Molecular Biology Reports, Journal Year: 2025, Volume and Issue: 52(1)
Published: April 25, 2025
Language: Английский
Molecular Biology Reports, Journal Year: 2025, Volume and Issue: 52(1)
Published: April 25, 2025
Language: Английский
Heliyon, Journal Year: 2024, Volume and Issue: 10(6), P. e27655 - e27655
Published: March 1, 2024
Cancer is a complex disease that caused by multiple genetic factors. Researchers have been studying protein domain mutations to understand how they affect the progression and treatment of cancer. These can significantly impact development spread cancer changing structure, function, signalling pathways. As result, there growing interest in these be used as prognostic indicators for prognosis. Recent studies shown provide valuable information about severity patient's response treatment. They may also predict resistance targeted therapy The clinical implications are significant, regarded essential biomarkers oncology. However, additional techniques approaches required characterize changes domains their functional effects. Machine learning other computational tools offer promising solutions this challenge, enabling prediction on structure function. Such predictions aid interpretation information. Furthermore, genome editing like CRISPR/Cas9 has made it possible validate significance mutants more efficiently accurately. In conclusion, hold great promise predictive Overall, considerable research still needed better define molecular heterogeneity resolve challenges remain, so full potential realized.
Language: Английский
Citations
4Epigenomics, Journal Year: 2025, Volume and Issue: 17(2), P. 125 - 140
Published: Jan. 19, 2025
Gliomas, highly aggressive tumors of the central nervous system, present overwhelming challenges due to their heterogeneity and therapeutic resistance. Glioblastoma multiforme (GBM), most malignant form, underscores this clinical urgency dismal prognosis despite treatment regimens. Recent advances in cancer research revealed signaling pathways epigenetic mechanisms that intricately govern glioma progression, offering multifaceted targets for intervention. This review explores dynamic interplay between events regulation context glioma, with a particular focus on crucial roles played by non-coding RNAs (ncRNAs). Through direct indirect targeting, ncRNAs emerge as key regulators shaping molecular landscape glioblastoma across its various stages. By dissecting these intricate regulatory networks, novel patient-tailored strategies could be devised improve patient outcomes devastating disease.
Language: Английский
Citations
0Biochimica et Biophysica Acta (BBA) - Reviews on Cancer, Journal Year: 2025, Volume and Issue: unknown, P. 189270 - 189270
Published: Jan. 1, 2025
Language: Английский
Citations
0Epigenomes, Journal Year: 2025, Volume and Issue: 9(1), P. 5 - 5
Published: Feb. 5, 2025
Genomic and epigenomic instability are defining features of cancer, driving tumor progression, heterogeneity, therapeutic resistance. Central to this process epigenetic echoes, persistent dynamic modifications in DNA methylation, histone modifications, non-coding RNA regulation, chromatin remodeling that mirror underlying genomic chaos actively influence cancer cell behavior. This review delves into the complex relationship between these illustrating how they collectively shape genome, affect repair mechanisms, contribute evolution. However, dynamic, context-dependent nature changes presents scientific ethical challenges, particularly concerning privacy clinical applicability. Focusing on lung we examine specific patterns function as biomarkers for distinguishing subtypes monitoring disease progression relapse.
Language: Английский
Citations
0European Journal of Pharmacology, Journal Year: 2025, Volume and Issue: 994, P. 177397 - 177397
Published: Feb. 18, 2025
Language: Английский
Citations
0Frontiers in Pharmacology, Journal Year: 2025, Volume and Issue: 16
Published: Feb. 19, 2025
Lung adenocarcinoma (LUAD) remains a major cause of cancer-related mortality worldwide, with high heterogeneity and poor prognosis. Epigenetic dysregulation plays crucial role in LUAD progression, yet its potential molecular classification therapeutic prediction largely unexplored. We performed an integrated multi-omics analysis 432 patients from TCGA 398 GEO datasets. Using consensus clustering random survival forest (RSF) algorithms, we established epigenetic-based system constructed prognostic model. The model's performance was validated multiple independent cohorts, biological implications were investigated through comprehensive functional analyses. identified two distinct subtypes (CS1 CS2) significant differences epigenetic modification patterns, immune microenvironment, clinical outcomes (P = 0.005). RSF-based model demonstrated robust both training (TCGA-LUAD) validation (GSE72094) time-dependent AUC values ranging 0.625 to 0.694. Low-risk exhibited enhanced cell infiltration, particularly CD8+ T cells M1 macrophages, showed better responses checkpoint inhibitors. Drug sensitivity revealed subtype-specific vulnerabilities, low-risk showing higher conventional chemotherapy targeted therapy. Our study establishes novel predictive for LUAD, providing valuable insights into patient stratification personalized treatment selection. ability predict immunotherapy response drug offers practical guidance decision-making, potentially improving precision medicine approaches.
