A Probable Risk Factor of Female Breast Cancer: Study on Benign and Malignant Breast Tissue Samples

2013 ◽  
Vol 157 (1) ◽  
pp. 24-29 ◽  
Author(s):  
Sohaila Rehman ◽  
Syed M. Husnain
Keyword(s):  
Breast Cancer ◽  
Risk Factor ◽  
Breast Tissue ◽  
Female Breast Cancer ◽  
Tissue Samples ◽  
Cancer Study ◽  
Female Breast ◽  
Malignant Breast Tissue ◽  
Breast Cancer Study ◽  
Malignant Breast

scholarly journals Association between cadmium and breast cancer

Medicina ◽  
2008 ◽  
Vol 44 (6) ◽  
pp. 415 ◽  
Author(s):  
Loreta Strumylaitė ◽  
Algirdas Boguševičius ◽  
Stanislovas Ryselis ◽  
Darius Pranys ◽  
Lina Poškienė ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Breast Tissue ◽  
Benign Tumor ◽  
Normal Breast Tissue ◽  
Cadmium Concentration ◽  
Normal Breast ◽  
Tissue Samples ◽  
Malignant Breast Tissue ◽  
Two Samples ◽  
Malignant Breast

Cadmium is a known human lung carcinogen, although some studies indicate a link between cadmium exposure and human breast cancer. The objective of this study was to assess cadmium concentration in breast tissue samples of patients with breast cancer and benign breast tumor. Material and methods. The concentration of cadmium was determined in breast tissue samples of 21 breast cancer and 19 benign tumor patients. Two samples of breast tissue from each patient, i.e. tumor and normal tissue close to tumor, were taken for the analysis. Cadmium was determined by atomic absorption spectrometry (Perkin-Elmer, Zeeman 3030). Results. In patients with breast cancer, the mean cadmium concentration was 33.1 ng/g (95% CI, 21.9– 44.4) in malignant breast tissue and 10.4 ng/g (95% CI, 5.6–15.2) in normal breast tissue (P=0.002). In patients with benign tumor, the corresponding values were 17.5 ng/g (95% CI, 8.4–26.5) and 11.8 ng/g (95% CI, 5.1– 18.5) (P=0.3144). There was a statistically significant difference in cadmium concentration between malignant and benign breast tissues (P=0.009). Conclusion. The data obtained show that cadmium concentration is significantly higher in malignant breast tissue as compared with normal breast tissue of the same women or benign breast tissue. Further studies are necessary to determine the association between cadmium concentration in malignant breast tissue and estrogen receptor level, and smoking.

Mutations in Human Interferon α2b Gene and Potential as Risk Factor Associated with Female Breast Cancer

2016 ◽  
Vol 31 (6) ◽  
pp. 199-208 ◽  
Author(s):  
Fayyaz Ahmed ◽  
Nasir Mahmood ◽  
Saman Shahid ◽  
Zahid Hussain ◽  
Ishtiaq Ahmed ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Risk Factor ◽  
Female Breast Cancer ◽  
Human Interferon ◽  
Female Breast ◽  
Interferon Α2b

scholarly journals Hyperglycemia-Induced miR-467 Drives Tumor Inflammation and Growth in Breast Cancer

Cancers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1346
Author(s):  
Jasmine Gajeton ◽  
Irene Krukovets ◽  
Santoshi Muppala ◽  
Dmitriy Verbovetskiy ◽  
Jessica Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Mouse Models ◽  
Breast Tissue ◽  
Fold Increase ◽  
Normal Breast ◽  
High Blood Glucose ◽  
Novel Mirna ◽  
Malignant Breast Tissue ◽  
Malignant Breast ◽  
Cancer Inflammation

The tumor microenvironment contains the parenchyma, blood vessels, and infiltrating immune cells, including tumor-associated macrophages (TAMs). TAMs affect the developing tumor and drive cancer inflammation. We used mouse models of hyperglycemia and cancer and specimens from hyperglycemic breast cancer (BC) patients to demonstrate that miR-467 mediates the effects of high blood glucose on cancer inflammation and growth. Hyperglycemic patients have a higher risk of developing breast cancer. We have identified a novel miRNA-dependent pathway activated by hyperglycemia that promotes BC angiogenesis and inflammation supporting BC growth. miR-467 is upregulated in endothelial cells (EC), macrophages, BC cells, and in BC tumors. A target of miR-467, thrombospondin-1 (TSP-1), inhibits angiogenesis and promotes resolution of inflammation. Systemic injections of a miR-467 antagonist in mouse models of hyperglycemia resulted in decreased BC growth (p < 0.001). Tumors from hyperglycemic mice had a two-fold increase in macrophage accumulation compared to normoglycemic controls (p < 0.001), and TAM infiltration was prevented by the miR-467 antagonist (p < 0.001). BC specimens from hyperglycemic patients had increased miR-467 levels, increased angiogenesis, decreased levels of TSP-1, and increased TAM infiltration in malignant breast tissue in hyperglycemic vs. normoglycemic patients (2.17-fold, p = 0.002) and even in normal breast tissue from hyperglycemic patients (2.18-fold increase, p = 0.04). In malignant BC tissue, miR-467 levels were upregulated 258-fold in hyperglycemic patients compared to normoglycemic patients (p < 0.001) and increased 56-fold in adjacent normal tissue (p = 0.008). Our results suggest that miR-467 accelerates tumor growth by inducing angiogenesis and promoting the recruitment of TAMs to drive hyperglycemia-induced cancer inflammation.

