scholarly journals COX-2 Expression in Carcinoma of the Breast and Surrounding Non-neoplastic Breast Tissue

2021 ◽  
pp. 29-36
Author(s):  
Namita Bhutani ◽  
Shilpi Moga ◽  
Pooja Poswal ◽  
Bhanu Sharma ◽  
Sunil Arora ◽  
...  

Background: Breast carcinoma is the most common malignant tumor and leading cause of cancer related death in women worldwide. Apart from traditional markers, estrogen receptor, progesterone receptor and Her-2neu, which are important for prognostication and staging purposes, a novel marker cyclooxygenase-2 (COX-2) is being studied extensively. We intend to study the spectrum of COX-2 expression in normal breast tissue, ductal carcinoma in situ (DCIS) adjacent to invasive cancer, and in invasive cancer and compare COX-2 expression with histological prognostic parameters and hormone receptor status.Methods: The present study is a prospective study that was conducted in the department of Pathology, SGT Medical College and Hospital, Gurugram (2019-2020). Fifty patients, aged between 21 and 70, suffering from primary breast cancer constituted the study group. Various histological prognostic parameters were assessed. Immunohistochemical profile of the tumor was assessed. COX-2 score was correlated with various clinicopathologic parameters.Results: Among the total of 50 patients suffering from invasive breast carcinoma, 94 percent (47/50) of cases showed the same COX-2 expression level in normal breast epithelium and corresponding tumor areas and this correlation was statistically significant. The correlation between the level of COX-2 expression in tumor and DCIS was highly significant.Conclusion: Inhibition of COX-2 may represent a potential target for preventing breast cancer oncogenesis and as an adjuvant treatment following surgery to reduce local recurrence.

Cancers ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3088 ◽  
Author(s):  
Kaoutar Ennour-Idrissi ◽  
Dzevka Dragic ◽  
Elissar Issa ◽  
Annick Michaud ◽  
Sue-Ling Chang ◽  
...  

Differential DNA methylation is a potential marker of breast cancer risk. Few studies have investigated DNA methylation changes in normal breast tissue and were largely confounded by cancer field effects. To detect methylation changes in normal breast epithelium that are causally associated with breast cancer occurrence, we used a nested case–control study design based on a prospective cohort of patients diagnosed with a primary invasive hormone receptor-positive breast cancer. Twenty patients diagnosed with a contralateral breast cancer (CBC) were matched (1:1) with 20 patients who did not develop a CBC on relevant risk factors. Differentially methylated Cytosine-phosphate-Guanines (CpGs) and regions in normal breast epithelium were identified using an epigenome-wide DNA methylation assay and robust linear regressions. Analyses were replicated in two independent sets of normal breast tissue and blood. We identified 7315 CpGs (FDR < 0.05), 52 passing strict Bonferroni correction (p < 1.22 × 10−7) and 43 mapping to known genes involved in metabolic diseases with significant enrichment (p < 0.01) of pathways involving fatty acids metabolic processes. Four differentially methylated genes were detected in both site-specific and regions analyses (LHX2, TFAP2B, JAKMIP1, SEPT9), and three genes overlapped all three datasets (POM121L2, KCNQ1, CLEC4C). Once validated, the seven differentially methylated genes distinguishing women who developed and who did not develop a sporadic breast cancer could be used to enhance breast cancer risk-stratification, and allow implementation of targeted screening and preventive strategies that would ultimately improve breast cancer prognosis.


2014 ◽  
Vol 50 ◽  
pp. S112
Author(s):  
H. Bergholtz ◽  
R. Lesurf ◽  
S. Myhre ◽  
V.D. Haakensen ◽  
A.L. Børresen-Dale ◽  
...  

2018 ◽  
Author(s):  
Corey Lourenco ◽  
Manpreet Kalkat ◽  
Kathleen E. Houlahan ◽  
Jason De Melo ◽  
Joseph Longo ◽  
...  

ABSTRACTThe potent MYC oncoprotein is deregulated in many human cancers, including breast carcinoma, and is associated with aggressive disease. To understand the mechanisms and vulnerabilities of MYC-driven breast cancer, we have generated anin vivomodel that mimics human disease in response to MYC deregulation. MCF10A cells ectopically expressing a common breast cancer mutation in the PI3 kinase pathway (PIK3CAH1047R) lead to the development of organized acinar structures in mice. However, expressing both PIK3CAH1047Rand deregulated-MYC lead to the development of invasive ductal carcinoma, thus creating a model in which a MYC-dependent normal-to-tumour switch occursin vivo. These MYC-driven tumors exhibit classic hallmarks of human breast cancer at both the pathological and molecular levels. Moreover, tumour growth is dependent upon sustained deregulated MYC expression, further demonstrating addiction to this potent oncogene and regulator of gene transcription. We therefore provide a MYC-dependent human model of breast cancer which can be assayed forin vivotumour initiation, proliferation, and transformation from normal breast acini into invasive breast carcinoma. Taken together, we anticipate that this novel MYC-driven transformation model will be a useful research tool to both better understand MYC’s oncogenic function and identify therapeutic vulnerabilities.Conflict of interest statementThe authors declare no potential conflicts of interest.


