Co-occurrence of metabolic disorders is a recognized risk factor for the development of colorectal cancer which is currently the leading cause of morbidity due to malignant neoplasms in the world. The pathogenesis of colorectal cancer is not well understood yet. Among the postulated neoplastic mechanisms is the activation of insulin-like growth factors, with both epidemiological and clinical observations of their role. In this paper, the authors synthesize the current knowledge about the importance of activation of insulin-like growth factors in the development of colorectal cancer.
Phosphatase and tensin homolog deleted on chromosome ten (PTEN) is a human suppressor gene. Its protein product is a bispecific phosphatase playing the complex role in the cell cycle regulating processes and apoptosis by the mechanism of signal transduction into the cell via tyrosine kinase B signaling pathway (PI3K/Akt/mTOR). Reduction or loss of PTEN function is implicated in the pathogenesis of many malignancies, including colorectal cancer. A gradual decrease in the function of PTEN in the sequence of transformations: normal tissue–polyp–adenocarcinoma – disseminated cancer was indicated. The relation between the PTEN loss and the higher clinical severity of colorectal cancer was observed, i.a. higher TNM status and higher tendency to form metastases, leading in some of the studies to shortened patients survival during the observation period. The potential predictive value of the PTEN function loss for the EGFR-targeted therapy in patients with advanced colorectal cancer is the subject of controversy. The potential application of PTEN assessment in clinical practice as a prognostic and/or predictive factor requires further well-designed prospective studies on larger patient population, using the unified methodology. The aim of the study is to summarize the current knowledge on the role of PTEN gene and PTEN protein in the pathogenesis of colorectal cancer and the role of PTEN in clinical practice.
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