scholarly journals Investigation of Methylation in E-cadherin Gene Promoter Regions and Interleukin-17 Gene Polymorphism in Breast Cancer Patients

2018 ◽  
Vol 26 (4) ◽  
pp. 94-103
Author(s):  
Sirous Naeimi ◽  
2021 ◽  
Author(s):  
Sadia Ajaz ◽  
Sani-e-Zehra Zaidi ◽  
Saleema Mehboob Ali ◽  
Aisha Siddiqa ◽  
Mohammad Ali Memon

In carcinomas, dissemination of cancer cells via blood or lymph circulation constitutes an early event. E-cadherin is a transmembrane calcium dependent adhesion protein. Cellular de-differentiation and plasticity, underlying metastasis, is attributed to the loss of function of E-cadherin (cdh1) gene. The loss of gene expression may arise from promoter hypermethylation, which has been reported in multiple cancers. In the present pilot project, sixty (60) blood samples were collected from the breast cancer patients at a tertiary care hospital in Karachi, Pakistan. DNA was isolated from the cells circulating in the peripheral blood of the participants. Promoter hypermethylation was investigated through sodium-bisulfite treatment of DNA followed by methylation-specific PCR. In 53.3% of the patients, E-cadherin gene promoter hypermethylation was observed. Promoter hypermethylation of E-cadherin has been reported in DNA isolated from the tissue specimen. However, to the best of our knowledge this is the first report of E-cadherin promoter hypermethylation in cells isolated from the peripheral blood of breast cancer patients from a geographically specific population. The results have important implications in tumour staging and selection of treatment regimens.


2010 ◽  
Vol 1 (4) ◽  
pp. 40 ◽  
Author(s):  
MushtaqA Siddiqi ◽  
Nidda Syeed ◽  
Safiya Abdullah ◽  
ASyed Sameer ◽  
SyedAkhtar Husain ◽  
...  

2019 ◽  
Vol 32 (11) ◽  
pp. 1574-1586 ◽  
Author(s):  
João Lobo ◽  
Sara Petronilho ◽  
Amy Hanlon Newell ◽  
Julia Coach ◽  
Greg Harlow ◽  
...  

2013 ◽  
Vol 46 (15) ◽  
pp. 1585-1589 ◽  
Author(s):  
G. Hofmann ◽  
M. Balic ◽  
N. Dandachi ◽  
M. Resel ◽  
W. Schippinger ◽  
...  

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 3880-3880
Author(s):  
Ameera Gaafar ◽  
Abdulla Al-Sulaiman ◽  
Alia Iqniebi ◽  
Adher Al-Sayed ◽  
Entezam Sahovic ◽  
...  

Abstract It has been well established that γδ T-cells play a role in innate anti-tumor immunity. However, the exact mechanism has not yet been fully elucidated. Most of these responses have been ascribed to Vγ9Vδ2 cells, which represent a major subset of the circulating γδ T-cells in humans (1–10%). IFN-γ and granzyme B are important molecules in the anti-tumor immune responses. Upon stimulation, γδ T-cells rapidly produce IFN-γ and cytotoxic molecules. In the present study we analyzed the immune responses by γδ T-cells in 30 newly diagnosed breast cancer patients and 30 normal controls before and after expansion with zoledronic acid. We also scanned the granzyme B gene polymorphism in breast cancer patients and controls. Our result revealed that γδ-T cells in PBMC were reduced in both frequency and function in breast cancer patients compared with the normal controls. Ex-vivo stimulation of γδ T-cells with zoledronic acid and IL-2 partially compensated for this deficiency, as it stimulates production of IFN- γ and release of cytotoxic molecules by these cells. However, the IFN- γ and granzyme B and cytotoxicity of the expanded γδ T-cells from breast cancer patients remained significantly below normal control. Genotypic analysis of granzyme B gene revealed significantly higher frequency of the RAH haplotype in breast cancer patients compared with normal controls. The prevalence of the wild genotype QPY/QPY was significantly higher in normal controls compared with the breast cancer patients. Cytotoxicity by γδ T-cells against various targets was reduced in breast cancer patients compared to normal controls. In conclusion, our analysis shows a defective immune function of γδ T-cells and granzyme B gene polymorphism in breast cancer patients. The γδ T-cell function defect in these patients can be partially corrected by zoledronic acid. Further studies of γδ T-cell function and granzyme B gene polymorphism in other cancers, as well as the therapeutic use of zoldedronic acid is warranted.


2004 ◽  
Vol 10 (18) ◽  
pp. 6189-6193 ◽  
Author(s):  
Essel Dulaimi ◽  
Jeanne Hillinck ◽  
Inmaculada Ibanez de Caceres ◽  
Tahseen Al-Saleem ◽  
Paul Cairns

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