Publications by authors named "T I Fetisov"
Undifferentiated pleomorphic sarcoma (UPS) is a highly malignant mesenchymal tumor that ranks as one of the most common types of soft tissue sarcoma. Even though chemotherapy increases the 5-year survival rate in UPS, high tumor heterogeneity frequently leads to chemotherapy resistance and consequently to recurrences. In this study, we characterized the cell composition and the transcriptional profile of UPS with resistance to chemotherapy at the single cell resolution.
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- * Current treatments primarily involve surgical resection for localized cases, with chemotherapy and radiotherapy as adjuncts, while targeted therapies remain limited.
- * There is a growing interest in exploring molecular characteristics of SS subtypes to identify new treatment targets, with innovative approaches including immune-based therapies and epigenetic modifiers being researched.
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- Glucocorticoids (GCs) are commonly used to treat blood cancers but can cause various side effects due to how they interact with glucocorticoid receptors (GRs).
- Selective GR agonists (SEGRAs) like CpdA aim to enhance the beneficial anticancer effects while minimizing side effects; however, CpdA faces challenges with chemical instability.
- The newly developed derivative, CpdA-03, shows improved stability and GR affinity, demonstrating significant anticancer activity in lymphoma models, with a tripling reduction in tumor volume compared to conventional treatments.
Article Synopsis
- 7-Methylguanine (7-MG) is a natural compound that inhibits key enzymes involved in cancer cell growth.
- Recent studies have shown that 7-MG is safe for use in mice, leading to a specific method for its administration.
- Research indicates that 7-MG effectively enters tumor tissues and reduces the growth of colon adenocarcinoma in various mouse models.
Combining chemotherapy and hormone therapy is a prevalent approach in breast cancer treatment. While the cytotoxic impact of numerous chemotherapy drugs stems from DNA damage, the exact role of these DNA alterations in modulating estrogen receptor α (ERα) machinery remains elusive. The present study aimed to analyze the impact of DNA damage agents on ERα signaling in breast cancer cells and assess the signaling pathways mediating the influence of DNA damage drugs on the ERα machinery.
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