Neoplasma ◽  
2020 ◽  
Author(s):  
Michaela Feriancová ◽  
Ingrid Walter ◽  
Christian F. Singer ◽  
Juraj Gazdarica ◽  
Kamil Pohlodek

2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Raja Alyusuf ◽  
Javed Fayyaz Wazir ◽  
Urmil Prabha Brahmi ◽  
Abdul Rahman Fakhro ◽  
Moiz Bakhiet

The role of estrogen and progesterone receptors in breast cancer biology is well established. In contrast, other steroid hormones are less well studied. Glucocorticoids (GCs) are known to play a role in mammary development and differentiation; thus, it is of interest to attempt to delineate their immunoexpression across a spectrum of mammary epithelia. Aim. To delineate the distribution pattern of glucocorticoid receptors (GRs) in malignant versus nonmalignant epithelium with particular emphasis on lactational epithelium. Materials and Methods. Immunohistochemistry (IHC) for GRs was performed on archival formalin-fixed paraffin-embedded tissue blocks of 96 cases comprising 52 invasive carcinomas, 21 cases with lactational change, and 23 cases showing normal mammary tissue histology. Results. Results reveal an overexpression of GRs in mammary malignant epithelium as compared to both normal and lactational groups individually and combined. GR overexpression is significantly more pronounced in HER-2-negative cancers. Discussion. This is the first study to compare GR expression in human lactating epithelium versus malignant and normal epithelium. The article discusses the literature related to the pathobiology of GCs in the breast with special emphasis on breast cancer. Conclusion. The lactational epithelium did not show overexpression of GR, while GR was overexpressed in mammary NST (ductal) carcinoma, particularly HER-2-negative cancers.


1994 ◽  
Vol 9 (3) ◽  
pp. 140-144 ◽  
Author(s):  
M.R. Giovagnoli ◽  
G. Reale ◽  
L. Cosentino ◽  
A. Manna ◽  
C. Midulla ◽  
...  

Two specific monoclonal antibodies for breast tissue (DF3 and MCAb-12) and the corresponding tumor markers CA15-3 and MCA in serum have been evaluated in 50 patients with breast cancer and in 15 controls. The expression of these antigens in tissue was poorly correlated with the common prognostic parameters. Their presence in serum was associated with an altered distribution of the antigens in the cell. The expression of these antigens in tissue enables us to select patients for serological follow-up and to evaluate tumor differentiation from a functional point of view.


2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e14645-e14645
Author(s):  
N. Kounalakis ◽  
S. Lau ◽  
D. Darling ◽  
M. Palomares ◽  
M. Senthil ◽  
...  

e14645 Background: Farnesoid X receptor (FXR), a nuclear receptor, is a ligand dependent transcriptional factor regulating cholesterol and carbohydrate metabolism. Recently, FXR was shown to have a contributing role in colorectal cancer. We hypothesize that FXR expression changes from normal to premalignant to malignant tissue in patients with breast cancer. Methods: We identified 16 paired formaldehyde fixed, paraffin embedded tissue (normal, premalignant, and malignant) from patients with receptor positive, early stage breast cancer. Clinical information was extracted from a prospective database initiated in 2006 under institutional approval. Immunohistochemical staining of FXR using a validated polyclonal antibody was completed with appropriate positive and negative controls. The slides were graded independently by two investigators using an agreed upon scale to detect the percentage of positively stained cells to the nearest 10th percentile. Statistical analysis was performed by ANOVA and Student's t-test. A p-value of 0.05 was considered significant in all analyses. Results: Normal tissue and invasive cancer was identified in all 16 patient specimens. Of the 16 invasive cancers, 12 were ductal and 4 were lobular. 8/16 (50%) of the specimens also contained non-invasive cancer. 5/16 patients (31%) had N1 disease. FXR expression did not correlate with grade, histology, stage, or lymph node status. However, FXR expression increases with malignant transformation of the breast cancer cell. The mean percentage of cells staining positive for FXR in normal breast tissue was 58%, non-invasive 72% and invasive 79%. FXR staining in normal breast tissue was significantly less when compared to both invasive and noninvasive cancer (p< 0.007). Conclusions: FXR expression is upregulated in breast cancer when compared with expression in normal tissue and appears to progressively increase along the continuum of malignancy. Our pilot study results warrant further evaluation into FXR as a predictive biomarker for breast cancer, given the ability to target FXR via development of non-toxic oral ligands. No significant financial relationships to disclose.


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