Oral Presentation Joint Scientific Meeting of the Australian & NZ Head & Neck Cancer Society & NZ Association of Plastic Surgeons

Presence of transcription factors involved in pluripotency in head and neck mucoepidermoid carcinoma (1378)

Umaima Khatoon 1 , Bridget Chang-McDonald 1 , Josie Patel 1 , Paul F Davis 1 , Swee T Tan 1 2 , Sean RR Hall 1
  1. Gillies McIndoe Research Institute, GMRI, Wellintgon, Wellington, New Zealand
  2. Wellington Regional Plastic, Maxillofacial & Burns Unit,, Hutt Hospital , Wellington, New Zealand


Mucoepidermoid carcinoma (MEC) is the most common malignant salivary gland tumour making up to 35% of malignant salivary gland tumours. There is accumulating evidence that cellular dedifferentiation whereby cells acquire a multipotent progenitor-like state regulated by the overexpression of key transcription factors, is a common feature in some solid tumors.


The aim of our study was to determine whether the transcription factors KLF4, SOX2 and c-MYC, which when co-expressed are central regulators of cellular dedifferentiation to pluripotency, are present in MEC.


Total RNA was extracted from MEC tissue to analyse gene expression of KLF4, SOX2, c-MYC and the epithelial cell adhesion marker EpCAM using real time quantitative PCR (RT-qPCR, n = 6, biological replicates). For spatial profiling, tissue was fixed and immunohistochemical staining (n = 9, biological replicates) was performed with KLF4, SOX2, and c-MYC. EpCAM was also included to identify tumour nests from stroma. Five control samples were stained for the same markers as the tumor samples.


Immunohistochemical staining and RT-qPCR demonstrated protein and mRNA expression of all three transcription factors and EpCAM, respectively. Serial immunohistochemical imaging of the tumour samples showed subpopulations of EpCAM positive tumour cells co-expressing KLF4, SOX2 and c-MYC.


Here we report the presence of transcription factors that have been shown to be involved in regulating pluripotency in MEC.  Further studies are warranted to determine the causative role of these subpopulations in MEC phenotype.