[Is there a claudin-low phenotype of breast cancer?].

The novel molecular subtype of breast cancer (BC), named "claudin-low", was described in 2007. It was characterized by the consistently low expression of genes involved in the formation of epithelial tight junctions in combination with the high activation of genes associated with the epithelial-to-mesenchymal transition, as well as tumor stem cell markers. The similar claudin- low subtype was later identified at the transcriptional level in bladder cancer, gastric cancer, and serous ovarian cancer.

Claudins as biomarkers of differential diagnosis and prognosis of tumors.

Claudins are a superfamily of transmembrane proteins, the optimal expression and localization of which are important for the normal physiological function of the epithelium and any imbalance may have pathological consequences. Not only insufficient but also excessive production of claudins in cancer cells, as well as their aberrant localization, equally manifest the formation of a malignant phenotype. Many works are distinguished by contradictory data, which demonstrate the action of the same claudins both in the role of tumor-growth suppressors and promoters in the same cancers.

[Role of tenascin С in triple-negative breast cancer].

Aim: to establish a relationship between the main markers tumor stem cells (TSCs), CD44, and CD24, the level of tenascin C production, and chemoresistance in triple-negative breast cancer (BC).

Subjects And Methods: Thirty biopsy specimens from triple-negative BC patients who had conventionally received preoperative chemotherapy followed by surgery were selected in the investigation. All the selected patients were conventionally assigned to neoadjuvant polychemotherapy (PCT) with paclitaxel and carboplatin.

[A change in the expression of membrane-associated proteins and cytoplasmic actin isoforms in the progression of human colon tumors].

Unlabelled: Tumor progression is a complex process that also involves the restructuring of the actin cytoskeleton and the weakening of intercellular adhesive contacts due to the tumor cells that pass through the epithelial-mesenchymal transition (EMT).

Aim: Тo identify correlations between clinical features, risk of progression and/or recurrence of human colon adenocarcinomas (CAC), and EMT-related tumor markers.

Material And Methods: Descending colon and sigmoid colon adenocarcinoma samples were examined immunohistochemically.