scholarly journals CD99 and HLA-II Immunostaining in Breast Cancer Tissue and Their Correlation with Lymph Node Metastasis

2013 ◽  
Vol 34 (5) ◽  
pp. 363-371 ◽  
Author(s):  
Amal Baccar ◽  
Imen Ferchichi ◽  
Wafa Troudi ◽  
Raja Marrakchi ◽  
Naziha Ben Hmida ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Intracellular Transport ◽  
Breast Tissue ◽  
Cancer Tissue ◽  
Node Metastasis ◽  
Malignant Breast Tissue ◽  
Malignant Breast ◽  
Lymph Node Stage

In an attempt to better unfold the antitumor immune response and invasion strategies perused by tumor cells, markers such as CD99 and HLA-II have been stained in breast tumors, some of them turned out to be important for prognosis and its outcome. CD99 is involved in the intracellular transport of HLA-II proteins. The expression of HLA-II and CD99 molecules has been demonstrated in a broader range of neoplastic tissues, including some epithelial tumors. In the present work, we stained CD99 and HLA-II in breast malignant and non-malignant tissues sections obtained from biopsies resected surgically from 80 Tunisian women. Data implied that CD99 marks malignant tissue significantly as compared to non-malignant breast tissue. HLA-II staining allowed determining the correlation between breast cancer and HLA-II with cytoplasmic localization. CD99 and HLA-II immunostaining was also examined in correlation with two of the most important breast cancer prognostication in routine clinical practice, the lymph node stage and the histological assessment. Results let suggest that CD99+HLA-II–is a marker of worst prognostic since this phenotype is strongly linked to lymph node metastasis in breast cancer.

scholarly journals Reproductive risk factor associations with lobular and ductal carcinoma in the Carolina Breast Cancer Study

2017 ◽  
Vol 29 (1) ◽  
pp. 25-32 ◽  
Author(s):  
Lindsay A. Williams ◽  
Hazel B. Nichols ◽  
Katherine A. Hoadley ◽  
Chiu Kit Tse ◽  
Joseph Geradts ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Risk Factor ◽  
Ductal Carcinoma ◽  
Reproductive Risk ◽  
Cancer Study ◽  
Breast Cancer Study ◽  
Carolina Breast Cancer Study

scholarly journals Hyperglycemia-Induced MIR-467 Drives Tumor Inflammation And Growth In Breast Cancer

2020 ◽  
Author(s):  
Jasmine Gajeton ◽  
Irene Krukovets ◽  
Santoshi Muppala ◽  
Dmitriy Verbovetskiy ◽  
Jessica Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Mouse Models ◽  
Breast Tissue ◽  
Fold Increase ◽  
Normal Breast ◽  
High Blood Glucose ◽  
Novel Mirna ◽  
Malignant Breast Tissue ◽  
Malignant Breast ◽  
Cancer Inflammation

Abstract Background: Tumor microenvironment contains the parenchyma, blood vessels, and infiltrating immune cells, including tumor-associated macrophages (TAMs). TAMs affect the developing tumor and drive cancer inflammation. Methods: We used mouse models of hyperglycemia and cancer and specimens from hyperglycemic breast cancer (BC) patients to demonstrate that miR-467 mediates the effects of high blood glucose on cancer inflammation and growth.Results: Hyperglycemic patients have a higher risk of developing breast cancer (BC). We have identified a novel miRNA-dependent pathway activated by hyperglycemia that promotes BC angiogenesis and inflammation supporting BC growth. miR-467 is upregulated in endothelial cells (EC), macrophages, BC cells, and in BC tumors. A target of miR-467, thrombospondin-1 (TSP-1), inhibits angiogenesis and promotes resolution of inflammation. Systemic injections of a miR-467 antagonist in mouse models of hyperglycemia resulted in decreased BC growth (P<.001). Tumors from hyperglycemic mice had a 2-fold increase in macrophage accumulation compared to normoglycemic controls (P<.001), and TAM infiltration was prevented by the miR-467 antagonist (P<.001). BC specimens from hyperglycemic patients had increased miR-467 levels, increased angiogenesis, decreased levels of TSP-1, and increased TAM infiltration in malignant breast tissue in hyperglycemic vs normoglycemic patients (2.17-fold, P=.002) and even in normal breast tissue from hyperglycemic patients (2.18-fold inc., P=.04). In malignant BC tissue, miR-467 levels were upregulated 258-fold in hyperglycemic patients compared to normoglycemic patients (P<.001) and increased 56-fold in adjacent normal tissue (P=.008). Conclusions: Our results suggest that miR-467 accelerates tumor growth by inducing angiogenesis and promoting the recruitment of TAMs to drive hyperglycemia-induced cancer inflammation.

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