Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2008, 152(1):21-25 | DOI: 10.5507/bp.2008.003
TPL-2/COT AND COX-2 IN BREAST CANCER
- a Laboratory of Molecular Pathology, Department of Pathology, Faculty of Medicine and Dentistry, Palacky University and University Hospital, 775 15 Olomouc, Czech Republic
- b Molecular and Cellular Biology Laboratory, Basic Science Division, University of Crete Medical School, Heraklion, Crete, Greece
- c Department of Histology and Embryology, Faculty of Medicine and Dentistry, Palacky University, 775 15 Olomouc, Czech Republic
Background: Breast cancer is the most common cancer in women worldwide and although mortality (129 000/year) stagnates, incidence (370 000/year) is increasing. In addition to histological type, grade, stage, hormonal and c-erbB2 status there is therefore a strong need for new and reliable prognostic and predictive factors.
Methods and results: This minireview focuses on two potential prognostic and predictive candidates Tpl2/Cot and COX-2 and summarise information about them.
Conclusion: Tumor progression locus 2 (Tpl2/Cot) is a serine/threonine protein kinase belonging to the family of MAP3 kinases. Activated Tpl2/Cot leads to induction of ERK1/2, JNK, NF-κB and p38MAPK pathways. The first study on Tpl2/Cot mRNA in breast cancer showed its increase in 40 % of cases of breast cancer but no available data exist on protein expression. Cyclo-oxygenase 2 (COX-2) is inducible by growth and inflammatory factors and contributes to the development of various tumours. Expression of COX-2 in breast cancer varied from 5-100 % in reviewed papers with significantly higher values in poorly differentiated tumours. Tpl2/Cot and COX-2 have their importance in different intracellular pathways and some of these are involved in cancer development. Briefly, the results from recent studies suggest that Tpl2/Cot and COX-2 could be prognostic factors in breast cancer.
Keywords: Tpl2, Cot, COX-2, Breast cancer
Received: February 10, 2008; Accepted: March 5, 2008; Published: June 1, 2008 Show citation
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