SciELO - Scientific Electronic Library Online

 
vol.51Regulation of aquaporins in plants under stressMinimal residual disease in prostate cancer patients after primary treatment: theoretical considerations, evidence and possible use in clinical management author indexsubject indexarticles search
Home Pagealphabetic serial listing  

Services on Demand

Journal

Article

Indicators

Related links

  • On index processCited by Google
  • Have no similar articlesSimilars in SciELO
  • On index processSimilars in Google

Share


Biological Research

Print version ISSN 0716-9760

Abstract

YADAV, Mukesh et al. A Nexus model of cellular transition in cancer. Biol. Res. [online]. 2018, vol.51, 23.  Epub Aug 29, 2018. ISSN 0716-9760.  http://dx.doi.org/10.1186/s40659-018-0173-8.

The exact cause of cancer is one of the most immutable medical questions of the century. Cancer as an evolutionary disease must have a purpose and understanding the purpose is more important than decoding the cause. The model of cancer proposed herein, provides a link between the cellular biochemistry and cellular genetics of cancer evolution. We thus call this model as the “Nexus model” of cancer. The Nexus model is an effort to identify the most apparent route to the disease. We have tried to utilize existing cancer literature to identify the most plausible causes of cellular transition in cancer, where the primary cancer-causing agents (physical, chemical or biological) act as inducing factors to produce cellular impeders. These cellular impeders are further linked to the Nexus. The Nexus then generates codes for epigenetics and genetics in cancer development.

Keywords : Cancer; The Nexus model; Biochemical stress; Epigenetics; Mutations; Genetics.

        · text in English     · English ( pdf )