# Common Molecular Mechanisms and Biomarkers in Breast, Colon and Ovarian Cancer
## 4 Discussion
This study prioritized validated data by using STRING's \"curated\" subset, minimizing noise and ensuring accuracy. GeneCodis was chosen for its multi-category analysis capability, allowing a broader evaluation of common cancer biomarkers. These methodological choices strengthen the reliability of the findings and their future experimental validation. The filtering process applied in this study has enabled the identification of biomarkers with the highest robustness and biological relevance in breast, colon, and ovarian cancer. The selection of 27 proteins and the validation of MSH2 and KIT as differential markers reinforce the existence of shared molecular mechanisms among these tumor types. The presence of an excessive number of biomarkers would have indicated a deficient filtering process, compromising the specificity of the analysis. On the contrary, the strict application of methodological and bioinformatics criteria ensures that the selected markers are representative of key processes, providing a solid foundation for future research and clinical validations. The statistical approach employed in this study, including the hypergeometric test and the application of a highly restrictive \(p\)-value threshold, reinforces the robustness of the identified associations. By minimizing the risk of false positives and ensuring high specificity in biomarker selection, these methodological choices strengthen confidence in the reported findings. Such stringent criteria align with best practices in biomarker discovery, and have been applied in previous studies to enhance result reliability and interpretability. However, one of the main limitations of this study is that the results are based on bioinformatics analyses, and the experimental validation in clinical samples performed is limited to patients from a single project (TCGA). Although the association between MSH2 and KIT expression and patient survival was modest, the observed trends suggest a possible prognostic value. These results highlight the need for further research with larger datasets and experimental validation to confirm their potential as reliable biomarkers. Nonetheless, this study provides an initial framework for considering MSH2 and KIT as potential biomarkers across breast, colon, and ovarian cancer. Therefore, it is essential to confirm the relevance of the identified biomarkers in other patient cohorts. Additionally, patient variability and tumor heterogeneity could affect the applicability of these biomarkers in all cases. Although RNA-seq expression analysis through GEPIA2 provides valuable insights into gene expression differences between tumor and normal tissues, it does not establish protein-level relevance, which is essential for understanding functional implications. As gene expression does not always correlate directly with protein abundance or activity, future studies should incorporate proteomic analyses, such as mass spectrometry, to confirm protein expression patterns in clinical samples. Additionally, immunohistochemical validation in independent patient cohorts could provide further evidence of the biological significance of MSH2 and KIT as potential biomarkers. These complementary approacheswill strengthen the translational impact of the findings and improve their applicability in personalized oncology. The association of high MSH2 and KIT expression with better survival outcomes in our analysis contrasts with previous reports wherein MSH2 loss leads to mismatch-repair deficiency, and KIT overexpression is implicated in oncogenesis in certain gastrointestinal tumors. This apparent paradox underscores the context-dependent role of these proteins across different cancer types. While MSH2 is essential for DNA repair, its differential expression may reflect compensatory mechanisms in tumors attempting to maintain genomic integrity. Similarly, KIT signaling can contribute to oncogenesis in specific tissues, but its regulation varies depending on genetic alterations, tumor microenvironment, and cellular context.