Imbalance of the mitochondrial pro- and anti-apoptotic mediators in neuroblastoma tumours with unfavourable biology.
Journal article, 2005

It has been proposed that a lack of apoptosis plays an important role in neuroblastoma (NB) progression. We therefore screened cDNA array filters, including 198 apoptotic genes, in order to identify mRNA transcripts that are differentially expressed in tumours with unfavourable versus favourable biology. Twenty-one genes were analysed further using real-time reverse-transcriptase-polymerase chain reaction (RT-PCR). Significantly lower levels of DNCL1 (PIN; P(c)(corrected) = 0.0054) and NTRK1 (TrkA; P(c) = 0.039) were found in NB tumours with unfavourable biology. In addition, BID, BCL2, APAF1, CASP2, CASP3 and CASP9 were found to be preferentially expressed in tumours with favourable biology, whereas CDKN1A (p21), IL2RA, and MCL1, were found to be preferentially expressed in NB tumours with unfavourable biology. In conclusion, mRNA levels of transcripts encoding pro-apoptotic mediators of the mitochondrial apoptotic pathway were found to be expressed to a lower extent in tumours with unfavourable biology. Our data also suggest that the mitochondrial pathway is suppressed in advanced stages of NB tumours, due to an imbalance between anti-apoptotic and pro-apoptotic mediators which is a finding that may have therapeutic significance.

pathology

pathology

genetics

genetics

genetics

genetics

Mitochondria

genetics

genetics

Reverse Transcriptase Polymerase Chain Reaction

RNA

methods

Messenger

RNA Precursors

Neuroblastoma

Apoptosis

DNA

Complementary

Humans

Author

Frida Abel

University of Gothenburg

Rose-Marie Sjöberg

University of Gothenburg

Staffan Nilsson

Chalmers, Mathematical Sciences, Mathematical Statistics

University of Gothenburg

Per Kogner

Karolinska University Hospital

Tommy Martinsson

University of Gothenburg

European Journal of Cancer

0959-8049 (ISSN)

Vol. 41 4 635-46

Subject Categories

MEDICAL AND HEALTH SCIENCES

DOI

10.1016/j.ejca.2004.12.021

More information

Created

10/7/2017