scholarly journals Immunohistochemical Distribution of a Breast Cancer-Associated Glycoprotein

1993 ◽  
Vol 11 (2-3) ◽  
pp. 91-101 ◽  
Author(s):  
P. D. Rye ◽  
R. A. Walker
Keyword(s):  
Breast Cancer ◽  
Epithelial Cells ◽  
Tissue Distribution ◽  
Normal Breast ◽  
Polyclonal Antiserum ◽  
Breast Carcinomas ◽  
Neoplastic Tissue ◽  
Wide Range ◽  
Malignant Breast ◽  
Breast Tissues

The tissue distribution and specificity of a glycoprotein of Mr230 OOOkDa which has previously been identified from breast carcinomas in culture and shown to be tumour-associated, has been assessed using a polyclonal antiserum. A wide range of tissues has been examined immunohistochemically. The tissue distribution of the glycoprotein show differences between normal, benign and malignant breast and other epithelial tissues, and are clearly specific for epithelial cells. This glycoprotein as detected by the polyclonal antiserum P5252-2, was either absent or showed a minimal presence in normal breast tissues. Evidence of the expression of the glycoprotein in hyperplastic breast was observed but was considerably less than that seen for carcinomas, for which 70% had greater than 50% of cells exhibiting reactivity with P5252-2. There was no relationship with grade or node status. Similar striking differences in glycoprotein expression between non-neoplastic and neoplastic tissue were observed for stomach, large intestine, thyroid and to lesser extent ovary. The di fferences in the expression of this glycoprotein between normal and malignant tissues is of obvious clinical and pathological potential.

Immunohistochemical Study of the BCAR1/p130Cas Protein in Non-Malignant and Malignant Human Breast Tissue

2001 ◽  
Vol 16 (3) ◽  
pp. 172-178 ◽  
Author(s):  
S. van der Flier ◽  
T.H. van der Kwast ◽  
C.J.C. Claassen ◽  
M. Timmermans ◽  
A. Brinkman ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Epithelial Cells ◽  
Tumor Cells ◽  
Intracellular Signaling ◽  
Immunohistochemical Study ◽  
Tamoxifen Treatment ◽  
Breast Carcinomas ◽  
Epithelial Tumor ◽  
Variable Expression ◽  
Malignant Breast

BCAR1/p130Cas is a docking protein involved in intracellular signaling pathways and in vitro resistance of estrogen-dependent breast cancer cells to antiestrogens. The BCAR1/p130Cas protein level in primary breast cancer cytosols was found to correlate with rapid recurrence of disease. A high BCAR1/p130Cas level was also associated with a higher likelihood of resistance to first-line tamoxifen treatment in patients with advanced breast cancer. Using antibodies raised against the rat p130Cas protein, we determined by immunohistochemical methods the BCAR1/p130Cas localization in primary breast carcinomas, in tumors of stromal origin, and in non-neoplastic breast tissues. The BCAR1/p130Cas protein was detected in the cytoplasm of non-malignant and neoplastic epithelial cells and in the vascular compartment of all tissue sections analyzed. Immunohistochemistry demonstrated variable intensity of BCAR1/p130Cas staining and variation in the proportion of BCAR1/p130Cas-positive epithelial tumor cells for the different breast carcinomas. Double immunohistochemical staining for BCAR1/p130Cas and estrogen receptor confirmed coexpression in non-malignant luminal epithelial cells and malignant breast tumor cells. The stromal cells in non-malignant tissues and tumor tissues as well as breast tumors of mesodermal origin did not stain for BCAR1/p130Cas. This immunohistochemical study demonstrates a variable expression of BCAR1/p130Cas in malignant and non-malignant breast epithelial cells, which may be of benefit for diagnostic purposes.

scholarly journals Aberrant epigenetic and transcriptional events associated with breast cancer risk

2021 ◽  
Author(s):  
Natascia Marino ◽  
Rana German ◽  
Ram Podicheti ◽  
Douglas B. Rush ◽  
Pam Rockey ◽  
...  
Keyword(s):  
Breast Cancer ◽  
High Risk ◽  
Breast Cancer Risk ◽  
Epithelial Cells ◽  
Cancer Risk ◽  
Breast Tissue ◽  
Cancer Susceptibility ◽  
Breast Cancer Susceptibility ◽  
Normal Breast ◽  
Breast Tissues

