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INTRODUCTION. Currently, the choice of tactics in the treatment of esophageal cancer remains an urgent problem. Important factors are: the stage of the disease, the functional state of the patient, as well as the morphological type of tumor. An integrated approach is today the standard for this pathology. However, after radical treatment, a significant number of complications are observed, in particular, the development of leakage of esophagogastroanastomosis. Today, according to world literature, it is generally accepted that the development of anastomotic leakage is associated with the detection of the disease in late stages, the consequences of radiation during combined chemoradiotherapy, and extensive surgical intervention for esophageal cancer.The OBJECTIVE was to improve the results of treatment of patients with malignant neoplasms of the esophagus and esophagogastric junction, through the use of an integrated approach.METHODS AND MATERIALS. During the period of 1988–2022, treated 2784 patients with cancer of the esophagus and esophagogastric junction were treated at the Republican Clinical Oncology Dispensary named after Prof. M. Z. Sigal. The study group included 1,799 patients who received surgical treatment, combined chemoradiotherapy in combination with surgery, and external beam radiation therapy in combination with surgery.RESULTS. Due to changes in treatment tactics for patients with cancer of the esophagus and esophagogastric junction, postoperative mortality after surgical complications decreased from 24.3 % to 6.2 %, and anastomotic leakage in the postoperative period decreased from 27.0 % to 8.1 %.CONCLUSION. Changes in the treatment of patients with cancer of the esophagus and esophagogastric junction made it possible to reduce the development of postoperative complications and increase life expectancy. The molecular genetic approach allows for effective analysis of screening, early diagnosis, treatment and rehabilitation.

Suppressor gene research is one of the main current trends in modern cancer research. Oncogenesis, including colorectal cancer (CRC), is a process strictly dependent on the proper functioning of the suppressor genes and their proteins. The molecular genetic studies of hereditary cases and sporadic forms of cancer conducted for several years have revealed that a significant feature of the occurrence and progression of neoplastic changes is silencing of the expression of tissue-specific suppressor genes. Restoring the proper activity of the respective suppressor proteins plays a key role in anti-cancer prevention and gives hope for the development of effective personalised therapy. This review presents the latest reports on the molecular mechanisms regulating the expression, activity, and function of suppressor genes, which were silenced in tissues and cell lines of colorectal cancer, and restoration of their correct expression inhibited the proliferation and invasion of CRC cells.

Mesenchymal stem cells (MSCs) are non-hematopoietic progenitor cells, which can be isolated from different types of tissues including bone marrow, adipose tissue, tooth pulp, and placenta/umbilical cord blood. There isolation from adult tissues circumvents the ethical concerns of working with embryonic or fetal stem cells, whilst still providing cells capable of differentiating into various cell lineages, such as adipocytes, osteocytes and chondrocytes. An important feature of MSCs is the low immunogenicity due to the lack of co-stimulatory molecules expression, meaning there is no need for immunosuppression during allogenic transplantation. The tropism of MSCs to damaged tissues and tumor sites makes them a promising vector for therapeutic agent delivery to tumors and metastatic niches. MSCs can be genetically modified by virus vectors to encode tumor suppressor genes, immunomodulating cytokines and their combinations, other therapeutic approaches include MSCs priming/loading with chemotherapeutic drugs or nanoparticles. MSCs derived membrane microvesicles (MVs), which play an important role in intercellular communication, are also considered as a new therapeutic agent and drug delivery vector. Recruited by the tumor, MSCs can exhibit both pro- and anti-oncogenic properties. In this regard, for the development of new methods for cancer therapy using MSCs, a deeper understanding of the molecular and cellular interactions between MSCs and the tumor microenvironment is necessary. In this review, we discuss MSC and tumor interaction mechanisms and review the new therapeutic strategies using MSCs and MSCs derived MVs for cancer treatment.

Two mutants were isolated in wheat that showed enhanced resistance towards Puccinia striiformis f. sp. tritici, the fungal causal agent of yellow rust. The altered phenotype of I3-48 is due to a minimum of two mutation events, each showing a partial, additive effect, with one mutation segregating with a deletion on the long arm of chromosome 4D. In the case of I3-54, the enhanced resistance is due to a single, dominant mutation. In both mutants, the expression of the enhanced resistance is growth-stage specific. With I3-54, the full resistance phenotype is apparent from the third seedling leaf onwards, while with I3-48, a full resistance phenotype is only seen on the tenth and subsequent leaves. In addition to the enhanced resistance towards yellow rust, I3-48 also shows enhanced resistance towards brown rust, and I3-54 shows enhanced resistance to powdery mildew.