Expression of polo‐like kinase (PLK1) in thin melanomas: a novel marker of metastatic disease

Abstract

Our results suggest that PLK1 expression in thin melanomas is a reliable marker to identify patients at high risk for metastases.

Polo-like kinase isoform expression is a prognostic factor in ovarian carcinoma

“…This hypothesis matches well with observations that PLK1 expression is a survival parameter in oesophageal carcinoma (Tokumitsu et al, 1999), lung carcinoma (Wolf et al, 1997) and squamous cell carcinoma of head and neck (Knecht et al, 1999), and serves as a marker for metastatic disease in malignant melanoma (Kneisel et al, 2002).…”

“…Studies on the expression of PLK1 have been performed on carcinomas of lung (Wolf et al, 1997), head and neck (Knecht et al, 1999), oesophagus and stomach (Tokumitsu et al, 1999), skin (Kneisel et al, 2002), breast , brain (Dietzmann et al, 2001), endometrium and ovary (Takai et al, 2001a, b). All studies consistently reported an overexpression of PLK1 in the respective tumour tissue compared to the corresponding nontransformed tissue of origin.…”

Getting in and out of mitosis with Polo-like kinase-1

“…Plk1 is overexpressed in a range of human tumors, including prostate tumors, ovarian carcinomas, hepatoblastomas and melanomas, and Plk1 overexpression was shown to coincide with bad prognosis (Kneisel et al, 2002;Weichert et al, 2004a, b;Yamada et al, 2004). Therefore, Plk1 is useful as a prognostic marker for outcome of disease.…”

Repression of mRNA for the PLK cell cycle gene after DNA damage requires BRCA1

“…The human Plk1 was identified on basis of its high expression levels in rapidly proliferating cells (Holtrich et al, 1994). More recent data have suggested that elevated Plk1 expression in the primary tumor is associated with an unfavorable clinical outcome (Knecht et al, 1999;Kneisel et al, 2002), and experimental silencing of Plk1 has been shown to inhibit proliferative capacity of tumor cells (Spa¨nkuch-Schmitt et al, 2002;Elez et al, 2003). Efficient tumor cell cycle arrest at the G 2 /M boundary following IR exposure requires intact function of the tumor-suppressor protein BRCA1 (Scully and Livingston, 2000), and here we report that the mechanism may involve repression of PLK gene expression.…”