Aims To broaden understanding of phenomena involved in progression from classical adenoid cystic carcinomas (ACCs) to tumours with high-grade transformation (ACC-HGT)
Methods Expression of proteins linked to cellular metabolism as well as the microvascular density (MVD) in conventional and transformed areas were analysed. Findings were compared with ordinary ACCs. In seven cases of ACC-HGT and in 18 ACCs the expressions of GLUT1, mitochondrial antigen (MTA), CD34 (for assessing MVD), α-SMA and P63 (for detection of myoepithelial cells) and Ki-67 (for evaluation of proliferation index) were examined.
Results The transformed component corresponded to adenocarcinomas with frequent (four cases) or scarce/absent (three cases) gland differentiation. In the latter, Ki-67 index was higher, two patients presented lymphatic metastasis and one died of disease. In the former, there was one long-term survivor and one with liver metastasis. Conventional areas of both ACC-HGT and ACC were negative for GLUT1 in most cases (83.3% and 81.3%, respectively) and exhibited low or no expression of MTA (100% and 66.7% of cases, respectively). In contrast, the HGT component presented increased expression of both proteins (GLUT1+ in 50% of cases; MTA+ in 100%). However, the degree of GLUT1 expression did not correlate with clinical outcome. MVD did not differ significantly between conventional and transformed components.
Conclusions Transformation of classical ACC into ACC-HGT encompasses adenocarcinomas with variable degrees of differentiation and seems to lead to metabolic changes without reflection in tumour vasculature. Despite the tumours' higher GLUT1 expression, this protein has no utility as a prognostic marker.
- adenoid cystic carcinoma
- undifferentiated carcinoma
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Funding This work was funded by Fundação de Amparo à pesquisa do Estado de São Paulo (FAPESP), grant number 07/55336-2.
Competing interests None.
Ethics approval This study was approved by the Committee of Ethics of the University of Campinas, Brazil.
Provenance and peer review Not commissioned; externally peer reviewed.