alexa Hallmarks of Cancer: Interpretation as Carcinogenic Hyp
ISSN: 2157-2518

Journal of Carcinogenesis & Mutagenesis
Open Access

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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: November 16, 2015; Accepted: February 01, 2016; Published: 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.
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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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