ABSTRACTBackgroundGenome-wide association studies have identified several breast cancer susceptibility loci. However, biomarkers for risk assessment are still missing. Here, we investigated cancer-related molecular changes detected in tissues from women at high risk for breast cancer prior to disease manifestation. Disease-free breast tissue cores donated by healthy women (N=146, median age=39 years) were processed for both methylome (MethylCap) and transcriptome (Illumina’s HiSeq4000) sequencing. Analysis of tissue microarray and primary breast epithelial cells was used to confirm gene expression dysregulation.ResultsTranscriptomic analysis identified 69 differentially expressed genes between women at either high and those at average risk of breast cancer (Tyrer-Cuzick model) at FDR<0.05 and fold change≥2. The majority of the identified genes were involved in DNA damage checkpoint, cell cycle, and cell adhesion. Two genes, FAM83A and NEK2, were overexpressed in tissue sections (FDR<0.01) and primary epithelial cells (p<0.05) from high-risk breasts. Moreover, 1698 DNA methylation aberrations were identified in high-risk breast tissues (FDR<0.05), partially overlapped with cancer-related signatures and correlated with transcriptional changes (p<0.05, r≤0.5). Finally, among the participants, 35 women donated breast biopsies at two time points, and age-related molecular alterations enhanced in high-risk subjects were identified.ConclusionsNormal breast tissue from women at high risk of breast cancer bears molecular aberrations that may contribute to breast cancer susceptibility. This study is the first molecular characterization of the true normal breast tissues and provides an opportunity to investigate molecular markers of breast cancer risk, which may lead to new preventive approaches.

scholarly journals Expression Pattern of a Homeotic Gene, HOXA5, in Normal Breast and in Breast Tumors

2006 ◽  
Vol 28 (5-6) ◽  
pp. 305-313
Author(s):  
Gregory S. Henderson ◽  
Paul J. van Diest ◽  
Horst Burger ◽  
Jose Russo ◽  
Venu Raman
Keyword(s):  
Breast Cancer ◽  
Expression Pattern ◽  
Breast Tumors ◽  
Normal Breast ◽  
Receptor Expression ◽  
Homeotic Genes ◽  
Breast Carcinomas ◽  
Expression Levels ◽  
Egfr Expression ◽  
Breast Tissues

Introduction: Homeotic (HOX) gene products are now known to be functionally associated with breast cancer biogenesis. Recent evidence has indicated that HOXA5 regulates both p53 and progesterone receptor expression levels in breast cancer cells. In addition, HOXA5 has been shown to interact and regulate the activity of another protein referred to as Twist. As homeotic genes play a pivotal role in development, we sought to decipher the expression pattern in both normal breast tissues and in breast carcinomas. Methods: RT-PCR and immunohistochemistry were performed, to assay the levels of HOXA5 expression, on a panel of normal breast tissue and its corresponding primary breast tumors. Results and Conclusions: We show that HOXA5 expression was maintained at stable levels at different reproductive stages of a woman's life, except during lactation. This evidence indicates that HOXA5 may play a role in maintaining the differentiated state within the breast epithelium. However, nearly 70% of all breast carcinomas had decreased HOXA5 protein levels as compared to normal breast tissues. In addition, we demonstrate that HOXA5 protein expression levels in breast carcinomas inversely co-relates with Epidermal Growth Factor Receptor (EGFR) expression. Furthermore, we found that the survival rate amongst the different low levels of HOXA5 expressing breast tumors was not significant, indicative of an early tumorigenesis process in the absence of innate levels of HOXA5 in normal breast cells.

scholarly journals FAM83A is a Potential Biomarker for Breast Cancer Initiation

2021 ◽  
Author(s):  
Natascia Marino ◽  
Rana German ◽  
Ram Podicheti ◽  
Pam Rockey ◽  
George E. Sandusky ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Epithelial Cells ◽  
Normal Breast ◽  
Mass Spectrometry Analysis ◽  
Breast Epithelial Cells ◽  
Potential Biomarker ◽  
Interaction Partners ◽  
Immortalized Cells ◽  
Breast Epithelial ◽  
Breast Tissues

