Breast cancer presents a significant challenge due to its heterogeneity and propensity for developing chemoresistance, particularly in the triple-negative subtype. c-Mesenchymal epithelial transition factor (c-Met), a receptor tyrosine kinase, presents a promising target for breast cancer therapy due to its involvement in disease progression and poor prognosis. However, the heterogeneous expression of c-Met within breast cancer subtypes and individual tumors complicates targeted therapy. Also, cancer cells can develop resistance to c-Met inhibitors through various mechanisms, including bypass signaling pathways and genetic mutations. The off-target effects of c-Met inhibitors further limit their clinical utility, necessitating the development of more selective agents. To overcome these challenges, personalized treatment approaches and combination therapies are being explored to improve treatment efficacy while minimizing adverse effects. Novel c-Met inhibitors with improved selectivity and reduced off-target toxicity show promise in preclinical studies. Additionally, targeted delivery systems aim to enhance drug localization and reduce systemic toxicity. Future directions involve refining inhibitor design and integrating c-Met inhibition into personalized treatment regimens guided by molecular profiling. This review explores the mechanisms by which c-Met contributes to chemoresistance in breast cancer and current challenges in targeting c-Met for breast cancer therapy. It discusses strategies to optimize treatment outcomes, ultimately improving patient prognosis and reducing mortality rates associated with this devastating disease.

Study’s Excerpt/Novelty Full Abstract It is believed that among others, magnetic nanoparticles possess the ability for stability, biocompatibility, and cost-effectiveness in biomedicine. Despite many types of magnetic materials, including non-noble metals like iron, cobalt, and nickel, the potential applications seem not to have been as explored as with noble metals like gold. This review aimed to give a broad overview of magnetic nanoparticles, more so their synthesis, characterization, and various applications in disease detection, such as cancer diagnostics. This was a literature review design; the data were sourced from peer-reviewed articles published within the last ten years. The criteria for selecting studies included that they had to directly address magnetic nanoparticle synthesis, design, and application. For this purpose, databases such as PubMed, Scopus, and Google scholar were tapped into to ensure the widest possible relevant coverage. Different approaches, such as chemical or mechanical ones, are used to create magnetic nanoparticles. The paper outlines the advantages of magnetic nanoparticles in the treatment of diseases. Furthermore, as most of the categorization techniques now in use are found to be inaccurate and unreliable, they have now shown certain flaws. Therefore, the use of magnetic nanoparticles in biomedical applications, especially in diagnosing and treating diseases, holds great promise. However, improvement in the methodology for the classification of nanoparticles is quite necessary. Such standard protocols for synthesizing and characterizing magnetic nanoparticles should be developed in the near future, with new therapeutic applications being explored in this domain.

Therapeutic resistance remains a serious challenge in breast cancer, and abnormal c-mesenchymal epithelial transition factor (c-Met) receptor tyrosine kinase (RTK) activation contributes to therapeutic resistance in many. Ubiquitin-specific peptidase 8 (USP8) has emerged as a modulator of RTK stability through deubiquitination and endosomal trafficking, and preclinical studies show that inhibition of USP8 speeds up ubiquitin-dependent degradation of RTKs, including c-Met and EGFR, suppresses PI3K/Akt and MAPK signaling, and reverses resistance phenotypes. In this review, we summarize mechanistic evidence for USP8 regulation of c-Met and related RTKs, explore preclinical studies that assess inhibition of USP8 as a strategy to sensitize RTK-driven tumors, and highlight translational limitations such as drug selectivity, toxicity, dosing, pharmacodynamics biomarkers, and patient selection that must be addressed prior to a clinical trial in breast cancer. While the therapeutic targeting of USP8 is promising, direct validation in breast cancer models and the development of robust pharmacodynamic markers and inhibitors that are clinically graded remain crucial next phase.

Breast cancer (BC) is a major cause of cancer-related mortality among women worldwide. Genetic polymorphisms, such as those in the Mesenchymal Epithelial T

Breast Tumour Kinase (BRK/PTK6) is a non-receptor tyrosine kinase that has attracted growing interest in breast cancer research due to its association with tumour progression, aggressive disease behaviour, therapy resistance, and prognosis. Although BRK is often discussed in relation to its expression in malignant breast tissues, its significance extends beyond expression level alone. Its activation, subcellular localisation, kinase-dependent signalling, and non-catalytic interactions all contribute to its influence on tumour behaviour. Across breast cancer models, BRK has been associated with disease progression, resistance-related signalling, and reduced treatment response, supporting its relevance as both a prognostic marker and a therapeutic target. Its role in breast cancer is not confined to a single pathway or mechanism, but reflects the combined contribution of kinase activity, functional interactions, activation status, localisation, and tumour subtype. This review examines the prognostic and therapeutic significance of BRK/PTK6 in breast cancer, with an emphasis on its roles in disease progression and therapy resistance, its potential as a biomarker, and emerging BRK-directed treatment strategies. Summary: This review explores the role of BRK/PTK6 in driving breast cancer progression and treatment resistance, emphasising its potential as a prognostic biomarker and discussing challenges in targeting BRK to improve breast cancer therapies.