Introduction
Background
Proliferation
Cell Cycle
Mutations
Euploidy
Polyploidy
Aneuploidy
Duesbergs/Rasnick Hypothesis
Pathology
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Methods
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Measurements
Multimodal Cell Analysis
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You are here Background | Duesbergs/Rasnick Hypothesis
   
How many mutated genes are involved in the development
of different cancers?
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The number of genes mentioned in the Sanger
Institute’s Catalogue of Somatic Mutations
in Cancer steadily increased
2005: 21, 2006: 870, 2008: 4.763
Two kinds of mutations are thought to cause cancer:

1. Mutations that convert normal cells to cancer cells, termed oncogenes
2. Mutations that inactivate tumour suppressor genes

 
 
Inconsistencies of the mutation-theory
 
So far no combinations of mutated genes were found that transform normal
to malignant cells
Mice with inherited, allegedly cancer causing genes survive many generations without cancer
Why does chromosomal aneuploidy occur in all tumours?
Why does it take many years for cancers to develop, whereas mutations have immediate effects?
Gene mutations are stable, yet cancer cells are highly unstable with a massively variable genome
Half of all known carcinogenes do not cause mutations yet, all carcinogenes that have been tested cause chromosomal aneuploidy
Why is carcinogenesis extremely time consuming?
Cancer is never present in newborns, whereas mutations are
The Risk to develop cancer increases exponentially with age
Carcinogenes, e.g. x-rays, even with highest dosage,
induce solid cancers only after 20 – 30 years:
 
 
Different latency periods from radiation by atomic bombs
and malignant transformation for leukemia and solid cancers
 
 
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How many different cancer genes do exist?

 

 

 

 




 

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Many observations
on cancers are not sufficienty explained
by the current mutation theory

 

 

 

 

 

 
 
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Chromosomal aneuploidy needs mitoses to occur

 

 

   
   
     
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