Abstract
Alpha-1 antitrypsin (1-AT) is a secretory glycoprotein mainly produced in the liver and monocytes. It is the most abundant serine protease inhibitor in human plasma. Proteolytic enzymes play a significant role in the expression of the malignant phenotype, including the loss of growth regulation, invasiveness and formation of metastases. Deficiency of 1-AT is an inherited disorder characterized by reduced serum level of 1-AT. Protease inhibitors Z (PiZ) and protease inhibitors S (PiS) are the most common deficient genotypes of 1-AT. The association of deficient 1-AT subtypes with several tumors such as primary liver carcinoma, lung cancer, bladder cancer and malignant hepatoma was reported. This study aimed to determine the incidence of 1-AT genotypes (PiZ and PiS) in breast cancer female patients. Blood samples were collected from 111 patients. DNA was isolated and the PCR technique was performed to amplify the regions contain the Z and S mutations in exon V and exon III, respectively. Genotyping of the Z and S alleles was performed by restriction fragment length polymorphism analysis using the Taq1 restriction enzyme. Our results demonstrated that 100% of the breast cancer patients were homozygous for the normal allele (PiMM) and no PiZ and PiS genotypes were found.
Highlights
We have shown that overexpression of TGF-β1 in mammary epithelial cells suppresses the development of carcinomas and that expression of a dominant negative type II TGF-β receptor (DNIIR) in mammary epithelial cells under control of the MMTV promoter/enhancer increases the incidence of erbB2 in carcinomas accompanied by Tgfbr2fspKO fibroblasts
We found that the frequency of the IVS10-6T>G is characterized by multiple physiologic abnormalities, including mutation was not increased in breast cancer cases as compared with neurodegeneration, immunologic abnormalities, cancer predisposition, controls
We examined the incidence of tumors the hypothesis that Single nucleotide polymorphisms (SNPs) in the regulatory regions of genes that create formed in these ERα knockout mice bearing the Wnt-1 transgene
Summary
Endocrine therapy for breast cancer is a major modality for the treatment of breast cancer, producing response rates between 30% and 40% of unselected patients with the minimum of toxicity. Several human genetic diseases are known to be or suspected to be due to defects in DNA repair or cell cycle control Some of these patients are radiation sensitive and/or predisposed for cancer as a cause of mutations in genes involved in these cellular pathways. Microarray-based comparative genomic hybridization (arrayCGH) allows the construction of high-resolution genome-wide maps of copy number alterations, and statistical software packages are available for exploring and analysing array-CGH data (see, for example, [2,3]), facilitating the delineation of the boundaries of CNAs in individual tumors and thereby localizing and identifying potential oncogenes and tumor suppressor genes. The aim of this study was to evaluate the prognostic value of gene expression-based classification as well as established prognostic markers, including mutation status of the TP53 gene, in a group of breast cancer patients with long-term (>10 years) fol The aim of this study was to compare MR spectroscopic findings from breast cancer tissue with histological grading of tumor and patient lymph node status
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