Tumor-suppressor genes in breast cancer progression

1994 ◽  
pp. 79-96 ◽  
Author(s):  
Helene S. Smith
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Cancer Progression ◽  
Tumor Suppressor Genes ◽  
Breast Cancer Progression ◽  
Suppressor Genes

scholarly journals Loss of Heterozygosity at Tumor Suppressor Genes Detectable on Fractionated Circulating Cell-Free Tumor DNA as Indicator of Breast Cancer Progression

2012 ◽  
Vol 18 (20) ◽  
pp. 5719-5730 ◽  
Author(s):  
Heidi Schwarzenbach ◽  
Corinna Eichelser ◽  
Jolanthe Kropidlowski ◽  
Wolfgang Janni ◽  
Brigitte Rack ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Loss Of Heterozygosity ◽  
Cancer Progression ◽  
Tumor Suppressor Genes ◽  
Breast Cancer Progression ◽  
Suppressor Genes ◽  
Tumor Dna

scholarly journals Detection of a novel mutation in exon 20 of the BRCA1 gene

2013 ◽  
Vol 18 (4) ◽  
Author(s):  
Abhijit Chakraborty ◽  
Atul Katarkar ◽  
Keya Chaudhuri ◽  
Ashis Mukhopadhyay ◽  
Jayasri Basak
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Hereditary Breast Cancer ◽  
Tumor Suppressor Genes ◽  
Novel Mutation ◽  
Mutation Screening ◽  
Brct Domain ◽  
Globular Domain ◽  
Suppressor Genes ◽  
Exon 20

AbstractHereditary breast cancer constitutes 5–10% of all breast cancer cases. Inherited mutations in the BRCA1 and BRCA2 tumor-suppressor genes account for the majority of hereditary breast cancer cases. The BRCA1 C-terminal region (BRCT) has a functional duplicated globular domain, which helps with DNA damage repair and cell cycle checkpoint protein control. More than 100 distinct BRCA1 missense variants with structural and functional effects have been documented within the BRCT domain. Interpreting the results of mutation screening of tumor-suppressor genes that can have high-risk susceptibility mutations is increasingly important in clinical practice. This study includes a novel mutation, p.His1746 Pro (c.5237A>C), which was found in BRCA1 exon 20 of a breast cancer patient. In silico analysis suggests that this mutation could alter the stability and orientation of the BRCT domain and the differential binding of the BACH1 substrate.

scholarly journals Reversal of hypermethylation and reactivation of glutathione S-transferase pi 1 gene by curcumin in breast cancer cell line

Tumor Biology ◽  
2017 ◽  
Vol 39 (2) ◽  
pp. 101042831769225 ◽  
Author(s):  
Umesh Kumar ◽  
Ujjawal Sharma ◽  
Garima Rathi
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Breast Cancer Cell ◽  
Breast Cancer Cell Line ◽  
Tumor Suppressor Genes ◽  
Cancer Cell Line ◽  
Methylation Pattern ◽  
Glutathione S Transferase ◽  
Suppressor Genes ◽  
Mcf 7

One of the mechanisms for epigenetic silencing of tumor suppressor genes is hypermethylation of cytosine residue at CpG islands at their promoter region that contributes to malignant progression of tumor. Therefore, activation of tumor suppressor genes that have been silenced by promoter methylation is considered to be very attractive molecular target for cancer therapy. Epigenetic silencing of glutathione S-transferase pi 1, a tumor suppressor gene, is involved in various types of cancers including breast cancer. Epigenetic silencing of tumor suppressor genes can be reversed by several molecules including natural compounds such as polyphenols that can act as a hypomethylating agent. Curcumin has been found to specifically target various tumor suppressor genes and alter their expression. To check the effect of curcumin on the methylation pattern of glutathione S-transferase pi 1 gene in MCF-7 breast cancer cell line in dose-dependent manner. To check the reversal of methylation pattern of hypermethylated glutathione S-transferase pi 1, MCF-7 breast cancer cell line was treated with different concentrations of curcumin for different time periods. DNA and proteins of treated and untreated cell lines were isolated, and methylation status of the promoter region of glutathione S-transferase pi 1 was analyzed using methylation-specific polymerase chain reaction assay, and expression of this gene was analyzed by immunoblotting using specific antibodies against glutathione S-transferase pi 1. A very low and a nontoxic concentration (10 µM) of curcumin treatment was able to reverse the hypermethylation and led to reactivation of glutathione S-transferase pi 1 protein expression in MCF-7 cells after 72 h of treatment, although the IC50 value of curcumin was found to be at 20 µM. However, curcumin less than 3 µM of curcumin could not alter the promoter methylation pattern of glutathione S-transferase pi 1. Treatment of breast cancer MCF-7 cells with curcumin causes complete reversal of glutathione S-transferase pi 1 promoter hypermethylation and leads to re-expression of glutathione S-transferase pi 1, suggesting it to be an excellent nontoxic hypomethylating agent.

scholarly journals JMJD2A contributes to breast cancer progression through transcriptional repression of the tumor suppressor ARHI

2014 ◽  
Vol 16 (3) ◽  
Author(s):  
Li-Liang Li ◽  
Ai-Min Xue ◽  
Bei-Xu Li ◽  
Yi-Wen Shen ◽  
Yu-Hua Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Cancer Progression ◽  
Transcriptional Repression ◽  
Breast Cancer Progression

scholarly journals Targeting DNA methylation for treating triple-negative breast cancer

2019 ◽  
Vol 20 (16) ◽  
pp. 1151-1157 ◽  
Author(s):  
Jia Yu ◽  
Jacqueline Zayas ◽  
Bo Qin ◽  
Liewei Wang
Keyword(s):  
Breast Cancer ◽  
Dna Methylation ◽  
Tumor Suppressor ◽  
Triple Negative Breast Cancer ◽  
Targeted Therapies ◽  
Tumor Suppressor Genes ◽  
Dna Methyltransferase ◽  
Triple Negative ◽  
Suppressor Genes ◽  
Dna Methyltransferase Inhibitors

Triple-negative breast cancer (TNBC) accounts for 15–20% of all invasive breast cancers and tends to have aggressive histological features and poor clinical outcomes. Unlike, estrogen receptor- or HER2-positive diseases, TNBC patients currently lack the US FDA-approved targeted therapies. DNA methylation is a critical mechanism of epigenetic modification. It is well known that aberrant DNA methylation contributes to the malignant transformation of cells by silencing critical tumor suppressor genes. DNA methyltransferase inhibitors reactivate silenced tumor suppressor genes and result in tumor growth arrest, with therapeutic effects observed in patients with hematologic malignancies. The antitumor effect of these DNA methyltransferase inhibitors has also been explored in solid tumors, especially in TNBC that currently lacks targeted therapies.

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