Studying the Expression of miR-1, EVI1 and Calreticulin in Invasive Breast Carcinoma: Relationship with Clinicopathological Parameters | ||||
| Benha Medical Journal | ||||
| Articles in Press, Accepted Manuscript, Available Online from 18 August 2025 PDF (1.13 MB) | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/bmfj.2025.379508.2388 | ||||
 View on SCiNiTO | ||||
| Authors | ||||
Hend E Nasr ; Omneya Y Bassyoni  ; omnia Y Habashy ; Lina A Mohammed
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| benha faculty of medicine - department of patholoy | ||||
| Abstract | ||||
| .Introduction: Breast cancer is the most prevalent cause of cancer-related mortality among women, with significant rates of morbidity and mortality. Although breast cancer is conventionally treated using various methods including surgery, chemotherapy and endocrine therapy , recurrence and metastasis still remain a serious issue in advanced stage patients. So, new therapeutic strategies are awfully needed. Objectives : In this research we tended to determine the expression of miR-1, EVI1, and calreticulin- in breast cancer and to associate their expression with clinicopathological parameters. Material & Methods: This retrospective study focused on EVI1 and calreticulin was conducted using paraffin-embedded blocks from 100 cases of breast cancer, and miR-1 gene expression analysis was performed . Results: miR-1 was downregulated in cancer patients in contrast to controls. Otherwise EVI1 & calreticulin were over-expressed. miR-1 was inversely correlated with T stage (p=0.01), lymph node metastasis (p=0.003), TNM stage (p=0.01) and ki67 (p=0.01). miR-1 was higher in the hormone-positive group. EVI1 and calreticulin were directly correlated with T stage (p=0.01 & p <0.001), lymph node metastasis (p=0.000 & p=0.01), stage (p=0.000) ki67(p=0.003), and triple-negative breast cancer (p <0.01). miR-1 was negatively correlated with both EVI1 and calreticulin (p=0.02, p= 0.000). Conclusion: miR-1, EVI1, and calreticulin might make a substantial contribution to the onset and spread of breast cancer. Therefore, upregulating miR-1 and blocking EVI1 could be possible targets for therapy in breast cancer treatment. Additionally, there might be a link between miR-1, EVI1, and calreticulin and E-cadherin in induction of epithelial–mesenchymal transition. | ||||
| Keywords | ||||
| Breast Cancer; MicroRNAs; CRT | ||||
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