Normal Breast Stem Cells, Malignant Breast Stem Cells, and the Perinatal Origin of Breast Cancer

2006 ◽  
Vol 2 (2) ◽  
pp. 103-110
Author(s):  
Todd M. Savarese ◽  
Hoi Pang Low ◽  
Inkyung Baik ◽  
William C. Strohsnitter ◽  
Chung-Cheng Hsieh
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Normal Breast ◽  
Breast Stem Cells ◽  
Malignant Breast

Normal breast stem cells, malignant breast stem cells, and the perinatal origin of breast cancer

2006 ◽  
Vol 2 (2) ◽  
pp. 103-109 ◽  
Author(s):  
Todd M. Savarese ◽  
Hoi Pang Low ◽  
Inkyung Baik ◽  
William C. Strohsnitter ◽  
Chung-Cheng Hsieh
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Normal Breast ◽  
Breast Stem Cells ◽  
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.

Bone Marrow Mesenchymal Stem Cells: Pre-Metastatic Niche For Breast Cancer

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 4859-4859 ◽  
Author(s):  
Leonardo Julio Feldman ◽  
Valeria B. Fernández Vallone ◽  
Hosoon Choi ◽  
Vivian Labovsky ◽  
Leandro M Martinez ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Bone Marrow ◽  
Primary Tumor ◽  
Tumor Tissue ◽  
T Test ◽  
Malignant Breast ◽  
Migration Capacity ◽  
Breast Tissues ◽  
Lower Expression

It has been described that the hematopoietic niche has to be considered as a dynamic system that could easily behave as a tumor niche because they share many structural and functional components. Bone marrow (BM) mesenchymal stem cells (MSC) are one of the actors that regulate homing, migration, proliferation and survival, quiescence and latency of hematopoietic SC or tumor cells. Since one of the chosen sites for breast cancer (BC) metastasis is BM/bone, we have been trying for many years to address how BM´s MSC could play a role as permissive promoters of this type of metastasis. In this regard, we have previously described that BM-MSC from untreated advanced BC patients, without BM/bone metastasis (BCP), had lower cloning efficiency to give fibroblast colony forming units (CFU-F), lower plasticity capacity towards osteogenic and adipogenic lineages as well as lower capacity to regulate the hematopoietic process. CD146 expression over MSC/osteoprogenitors is diminished while they are enriched in CD49b. These last observations added to lower expression of VCAM-1 and lower levels of SDF-1 released by patient´s MSC plus the lower expression of phosphorylated β-catenin could be related to their poor transmigration capacity and so higher retention in BM. We tried, then, to analyze the migration capacity of BM-MSC of untreated advanced BCP (infiltrative ductal carcinoma, IIIB clinical stage) compared to those coming from healthy volunteers (HV) and the possible factors that influence it. Finally, since these MSC are the ones remaining in BM after the development of the primary tumor and could act as tumor niche we investigated how capable are those for tumor cells recruitment. Materials and Methods BCP (n=5) were in menopause with an age range between 50-65 years old. Patients were free of metabolic bone disease, such as vitamin D deficiency, thyroid disease, parathyroid disease or kidney damage. HV (n=6) were healthy females adult bone marrow donors for allogeneic BM transplantation. BM aspirates, peripheral blood plasma (PBP) and primary tumor tissue biopsies were used for this work. All individuals gave consent prior to participating in these studies. The investigations were approved by the IBYME Ethical Committee and performed in accordance with the principles of the Helsinki Declaration. Transwell co-culture assays were performed to observe BM-MSC migration capacity towards BC cells (human lines: MDA-MB231 and MCF-7) and vice versa. ELISA and immunohistochemistry assays were done to study the factors and receptors implicated in the process. IHC studies were carry out on paraffin blocks from 5 primary tumor tissue biopsies of these BCP and 5 non-malignant breast tissues. The controls “non- malignant” tissue were breast biopsies from women who had negative results of BC (non-neoplastic breast tissue). Also these women were in menopause and did not present compromise in their BM and bone metabolism. Results BM-MSC from BCP showed lower migration capacity towards both BC cell lines compared with MSC from HV. These observations could be related to the lower levels (mean±SE, pg/ml) of SDF-1 (54 ± 28 and 117 ± 25; unpaired t-test, p<0.05) and G-CSF (250 ± 113 and 1076 ± 325; unpaired t-test, p<0.05) as well as high levels of MIF (4,564±591 and 2,265±402; unpaired t-test, p<0.05) found in PBP from BCP compared with HV. Both type of BC cells migrated in higher proportion towards MSC from BCP than those from HV. The higher migration % was significant for the more invasive line MDA-MB231 (Mann Whitney test, p= 0.0159). These last observations could be related to the higher expression of membrane RANKL and IL-6 observed in BM-MSC of BCP respect to HV and the presence of its correspondent receptors in epithelial localization seen over primary breast tumor biopsies from advanced BCP compared with non-malignant breast tissues. Conclusion These findings suggest that early therapeutic intervention may be required to oppose the tumor-induced changes to the BM-MSC and haematopoietic microenvironment, and thus, future bone metastatic development Disclosures: No relevant conflicts of interest to declare.

