Cancer Letters, Journal Year: 2024, Volume and Issue: 611, P. 217382 - 217382
Published: Dec. 4, 2024
Language: Английский
Cancer Letters, Journal Year: 2024, Volume and Issue: 611, P. 217382 - 217382
Published: Dec. 4, 2024
Language: Английский
Journal of Hematology & Oncology, Journal Year: 2024, Volume and Issue: 17(1)
Published: June 6, 2024
Abstract Ferroptosis, an iron-dependent form of cell death characterized by uncontrolled lipid peroxidation, is governed molecular networks involving diverse molecules and organelles. Since its recognition as a non-apoptotic pathway in 2012, ferroptosis has emerged crucial mechanism numerous physiological pathological contexts, leading to significant therapeutic advancements across wide range diseases. This review summarizes the fundamental mechanisms regulatory pathways underlying ferroptosis, including both GPX4-dependent -independent antioxidant mechanisms. Additionally, we examine involvement various conditions, cancer, neurodegenerative diseases, sepsis, ischemia–reperfusion injury, autoimmune disorders, metabolic disorders. Specifically, explore role response chemotherapy, radiotherapy, immunotherapy, nanotherapy, targeted therapy. Furthermore, discuss pharmacological strategies for modulating potential biomarkers monitoring this process. Lastly, elucidate interplay between other forms regulated death. Such insights hold promise advancing our understanding context human health disease.
Language: Английский
Citations
51Hematology/Oncology Clinics of North America, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 1, 2025
Language: Английский
Citations
0Seminars in Radiation Oncology, Journal Year: 2025, Volume and Issue: 35(2), P. 224 - 242
Published: March 14, 2025
Language: Английский
Citations
0Molecular Cancer, Journal Year: 2025, Volume and Issue: 24(1)
Published: March 22, 2025
Abstract Background Recurrent/metastatic head and neck squamous cell carcinoma (R/M-HNSCC) is a severe, frequently lethal condition. Oncogene addiction to epidermal growth factor receptor (EGFR) hallmark of HNSCC, but the clinical efficacy EGFR-targeted therapies remains low. Understanding molecular networks governing EGFR-driven progression paramount exploration (co)-treatment targets predictive markers. Methods We performed function-based mapping differentially expressed genes in EGFR-mediated local invasion (fDEGs) using photoconvertible tracers RNA-sequencing (RNA-seq) cellular 3D-model. Results Upon alignment with public single-cell RNA-seq (scRNA-seq) datasets HNSCC-specific regulons, gene regulatory network (invGRN) was inferred from expression data, which overrepresented budding tumors. InvGRN comprises central hubs inhibin subunit beta alpha ( INHBA ) snail family transcriptional repressor 2 SNAI2 ), druggable fDEGs integrin 4 ITGB4 laminin 5 LAMB3 / LAMC2 sphingosine kinase 1 SPHK1 ). Blockade repressed reverted by activin A, 5, sphingosine-1-phosphate, demonstrating functional interconnectivity invGRN. Epithelial-to-mesenchymal transition (EMT) malignant cells invGRN are induced newly defined EGFR-activity subtypes prognostic value that promoted amphiregulin AREG epiregulin EREG Importantly, co-inhibition showed synthetic effects on Cetuximab-mediated blockade high selected associated response Cetuximab patient-derived xenotransplantation (PDX) R/M-HNSCC patients. Conclusions describe an actionable define effectors potential regarding Cetuximab.
Language: Английский
Citations
0Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16
Published: April 1, 2025
The prognosis for head and neck squamous cell carcinoma (HNSCC) remains unfavorable, primarily due to significant therapeutic resistance the absence effective interventions. A major obstacle in cancer treatment is persistent of cells a variety modalities. tumor microenvironment (TME) which includes encompasses all non-malignant components their metabolites within tissue, plays crucial role this context. distinct characteristics HNSCC TME facilitate growth, invasion, metastasis, treatment. This review provides comprehensive overview components, with particular focus on tumor-associated macrophages (TAMs), regulatory T (Tregs), myeloid-derived suppressor (MDSCs), cancer-associated fibroblasts (CAFs), extracellular matrix, reprogrammed metabolic processes, products. It elucidates contributions modulating chemotherapy, radiotherapy, targeted therapy, immunotherapy HNSCC, explores novel strategies targeting management.
Language: Английский
Citations
0Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16
Published: April 10, 2025
Tumor metabolic reprogramming is a highly complex process that enables tumor survival in the presence of limited nutrients, involving multiple signaling pathways, non-coding RNAs (ncRNAs), and transcription factors. Lately, glutamine has been found to enhance growth, spread, drug resistance cancer cells, while also fostering an immunosuppressive microenvironment aids development. However, some tumors, such as pancreatic melanoma, additional can inhibit proliferation this mechanism closely related regulation immune microenvironment. Therefore, further exploration metabolism tumors essential for understanding pathogenesis developing new metabolically targeted therapies. We systematically review latest research on its role system regulation. Additionally, we clinical progress therapies their application combination with current anti-tumor treatments. Ultimately, address challenges prospects involved anti-cancer strategies aimed at metabolism.
Language: Английский
Citations
0Cancer Letters, Journal Year: 2024, Volume and Issue: 611, P. 217382 - 217382
Published: Dec. 4, 2024
Language: Английский
Citations
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