Tumors of the Pancreas: From Genes to Diagnostic Pathology

Discrepancies have been reported between HER2 status[ERBB2 gene] in primary breast cancer[Breast cancer] and micrometastatic cells[Cell] in bone marrow. The aim of this study was to assess HER2 gene status[ERBB2 gene] in micrometastatic cells[Cell] in bone marrow and corresponding primary tumour[Neoplasm]. Micrometastatic cells[Cell] were detected in bone marrow aspirations in a prospective series of 27 breast cancer patients[Patient] by immunocytochemistry[Immunocytochemical procedure] (pancytokeratin antibody). HER2 status of micrometastatic cells[ERBB2 gene] was assessed by fluorescence in situ hybridisation (FISH)[Hybridization], respectively in 24 out of 27. Primary tumour HER2 status[ERBB2 gene] was assessed by immunohistochemistry[Immunohistochemistry] (CB11 antibody) and by FISH[Hybridization] in 20 out of 27 of the cases. HER2[ERBB2 gene] was amplified or overexpressed in five out of 27 (18.5%) primary tumours and in four out of 27 (15%) micrometastatic cells[Cell]. In two cases, HER2[ERBB2 gene] was overexpressed and amplified in primary tumour[Neoplasm], but not in micrometastatic cells[Cell], whereas, in one case, HER2[ERBB2 gene] presented a low amplification rate (six copies) in micrometastatic cells[Cell] not found in the primary tumour[Neoplasm]. We demonstrated that negative and positive HER2 status[ERBB2 gene] remained, in the majority of the cases, stable between the bone marrow micrometastasis and the primary tumour[Neoplasm]. Therefore, the efficiency of anti-HER2 adjuvant therapy[adjuvant therapy] could be evaluated, in a clinical trial, by sequential detection of HER2-positive micrometastatic cells[Cell] within the bone marrow, before and after treatment.