Cancer Genetics and Epigenetics, 2025, Vol.13, No.1, 21-31 http://medscipublisher.com/index.php/cge 22 for treatment decisions in advanced patients. This study aims to integrate multidisciplinary research evidence to provide theoretical support for optimizing clinical practice and future research directions, with the expectation of enhancing the survival benefits of patients. 2 Research Progress on the Pathogenic Mechanism of Prostate Cancer 2.1 Biological characteristics and disease course evolution of the disease Prostate cancer exhibits a unique genetic variation spectrum, including chromosomal structural abnormalities, gene fragment loss, and defects in DNA repair function, etc. These changes jointly promote the formation and deterioration of tumors. Studies have shown that approximately 20% of cases in the metastatic castration resistance stage have defects in homologous recombination repair, among which gene mutations such as BRCA2 and ATMare the most typical (Grypari et al., 2023). The core turning point of the disease course development is the transformation from a hormone-dependent state to a castration-resistant state. At this time, even with hormone treatment, the disease continues to deteriorate, marking that the disease enters a highly invasive stage (Ceder et al., 2016; Ramalingam et al., 2017). The evolutionary process of tumors stems from the synergistic effect of gene mutations and epigenetic regulation. Specifically, epigenetic dysregulation of key growth regulatory genes, combined with the effect of the chronic inflammatory microenvironment, can drive the development of precancerous lesions (Gonzalgo and Isaacs, 2003). It should be focused on that this malignant tumor shows significant heterogeneity characteristics at the early stage, which suggests the urgent need to construct a prediction system to assess the risk of deterioration (Shtivelman et al., 2014). With the progression of the disease, the evolution of drug resistance is widespread, highlighting the urgency of developing innovative treatment options (Ceder et al., 2016). 2.2 Classical signaling pathways and current treatment systems The androgen receptor (AR) signaling network dominates the tumor proliferation process. Currently, the conventional clinical regimens are mainly designed around this pathway, among which hormone blockade therapy is the standard therapy during the hormone-sensitive period (Pisano et al., 2020; Maekawa et al., 2024). However, long-term treatment is prone to cause drug resistance, leading the disease to enter the castration resistance stage. At this time, the tumor still continues to progress in a low androgen environment (Ceder et al., 2016). In addition to the core signaling pathway of AR, molecular mechanisms such as the PI3K/AKT/mTOR regulatory network and the DNA damage response system are collaboratively involved in the development of the disease. These systems not only drive the compensation pathways for the deterioration of the condition but also form potential therapeutic targets. Clinical trials have shown that PI3K/AKT pathway-specific inhibitors demonstrate clinical application prospects in the castration resistance stage (Sarker et al., 2009). The interaction of multiple mechanisms reveals the complex nature of the disease and suggests that multi-target combined intervention may become an effective control strategy (Pisano et al., 2020). 2.3 The transformational significance of the new mechanism research Although important breakthroughs have been made in molecular mechanism research, there are still significant bottlenecks in the treatment of advanced prostate cancer. The current plan has deficiencies in dealing with drug resistance, promoting the scientific research community to develop new sites of action (Maekawa et al., 2024). The latest research has found that processes such as abnormal gene repair mechanisms and dysregulation of the immune regulatory system are closely related to the progression of diseases. For instance, defects in repair genes such as BRCA1/2 are not only associated with high invasiveness, but the related defects can also serve as biomarkers for PARP-targeted therapy (Ciccarese et al., 2017; Grypari et al., 2023). It is particularly worth noting that the ecological environment around the tumor affects the behavior of cancer cells in multiple ways, which provides a theoretical basis for the development of new intervention methods (Corn, 2012). An in-depth analysis of these emerging mechanisms will become the key path to achieving breakthroughs in precision medicine.
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