Introduction
Background
Proliferation
Cell Cycle
Mutations
Euploidy
Polyploidy
Aneuploidy
Duesbergs/Rasnick Hypothesis
Pathology
Indications
Methods
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Multimodal Cell Analysis
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You are here Background | Duesbergs/Rasnick Hypothesis
   
Which theory of carcinogenesis is plausible?
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The current mutation theory claims that a combination of 4–7 specific mutations transforms normal to cancer cells by elimination of normal growth control, i. e. tumour suppressor genes and by converting other genes to oncogenes

This implies the postnatal acquisition of 4–7 somatic mutations

In cases of inherited disposition for cancer, heritable mutations may predispose for an early occurence of chromosomal aneuploidy (e.g. Fanconi anemia, Xeroderma pigmentosum,…)
 
Normal chromosomes Damaged chromosomes  
 
The chromosomal theory of carcinogenesis had been abandoned
 
The original chromosomal theory of carcinogenesis (von Hansemann, 1890; Boveri, 1902) had been abandoned 50 years ago, because cancer-specific chromosomal patterns or karyotypes had not been found
 
Yet, since the 1960es biologists identified non random chromosomal aberrations in most tumours
 
Cancer-specific aneuploidy leads to abnormal transcription which generate cancer-specific phenotypes
 
 
Papillary renal cell carcinoma with typical primary chromosomal aberrations
(trisomy of no. 7, 12, 17, monosomy X)
 
What is chromosomal aneuploidy?
 
 
Diploid (euploid) chromosomal set of a normal human cell by spectral karyotyping
  Aneuploid chromosomal set of a cancer cell with many numerical and structural chromosomal aberrations  
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Carcinogens are
aneuploidogenes

 

 

 

 

 

 

 

 

 
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Specific chromosomal
aberrations may cause cancer

 

 

 

 

 

 

 

 

 

 

 

 

 

 





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Chromosomal aneuploidy means gains or losses of chromosomes or their segments

 

 

 

 

 

   
     
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