Imbalance of the mitochondrial pro- and anti-apoptotic mediators in neuroblastoma tumours with unfavourable biology.
Artikel i vetenskaplig tidskrift, 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

Författare

Frida Abel

Göteborgs universitet

Rose-Marie Sjöberg

Göteborgs universitet

Staffan Nilsson

Chalmers, Matematiska vetenskaper, matematisk statistik

Göteborgs universitet

Per Kogner

Karolinska universitetssjukhuset

Tommy Martinsson

Göteborgs universitet

European Journal of Cancer

0959-8049 (ISSN)

Vol. 41 4 635-46

Ämneskategorier

MEDICIN OCH HÄLSOVETENSKAP

DOI

10.1016/j.ejca.2004.12.021

Mer information

Skapat

2017-10-07