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

Journal of Carcinogenesis & Mutagenesis
Open Access

Like us on:
OMICS International organises 3000+ Global Conferenceseries Events every year across USA, Europe & Asia with support from 1000 more scientific Societies and Publishes 700+ Open Access Journals which contains over 50000 eminent personalities, reputed scientists as editorial board members.

Open Access Journals gaining more Readers and Citations

700 Journals and 15,000,000 Readers Each Journal is getting 25,000+ Readers

This Readership is 10 times more when compared to other Subscription Journals (Source: Google Analytics)

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.
Related article at Pubmed, Scholar Google


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.


Share This Page

Additional Info

Loading Please wait..
Peer Reviewed Journals
Make the best use of Scientific Research and information from our 700 + peer reviewed, Open Access Journals
International Conferences 2017-18
Meet Inspiring Speakers and Experts at our 3000+ Global Annual Meetings

Contact Us

© 2008-2017 OMICS International - Open Access Publisher. Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version