG8 is derived from epithelial cancer cells or from infiltrated leukocytes which are known to highly express TDAG8 [20, 21, 70, 71]. [...]TDAG8 expression is consistently down-regulated in hematological malignancies when compared to normal blood cells and tissues (Table 1 and Fig. 1). [...]functional results from this study, together with previous studies [22, 23], suggest that TDAG8 acts as a contextual tumor suppressor in hematological malignancies.




