# Common Molecular Mechanisms and Biomarkers in Breast, Colon and Ovarian Cancer
## 4 Discussion
Some of these proteins have been previously described in the literature as key players in cancer biology, further validating the approach of this research [34; 35; 36; 37; 38]. These shared proteins participate in a variety of key biological processes, including those related to DNA damage response, cell proliferation, apoptosis, and DNA repair. Among the most significant biological processes, the response to gamma radiation and the regulation of apoptosis in response to genetic damage stand out. These processes are fundamental to carcinogenesis and could be implicated in resistance to treatments, such as radiotherapy and chemotherapy. Through the PPI analysis and the application of the MCODE algorithm, three key clusters were identified, grouping densely interconnected proteins. These clusters showed a strong relation to several metabolic and signaling pathways, including those involved in the regulation of apoptosis, cellular metabolism, and cellular senescence. These observations suggest that cellular control processes like apoptosis and DNA repair could be crucial points in the progression of the three cancer types studied. The validation of gene expression using the GEPIA2 database showed that several of the proteins studied exhibited significant differential expression in tumor tissues compared to normal tissues. Although the differential expression levels of MSH2 and KIT may be considered modest, their consistent presence across all three cancer types and involvement in key biological processes, such as DNA repair and cell proliferation, support their functional relevance. This consistency, unlike the variability observed in other proteins, strengthens the rationale for further validation studies to explore their potential as shared biomarkers in cancer research. More importantly, survival analysis revealed that the higher expression of MSH2 and KIT was associated with a better prognosis in patients, suggesting that these genes could serve as key indicators of disease progression and treatment response. By analyzing survival data collectively, this study identifies trends that may be relevant across multiple cancer types, highlighting potential biomarkers with cross-cancer applicability. Despite biological differences, this approach allows for the detection of shared molecular mechanisms that could inform future research into diagnosis and treatment strategies. The identification of shared proteins also enabled the evaluation of their involvement in various signaling pathways, including those related to cancer and responses to viral infections. These pathways include PI3K-Akt, MAPK, P53, and pathways related to drug resistance, such as platinum drug resistance. In this regard, previous reports from our laboratory have documented the relationship between multiple dysregulatedproteins and resistance to cisplatin [39], as well as the expression of multiple resistance mechanisms to radiation in tumor cells [40]. Although some studies have suggested potential interactions between these phenomena, these associations remain speculative and require further mechanistic validation. [PERSON] [41] describes that the transformation caused by the Epstein-Barr virus in mammary cells induces the genetic disruption of essential functions for protection against carcinogenesis, suggesting a possible link to tumor progression, though additional experimental studies are necessary to confirm these mechanisms. While the identified viral pathways and radiation resistance mechanisms provide interesting insights, it is important to interpret these findings with caution. The current evidence is based on bioinformatics analyses and previously reported associations, but experimental validation is required to confirm direct mechanistic links. Future studies should include functional assays to determine the extent to which viral-related signaling pathways influence resistance mechanisms in breast, colon, and ovarian cancer.