Aberrant EGFR-ASAP1 signalling enhances hepatoblastoma invasiveness

20170104101000

EGFR-ASAP1 signalling may contribute to hepatoblastoma (HBL) tumorigenesis and invasiveness, say US-based researchers.

In their study, they used whole tumour transcriptome sequencing of 10 HBL tumours sourced from children with unresectable HBL requiring transplantation as well as immunohistochemistry analyses of residual formalin-fixed paraffin-embedded tissue samples from 60 children with HBL tumours (39 of which were resectable) to determine whether EGFR, ASAP1, ERBB2, or ERBB4 were predictive of the invasiveness of HBL tumours. [Sci Rep 2016;6:38347]

HBL tumours requiring transplantation were found to be enriched for most cancer signalling pathways, including Wnt-β-catenin, EGF, and ERBB. Compared with well-differentiated foetal cells, a progressive loss in EGFR and ASAP1 expression was observed in less differentiated embryonal and undifferentiated small cells (SCU). This trend was exaggerated in unresectable locally invasive or metastatic tumours: embryonal cells were EGFR-negative and SCU were both EGFR- and ASAP1-negative.

The researchers concluded that their findings indicate that loss of EGFR-ASAP1 signalling is characteristic of undifferentiated and invasive HBL and, if validated in future prospective studies, may facilitate the development of a novel immunohistochemistry panel for individualized risk stratification of HBL tumours.