[The alternative way of colorectal cancer developing. The histogenetic and molecular features of serrated lesions (review, continued)].

The occurrence of colorectal cancer can be traced in two ways: from conventional adenomas with the APC-gene mutation (model Fearon-Vogelstein) and the "serrated way", that has a unique genetic profile and morphological characteristics at the early stages. These neoplasms are determined from 7 to 9%. The risk of developing cancer of them is 7.5-15%. Precursors of epithelial neoplasia are aberrant crypts foci. About 20% of colorectal cancer demonstrated the common defects in DNA methylation (CIMP-positive profile), mutations BRAF (KRAS)--oncogenes, microsatellite instability (MSI). The serrated lesions may have these mutations. Serrated polyposis syndrome has specific genetic changes associated with biallelic mutation MUTYH also. Risk of colorectal cancer is very high in this syndrome and is more than 50%. Often the synchronous or metachronous cancers presence. They are usually accompanied by MSI-H and represented serrated morphology too. Understanding epigenetic ways and molecular features of serrated lesions gives an knowledge of their clinical significance and provides the evidence for the treatment and monitoring of patients with this disease. This review is devoted to these issues.

[Modern aspects of photodynamic therapy of esophageal].

This review presents the current possibilities of photodynamic therapy in the treatment of precancerous lesions and cancer of the esophagus. Mechanisms of photodynamic effects on tumor and especially the accumulation of photosensitizer in tumor tissue, results of studies on the use of photodynamic therapy in the treatment of early esophageal cancer, esophageal cancer stenosis and combinations with other treatment techniques. Results of treatment of Barrett's esophagus using photodynamic therapy were analyzed and a compared with other methods of treatment.