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ISSN: 2157-2518

Journal of Carcinogenesis & Mutagenesis
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Review Article

Hallmarks of Cancer: Interpretation as Carcinogenic Hypercycle

Malzev VN*

Department Practice of Urologie, Bahnhofstr 1, 30159 Hanover, Germany

*Corresponding Author:
Malzev VN
Urologische Praxis, Bahnhofstr. 1
30159 Hanover, Germany
Tel: +49 511 32 75 74
E-mail: [email protected]

Received date: November 16, 2015; Accepted date: February 01, 2016; Published date: February 04, 2016

Citation: Malzev VN (2016) Hallmarks of Cancer: Interpretation as Carcinogenic Hypercycle. J Carcinog Mutagene 7:252. doi: 10.4172/2517-2518.1000252

Copyright: © 2016 Malzev VN. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

The mechanism that is the base of all hallmarks is the genetic instability as a result of continuously occurring mutations and egipenomic DNA modifications in a cancer cell. It cannot be explained by simple accumulation of genome mutations. Continuous mutation and epigenetic modification are only possible as a result of continuous impact of a mutagenic factor. Cyclic DNA replication reaction and/or RNA of mobile genetic elements are this mutagenic agent. These elements are generated as a result of inner-cell chaos of molecular biological processes that is caused by the impact of a cancerogenic factor. After their generation, they can create a hypercyclic link to the cell DNA replication cycle and hence cause mutations and epigenetic modifications in this cell. A new type of selforganisation of inner-cell processes and structures named primary cancerogenic hypercycle is generated. These changes progress, but remain hidden until they affect certain weak points of the cell genome. As a result, additional cyclic processes are generated that support the primary cancerogenic hypercycle and entail the generation of a second-order hypercycle. Hypercycles of the second order and over are hallmarks of cancer, and they ensure a competitive advantage with regard to the cyclic DNA replication reaction of environmental healthy cells. Since this moment, a pre-cancer cell becomes a cancerous one. The primary cancerogenic hypercycle remains a homogenous structure during the whole cancerogenesis. This hypothesis reveals new principles of cancer treatment that are described in the article.

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