Abstract Background: Family with sequence similarity 83 member A (FAM83A) presents oncogenic properties in several cancers including breast cancer (BC). Recently, we reported FAM83A overexpression in normal breast tissues from women at high risk of breast cancer. We now hypothesize that FAM83A is a key factor in BC initiation. Methods: Immunohistochemical staining was used to evaluate FAM83A protein levels in both a normal breast tissue microarray (TMA, N=411) and a breast tumor TMA (N=349). EGFR staining and its correlation with FAM83A expression were also assessed. Lentivirus-mediated manipulation of FAM83A expression in primary and hTERT-immortalized breast epithelial cells was employed. Biological and molecular alterations upon FAM83A overexpression/downregulation and FAM83A’s interaction partners were investigated.Results: TMA analysis revealed a 1.5-fold increase in FAM83A expression level in BC cases as compared with normal breast tissues (p<0.0001). FAM83A protein expression was directly correlated with EGFR level in both normal and BC tissues. In in vitro assays, exogenous expression of FAM83A in either primary or immortalized breast epithelial cells promoted cell viability and proliferation. Additionally, Ingenuity Pathway Analysis (IPA) revealed that in normal cells FAM83A is involved in cellular morphology and metabolism. Mass spectrometry analysis identified DDX3X and LAMB3 as potential FAM83A interaction partners in primary cells, while we detected FAM83A interaction with cytoskeleton reorganization factors, including LIMA1, MYH10, PLEC, MYL6 in the immortalized cells.Conclusions: This study shows that FAM83A promotes metabolic activation in primary epithelial cells and survival in immortalized cells. These findings support its role in early breast oncogenesis.

Repression of protocadherin 17 is correlated with elevated angiogenesis and hypoxia markers in female patients with breast cancer

2021 ◽  
pp. 1-10
Author(s):  
Sanaa A. El-Benhawy ◽  
Samia A. Ebeid ◽  
Nadia A. Abd El Moneim ◽  
Rabie R. Abdel Wahed ◽  
Amal R.R. Arab
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Clinical Stage ◽  
Suppressor Gene ◽  
Normal Breast ◽  
Vital Role ◽  
Control Group ◽  
Breast Cancer Patients ◽  
Cd34 Cells ◽  
Breast Tissues

BACKGROUND: Altered cadherin expression plays a vital role in tumorigenesis, angiogenesis and tumor progression. However, the function of protocadherin 17 (PCDH17) in breast cancer remains unclear. OBJECTIVE: Our target is to explore PCDH17 gene expression in breast carcinoma tissues and its relation to serum angiopoietin-2 (Ang-2), carbonic anhydrase IX (CAIX) and % of circulating CD34+ cells in breast cancer patients (BCPs). METHODS: This study included Fifty female BCPs and 50 healthy females as control group. Cancerous and neighboring normal breast tissues were collected from BCPs as well as blood samples at diagnosis PCDH17 gene expression was evaluated by RT-PCR. Serum Ang-2, CAIX levels were measured by ELISA and % CD34+ cells were assessed by flow cytometry. RESULTS: PCDH17 was downregulated in cancerous breast tissues and its repression was significantly correlated with advanced stage and larger tumor size. Low PCDH17 was significantly correlated with serum Ang-2, % CD34+ cells and serum CAIX levels. Serum CAIX, Ang-2 and % CD34+ cells levels were highly elevated in BCPs and significantly correlated with clinical stage. CONCLUSIONS: PCDH17 downregulation correlated significantly with increased angiogenic and hypoxia biomarkers. These results explore the role of PCDH17 as a tumor suppressor gene inhibiting tumor growth and proliferation.

scholarly journals Expression of estrogen receptor β isoforms in normal breast epithelial cells and breast cancer: regulation by methylation

Oncogene ◽  
2003 ◽  
Vol 22 (48) ◽  
pp. 7600-7606 ◽  
Author(s):  
Chunyan Zhao ◽  
Eric W-F Lam ◽  
Andrew Sunters ◽  
Eva Enmark ◽  
Manuela Tamburo De Bella ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Epithelial Cells ◽  
Normal Breast ◽  
Estrogen Receptor Β ◽  
Breast Epithelial Cells ◽  
Breast Epithelial ◽  
Normal Breast Epithelial Cells

scholarly journals Long non-coding RNA ARAP1-AS1 accelerates cell proliferation and migration in breast cancer through miR-2110/HDAC2/PLIN1 axis

