ArticleVirchows Archiv : an international journal of pathology2011
Detection of Slit2 promoter hypermethylation in tissue and serum samples from breast cancer patients.
Article in Virchows Archiv : an international journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Cancer Biomarkers in Liquid Biopsy for Early Detection of Breast Cancer: A Systematic Review.Clinical Medicine Insights. Oncology · 2022Review
- FOXP1 negatively regulates tumor infiltrating lymphocyte migration in human breast cancer.EBioMedicine · 2019Article
- Combined Analysis of the Aberrant Epigenetic Alteration of Pancreatic Ductal Adenocarcinoma.BioMed research international · 2019Article
- Suppression of Slit3 induces tumor proliferation and chemoresistance in hepatocellular carcinoma through activation of GSK3β/β-catenin pathway.BMC cancer · 2018Article
- Function of Slit/Robo signaling in breast cancer.Frontiers of medicine · 2015Review
- Low Expression of Slit2 and Robo1 is Associated with Poor Prognosis and Brain-specific Metastasis of Breast Cancer Patients.Scientific reports · 2015Article
- Differential promoter methylation of kinesin family member 1a in plasma is associated with breast cancer and DNA repair capacity.Oncology reports · 2014Article
- Loss of expression and promoter methylation of SLIT2 are associated with sessile serrated adenoma formation.PLoS genetics · 2013Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Promoter hypermethylation has been shown to be a common mechanism for inactivation of tumor suppressor genes in breast cancer. The aim of this study was to investigate the prevalence of Slit2 promoter hypermethylation in both the tumor and serum samples of breast cancer patients with ductal carcinoma in situ (DCIS) or invasive breast carcinoma (IBC). The methylation status of Slit2 was investigated in 210 tissue samples (15 breast with no pathological findings, 26 DCIS, and 169 IBC samples) and 123 corresponding serum samples (15 breast with no pathological findings, 26 DCIS, and 82 IBC samples) using methylation-specific polymerase chain reaction. Immunohistochemical staining for Slit2 was also performed using tissue microarray blocks to determine whether Slit2 promoter hypermethylation correlated with loss of Slit2 expression. Slit2 promoter hypermethylation was not detected in breast tissue and serum samples from patients with no pathological findings. DCIS or IBC showed a statistically higher frequency of Slit2 promoter hypermethylation compared to breast with no pathological findings in both the tissue and serum samples; however, there were no statistically significant differences between DCIS and IBC samples. Similar Slit2 promoter hypermethylation patterns were seen in the tissue samples and corresponding serum specimens (p < 0.001). Slit2 promoter hypermethylation was associated with loss of Slit2 expression. These results suggest that Slit2 promoter hypermethylation appears to be responsible for functionally silencing Slit2 expression. Slit2 promoter hypermethylation may be considered as a possible serum marker for early detection of breast cancer.
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