fig2

The genetic architecture of bone metastases: unveiling the role of epigenetic and genetic modifications in drug resistance

Figure 2. Genetic mutations and their role in drug resistance and cancer progression. This illustration depicts the intricate network of genetic mutations that underpin drug resistance and cancer progression. Mutations in the BRCA gene, represented by the red circle, impair DNA repair mechanisms, increasing susceptibility to further genetic aberrations that may lead to cancer. Similarly, alterations in the KRAS gene, shown in green, trigger hyperactive signaling pathways that foster cancer cell growth and survival. The purple oval indicates mutations in the EGFR, specifically in the kinase domain, which activate downstream signaling pathways independently of ligand binding, thereby promoting unregulated cell proliferation. The magenta oval represents the loss of function in the RB1 gene, leading to disrupted cell cycle control and unchecked cell proliferation. Additionally, mutations in the TP53 gene, shown in blue, result in the loss of apoptosis, allowing cells with damaged DNA to survive. These genetic alterations collectively enhance survival signaling, evade apoptosis, and facilitate unchecked cell proliferation, culminating in therapy failure, as depicted by the grey circles. This figure highlights how these mutations collectively contribute to the complexity of drug resistance in cancer therapy. Created in BioRender. Mohammad, K. (2025) https://BioRender.com/86cygfh. EGFR: Epidermal growth factor receptor.

Cancer Drug Resistance
ISSN 2578-532X (Online)

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