Dysplasia caused by HR-HPV
|
Fig. 1: Scheme of p16INK4a immunostaining in dysplasia: gradual increase in p16INK4a positivity with progression of dysplasia, starting from basal layer.Upregulation of p16INK4a has been suggested to be a consequence of the functional inactivation of the retinoblastoma protein (pRb).In the case of cervical cancer, inactivation of pRb is mediated by binding of the E7 oncoprotein of high risk human papillomaviruses (HR-HPV) to pRb. Since expression of p16INK4a underlies a negative feedback control through functional pRb, overexpression might represent a useful biomarker for cells with active expression of HPV oncogenes. p16INK4a in cervical dysplasia is unrelated to differentiation /maturation and can therefore be expressed in dysplastic, i.e. proliferating cells. In these cells, strongly overexpressed p16INK4a is easily detectable with immunochemical means. |
® mtm laboratories AG, all rights reserved