Mitochondria are sub-cellular organelles that produce adenosine triphosphate (ATP) through oxidativephosphorylation (OXPHOS). As suggested over 70 years ago by Otto Warburg and recently confirmed with moleculartechniques, alterations in respiratory activity and in mitochondrial DNA (mtDNA) appear to be common features ofmalignant cells. Somatic mtDNA mutations have been reported in many types of cancer cells, and some reportsdocument the prevalence of inherited mitochondrial DNA polymorphisms in cancer patients. Nevertheless, a carefulreanalysis of methodological criteria and methodology applied in those reports has shown that numerous papers can'tbe used as relevant sources of data for systematic review, meta-analysis, or finally for establishment of clinicallyapplicable markers.In this review technical and conceptual errors commonly occurring in the literature are summarized. In the first placewe discuss, why many of the published papers cannot be used as a valid and clinically useful sources of evidence in thebiomedical and healthcare contexts. The reasons for introduction of noise in data and in consequence - bias for theinterpretation of the role of mitochondrial DNA in the complex process of tumorigenesis are listed. In the second partof the text practical aspects of mtDNA research and requirements necessary to fulfill in order to use mtDNA analysis inclinics are shown. Stringent methodological criteria of a case-controlled experiment in molecular medicine areindicated. In the third part we suggest, what lessons can be learned for the future and propose guidelines for mtDNAanalysis in oncology. Finally we conclude that, although several conceptual and methodological difficulties hinder theresearch on mitochondrial patho-physiology in cancer cells, this area of molecular medicine should be considered ofhigh importance for future clinical practice.
|Numero di pagine||15|
|Rivista||Journal of Biomedical Science|
|Stato di pubblicazione||Published - 2010|