Putative Status of Actively Operative Performance Attributes as Determinants of Minimal Platform Oncogenesis in C-Myc Amplification

The combinatorial complex-action of amplified c-Myc in inducing both increased proliferation and also apoptosis of target cells implicates a derivative dysfunctional relationship of intrinsic tumor suppressor function within the dysfunctional mediating actions of a master oncogene. Increased proline biosynthesis in carcinogenesis by MYC, links the reprogramming of glucose, glutamine and pyridine nucleotides. In such manner, promotional effects of increased cell proliferation must be interpreted within the substantial dysregulation and loss of terminal differentiation of these induced cells. Microarray gene expression profiling in osteosarcoma has revealed relationships of this tumor type and of recurrent medulloblastoma with c-Myc.

Realization of essential dynamics of turnover of proliferating cells appears to promote the emergence both of “escapers” of such proliferative clones of cells and also of “dormant” cells, that is, cells that are non-proliferative but still capable, in future, to resume increased proliferative activity. Nuclear factor, erythroid 2-like 2 (NFE2L2)- associated molecular signature is a robust prognostic gene signature independent of MYC level and lung cancer stage.

Dimensions of a minimal platform for the induction and progression of transformation per se would implicate the potentiality for further evolutionary pathways through dysregulation and enhanced activity of abnormal c-Myc homeostasis. Micro-R675 appears involved in epigenetic regulation of histones for gene expression during hepatocarcinogenesis including that of c-Myc