A recent review published in Genes & Diseases offers a comprehensive overview of the molecular mechanisms, diagnostic approaches, and therapeutic strategies driving current and future management of this lethal disease. ATC, accounting for a small percentage of thyroid cancers, progresses rapidly and resists conventional therapies, underscoring the urgency for innovative treatment paradigms. At the core of ATC's pathogenesis are genetic aberrations, with prominent alterations in MAPK and PI3K-AKT-mTOR signaling pathways. These dysregulated pathways promote unchecked cellular proliferation, survival, and metastasis. Mutations in genes such as BRAF, RAS, PIK3CA, TP53, and TERT have emerged as key drivers of ATC development and progression. Understanding the interplay between these mutations has enabled refined subclassifications of ATC, potentially informing personalized therapeutic approaches. The review emphasizes the significance of targeted therapies, especially BRAF and MEK inhibitors, in improving patient outcomes. While trimodal therapy—a combination of surgery, chemotherapy, and radiation—remains the cornerstone for localized disease, its limitations in advanced ATC highlight the need for additional therapeutic avenues. Immunotherapy has gained traction as a complementary modality. The tumor microenvironment of ATC, marked by immune cell infiltration and PD-L1 overexpression, presents opportunities for immune checkpoint inhibitors. Diagnostic innovations are also covered in detail, including the comparative efficacy of fine needle aspiration (FNA) versus core needle biopsy (CNB) and the utility of 18F-FDG PET/CT imaging in staging and treatment planning. Advances in immunohistochemical markers and liquid biopsies hold promise for earlier detection and real-time monitoring of therapeutic response. The article concludes by highlighting the emerging role of mitochondrial metabolism as a therapeutic target and the potential of novel agents, including nanoparticles and oncolytic viruses, to enhance radioiodine uptake and overcome therapeutic resistance. Anaplastic thyroid cancer: Genetic roles, targeted therapy, and immunotherapy. Dr. Pascale Allotey advocates for comprehensive maternal health policies, stressing the importance of women's voices in shaping effective healthcare solutions. News-Medical.Net provides this medical information service in accordance with these terms and conditions. Please note that medical information found on this website is designed to support, not to replace the relationship between patient and physician/doctor and the medical advice they may provide. Hi, I'm Azthena, you can trust me to find commercial scientific answers from News-Medical.net. Registered members can chat with Azthena, request quotations, download pdf's, brochures and subscribe to our related newsletter content. A few things you need to know before we start. Please check the box above to proceed. While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles. Please do not ask questions that use sensitive or confidential information.

A new review published in Genes & Diseases highlights the transformative role of microRNAs (miRNAs) in regulating and potentially reversing adipose tissue fibrosis, a condition closely linked to obesity, diabetes, and cardiovascular disease. Fibrosis, driven by abnormal extracellular matrix (ECM) accumulation, disrupts normal adipose tissue function and contributes to broader organ dysfunction. The review explores how miRNAs act as potent molecular regulators, capable of fine-tuning signaling pathways and gene expression patterns that influence fibrotic progression. miRNAs, a class of small non-coding RNAs, can suppress or promote the translation of target genes involved in fibrogenic processes. Within adipose tissue, their regulation of pathways such as TGF-β/Smad, PI3K/AKT, and PPAR-γ plays a pivotal role in determining the balance between healthy tissue maintenance and pathological fibrosis. Specific miRNAs such as miR-122, miR-140, miR-150, miR-30b, and miR-155 demonstrate diverse functions, from blocking collagen synthesis to preventing the conversion of adipogenic cells into fibrogenic ones. These engineered cells produce a secretome—a vesicle-rich fluid carrying anti-fibrotic miRNAs—that can be delivered to affected tissues without triggering immune rejection. This approach enables precise molecular intervention, targeting key proteins like Smad3, PDGFR-β, Runx1, and PPAR-γ, which are central to fibrosis development. The review also draws attention to miRNAs' systemic impact, noting how alterations in adipose tissue can influence fibrosis in distant organs, including the liver, heart, and kidneys. Conversely, restoring miR-140 or delivering miR-30b can mitigate these fibrotic responses. Ultimately, the findings underscore the potential of miRNA-based therapies as a non-invasive, targeted strategy to combat fibrosis in both adipose tissue and other organs. MicroRNAs in adipose tissue fibrosis: Mechanisms and therapeutic potential. Dr. Pascale Allotey advocates for comprehensive maternal health policies, stressing the importance of women's voices in shaping effective healthcare solutions. News-Medical.Net provides this medical information service in accordance with these terms and conditions. Please note that medical information found on this website is designed to support, not to replace the relationship between patient and physician/doctor and the medical advice they may provide. Hi, I'm Azthena, you can trust me to find commercial scientific answers from News-Medical.net. Registered members can chat with Azthena, request quotations, download pdf's, brochures and subscribe to our related newsletter content. A few things you need to know before we start. Please check the box above to proceed. While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles. Please do not ask questions that use sensitive or confidential information.