Language: Английский
Citations
0Extracellular Vesicles and Circulating Nucleic Acids, Journal Year: 2025, Volume and Issue: 6(1), P. 112 - 27
Published: Feb. 24, 2025
The role of extracellular vesicles (EVs) in mediating chemoresistance has gained significant attention due to their ability transfer bioactive molecules between drug-resistant and drug-sensitive cells. In particular, they have been demonstrated play an active part breast cancer by the horizontal genetic protein material. This review highlights EVs, particularly miRNA cargo, driving drug resistance cancer. EVs derived from chemoresistant cells carry miRNAs lncRNAs, which are known modulate gene networks involved cell proliferation survival. These cargo suppress apoptosis targeting pro-apoptotic genes like PTEN BIM, promote epithelial-mesenchymal transition (EMT) through regulation pathways such as TGF-β Wnt/b-catenin, contribute tumor growth enhancing angiogenesis modulating microenvironment. Beyond RNA-mediated effects, also functional proteins, including P-glycoprotein Hsp70, impact cellular metabolism survival pathways. Our findings underscore significance chemoresistance, suggesting potential involvement possible prognostic factors predict therapy response therapeutic targets combination with usual therapy.
Language: Английский
Citations
0International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(5), P. 1988 - 1988
Published: Feb. 25, 2025
Colorectal cancer (CRC) is a major cause of cancer-related mortality worldwide, with significant impact on public health. Current treatment options include surgery, chemotherapy, radiotherapy, molecular-targeted therapy, and immunotherapy. Despite advancements in these therapeutic modalities, resistance remains challenge, often leading to failure, poor progression-free survival, recurrence. Mechanisms CRC are multifaceted, involving genetic mutations, epigenetic alterations, tumor heterogeneity, the microenvironment. Understanding mechanisms at molecular level crucial for identifying novel targets developing strategies overcome resistance. This review provides an overview diverse driving drug sporadic discusses currently under investigation counteract this Several promising being explored, including targeting transport, key signaling pathways, DNA damage response, cell death modifications, stem cells, The integration emerging approaches that target aims enhance efficacy current treatments improve patient outcomes.
Language: Английский
Citations
0Cells, Journal Year: 2025, Volume and Issue: 14(5), P. 382 - 382
Published: March 5, 2025
The peremptory need to circumvent challenges associated with poorly differentiated epithelial endometrial cancers (PDEECs), also known as Type II (ECs), has prompted therapeutic interrogation of the prototypically intractable and most prevalent gynecological malignancy. PDEECs account for cancer-related mortalities due their aggressive nature, late-stage detection, poor response standard therapies. are characterized by heterogeneous histopathological features distinct molecular profiles, they pose significant clinical propensity rapid progression. Regardless complexities around PDEECs, still being administered inefficiently in same manner clinically indolent readily curable type-I ECs. Currently, there no targeted therapies treatment PDEECs. realization new options transformed our understanding enabling more precise classification based on genomic profiling. transition from a provided critical insights into underlying genetic epigenetic alterations these malignancies. This review explores landscape focus identifying key subtypes mutations that variants. Here, we discuss how correlates outcomes can refine diagnostic accuracy, predict patient prognosis, inform strategies. Deciphering underpinnings led advances precision oncology protracted remissions patients untamable
Language: Английский
Citations
0Cancer Treatment and Research Communications, Journal Year: 2025, Volume and Issue: unknown, P. 100918 - 100918
Published: March 1, 2025
Breast cancer (BC) is one of the leading causes cancer-related deaths among women worldwide. Paclitaxel (PTX), a chemotherapeutic agent derived from taxane family, commonly used in treating BC due to its ability disrupt microtubule dynamics and induce cell death. However, resistance PTX presents significant challenge, as it diminishes drug's effectiveness can lead treatment failure. This review explores mechanisms by which exerts effects various factors contributing resistance. These include genetic mutations that affect tubulin dynamics, role non-coding RNAs, molecular pathways involved chemoresistance, epigenetic changes, post-transcriptional modifications, increased activity ABC transporters promote drug efflux, immunosuppressive interactions within tumor microenvironment, mediated autophagy. also strategies overcome resistance, including innovations, combination therapies, nanotechnology-based approaches. may improve efficacy enhance outcomes for patients.
Language: Английский
Citations
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