2020 ◽  
Vol 40 (4) ◽  
Author(s):  
Chong Lu ◽  
Xiuhua Wang ◽  
Xiangwang Zhao ◽  
Yue Xin ◽  
Chunping Liu
Keyword(s):  
Breast Cancer ◽  
Normal Breast ◽  
Tumor Promoter ◽  
Women Health ◽  
Non Coding Rna ◽  
Non Coding Rnas ◽  
And Migration ◽  
Breast Tissues ◽  
Long Non Coding Rna

Abstract Breast cancer (BC) poses a great threaten to women health. Numerous evidences suggest the important role of long non-coding RNAs (lncRNAs) in BC development. In the present study, we intended to investigate the role of ARAP1-AS1 in BC progression. First of all, the GEPIA data suggested that ARAP1-AS1 was highly expressed in breast invasive carcinoma (BRAC) tissues compared with the normal breast tissues. Meanwhile, the expression of ARAP1-AS1 was greatly up-regulated in BC cell lines. ARAP1-AS1 knockdown led to repressed proliferation, strengthened apoptosis and blocked migration of BC cells. Moreover, ARAP1-AS1 could boost HDAC2 expression in BC through sponging miR-2110 via a ceRNA mechanism. Of note, the UCSC predicted that HDAC2 was a potential transcriptional regulator of PLIN1, an identified tumor suppressor in BC progression. Moreover, we explained that the repression of HDAC2 on PLIN1 was owing to its deacetylation on PLIN1 promoter. More importantly, depletion of PLIN1 attenuated the mitigation function of ARAP1-AS1 silence on the malignant phenotypes of BC cells. To sum up, ARAP1-AS1 serves a tumor-promoter in BC development through modulating miR-2110/HDAC2/PLIN1 axis, which may help to develop novel effective targets for BC treatment.

scholarly journals FGF12 is differentially expressed in the brain metastases of patients with metastatic breast cancer.

2020 ◽  
Author(s):  
Shahan Mamoor
Keyword(s):  
Breast Cancer ◽  
Metastatic Breast Cancer ◽  
Brain Metastases ◽  
Metastatic Breast ◽  
Metastatic Tumor ◽  
Clinical Problem ◽  
Normal Breast ◽  
Primary Tumors ◽  
Breast Tissues ◽  
The Brain

Metastasis to the brain is a clinical problem in patients with breast cancer (1-3). We mined published microarray data (4, 5) to compare primary and metastatic tumor transcriptomes to discover genes associated with brain metastasis in patients with metastatic breast cancer. We found that the fibroblast growth factor 12, encoded by FGF12, was among the genes whose expression was most different in the brain metastases of patients with metastatic breast cancer as compared to normal breast tissues. FGF12 mRNA expression was significantly higher in brain metastatic tissues as compared to primary tumors of the breast. Up-regulation of FGF12 expression may contribute to metastasis of tumor cells from the breast to the brain in humans with metastatic breast cancer.

scholarly journals C1R is differentially expressed in the brain metastases of patients with metastatic breast cancer.

2020 ◽  
Author(s):  
Shahan Mamoor
Keyword(s):  
Breast Cancer ◽  
Metastatic Breast Cancer ◽  
Brain Metastases ◽  
Metastatic Breast ◽  
Metastatic Tumor ◽  
Clinical Problem ◽  
Normal Breast ◽  
Primary Tumors ◽  
Breast Tissues ◽  
The Brain

Metastasis to the brain is a clinical problem in patients with breast cancer (1-3). We mined published microarray data (4, 5) to compare primary and metastatic tumor transcriptomes to discover genes associated with brain metastasis in patients with metastatic breast cancer. We found that the complement component 1, r subcomponent, encoded by C1R, was among the genes whose expression was most different in the brain metastases of patients with metastatic breast cancer as compared to normal breast tissues. C1R mRNA was present at significantly reduced quantities in brain metastatic tissues as compared to primary tumors of the breast. Down-regulation of C1R expression may contribute to metastasis of tumor cells from the breast to the brain in humans with metastatic breast cancer.

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