Cancer: (Prevention and Cure)

 THEORY Of METASTASIS  : (Metastatic Cancer is the NEMESIS) 

Tumorigenesis :

During tumor initiation, cells intially divide, to form a cluster of cells. This cell division, is based on the evolutionary theory of Darwin, i.e. natural selection.

Tumor cell circulation :

 These cluster of cells, circulate through blood in inhospitable environments, to newer sites. At the newer sites, they secrete tumor-suppressive molecules which block inhibitory factors, that prevent the seeding of cancer seed cells in newer environments. This leads to the hypothesis that the transcriptional machinery (involving RNA and transcriptional factors),  adsorbed by the promoters of tumor-suppressors. The assumption is that, the quantitative relation between oncogenes and tumor-suppressors is an inverse one. 

Metastasis :

With excessive levels of tumor suppressors, a negative feedback loop functions to prevent apoptosis (programmed cell death), of cells  in-order that cell survival ensues. This leads to the increase in levels of oncogenes to counteract the excessive levels of tumor-suppressors,that could be termed as ADAPTATION (Jean-Baptiste Lamarck; French Natural Philosopher); further increase in oncogenic levels/activity ensues, leading to cell division and and metastatic tumors at secondary sites. 

Nomenclature (Terminology)

This progress of events could be termed Dar-Lam-Da or alternatively Darwinian survival-Lamarckian Adaptation followed by Darwinian survival.          

 

 Assumption 

The theoretical assumption is that,   neo-antigens in tumor cells are probably oncogenes which may be poorly presented on the cell surface. This could be due to low expression levels, or inappropriate interaction of cell-surface neo-antigens, with MHC II molecules, more specifically the  inhibitory peptide. This inhibitory peptide, could form unstable complexes with the neo-antigen and MHC II, resulting in failed neoantigen-presentation. Thus the tumor survivesthe   immunosurveillance process.

The tumor suppressor polypeptide (based on the amino acid sequence) could fold in such a way that it forms stable complexes with MHC II, that is not inhibited by the inhibitory peptide. This leads to proper antigen-presentation. In this instance, the tumor is targeted by the immune system (cell-defense mechanism) and gets eliminated.

A successful cancer vaccine would override the above biology, for example an adjuvant such as an emulsion, could cloak the inhibitory peptide in the case of a neo-antigen/oncogenic polypeptide resulting in stable complexes, that leads to successful antigen-presentation, and elimination of the tumor.

Therapy/Cure ensues.