Lipid metabolism has emerged as a central player in the progression and therapy resistance of breast cancer, particularly the aggressive subtype known as triple-negative breast cancer (TNBC). This review article highlights how disruptions in lipid regulation can significantly influence the behavior of breast cancer cells, impacting their growth, metastasis, and response to treatment. Alterations in the metabolism of fatty acids, cholesterol, sphingolipids, and glycolipids are profoundly intertwined with breast cancer cell survival and invasiveness. The uptake and biosynthesis of fatty acids are notably upregulated in tumor cells, which not only fuels cellular energy demands but also supports membrane synthesis and intracellular signaling. In cholesterol metabolism, the focus falls on how elevated cholesterol synthesis and its potent metabolite 27-hydroxycholesterol (27HC) accelerate tumor progression and interfere with immune responses. The interplay of 27HC with estrogen receptors and immune-modulatory pathways further complicates therapeutic strategies, particularly in hormone-sensitive and resistant tumors. The dual nature of sphingolipid metabolism, especially the contrasting roles of ceramide and its glycosylated derivatives, underscores a complex metabolic paradox. While ceramide accumulation exhibits tumor-suppressive effects, including enhanced apoptosis and chemotherapy sensitization, glycosylated forms such as Globo-H ceramide and GD2 are linked to tumorigenesis, angiogenesis, and cancer stem cell maintenance. A crucial outcome of lipid reprogramming is its role in promoting epithelial-mesenchymal transition (EMT), a process associated with enhanced migratory ability and drug resistance. Beyond intrinsic cancer cell metabolism, the surrounding tumor immune microenvironment (TIME) also adapts in response to lipid cues. M2 macrophages, cancer-associated fibroblasts, and CD8+ T cells exhibit lipid-driven phenotypic shifts that support tumor evasion and therapy failure. Resistance to standard treatments—including chemotherapy, endocrine therapy, HER2-targeted therapy, and immune checkpoint inhibitors—is intimately linked to lipid metabolic rewiring. Upregulation of CD36, FASN, CPT1, and GPR120 exemplifies how tumor cells exploit lipid pathways to avoid apoptosis, reduce drug accumulation, and sustain stemness. Lipid metabolism involved in progression and drug resistance of breast cancer. Dr. Pascale Allotey advocates for comprehensive maternal health policies, stressing the importance of women's voices in shaping effective healthcare solutions. News-Medical.Net provides this medical information service in accordance with these terms and conditions. Please note that medical information found on this website is designed to support, not to replace the relationship between patient and physician/doctor and the medical advice they may provide. Hi, I'm Azthena, you can trust me to find commercial scientific answers from News-Medical.net. Registered members can chat with Azthena, request quotations, download pdf's, brochures and subscribe to our related newsletter content. A few things you need to know before we start. Please check the box above to proceed. While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles. Please do not ask questions that use sensitive or confidential information.