scholarly journals MicroRNA93 Regulates Proliferation and Differentiation of Normal and Malignant Breast Stem Cells

PLoS Genetics ◽  
2012 ◽  
Vol 8 (6) ◽  
pp. e1002751 ◽  
Author(s):  
Suling Liu ◽  
Shivani H. Patel ◽  
Christophe Ginestier ◽  
Ingrid Ibarra ◽  
Rachel Martin-Trevino ◽  
...  
Keyword(s):  
Stem Cells ◽  
Proliferation And Differentiation ◽  
Breast Stem Cells ◽  
Malignant Breast

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 Immunohistochemical Expression of p63 in Benign and Malignant Breast Lesions

2021 ◽  
Author(s):  
Abhishek Saini ◽  
Swaran Kaur Saluja ◽  
MK Garg ◽  
Deepti Agarwal ◽  
Amrita Kulhria ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Myoepithelial Cells ◽  
Normal Breast ◽  
High Morbidity ◽  
Breast Lesions ◽  
Benign Lesions ◽  
Medical College ◽  
Malignant Breast ◽  
Malignant Lesions

Introduction: Breast carcinoma demands attention as it causes high morbidity and mortality. It is important to recognise benign lesions to distinguish them from in situ and invasive breast cancer and to assess a patient’s risk of developing breast cancer, so that the most appropriate treatment modality for each case can be established. The p63 has been characterised as a reliable marker of myoepithelial cells of lactiferous duct. It is exclusively expressed in myoepithelial cells of normal breast tissue. Hence, p63 can be of great help in the differential diagnosis involving benign lesions. Also, p63 may aid in distinguishing benign from malignant lesions. Aim: To study the Immunohistochemistry (IHC) expression of p63 in benign and malignant breast lesions. Materials and Methods: The prospective study was conducted on 76 breast specimens for a period of one year, from 1st December 2018 to 30th November 2019 in the Department of Pathology, Bhagat Phool Singh, Government Medical College for Women, Khanpur Kalan, Sonepat, Haryana, India. IHC assessment for p63 nuclear protein was performed. The intensity of p63 expression was evaluated as continuous positive, discontinuous positive and negative. The extent was scored on the basis of percentage of positive cells and assigned a score of negative (0%), 1 (<25%), 2 (26-90%) and 3 (91-100%). Results: Out of 76 cases, 38 cases were diagnosed as benign and 38 cases as malignant. IHC staining with p63 showed nuclear positivity in all benign lesions. Among malignant lesions, four were positive and 34 were negative. Conclusion: According to the above results, p63 is a very useful IHC marker in diagnosing difficult cases, cases of carcinoma in situ, borderline cases and cases with inconclusive histomorphological diagnosis.

scholarly journals Cancer Stem Cells and Somatic Stem Cells as Potential New Drug Targets, Prognosis Markers, and Therapy Efficacy Predictors in Breast Cancer Treatment

Biomedicines ◽  
2021 ◽  
Vol 9 (9) ◽  
pp. 1223
Author(s):  
Olga Pershina ◽  
Natalia Ermakova ◽  
Angelina Pakhomova ◽  
Darius Widera ◽  
Edgar Pan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Tumor Cells ◽  
Drug Targets ◽  
Breast Tissue ◽  
Normal Breast Tissue ◽  
Normal Breast ◽  
Epithelial Tumor

New drug targets, markers of disease prognosis, and more efficient treatment options are an unmet clinical need in breast cancer (BC). We have conducted a pilot study including patients with luminal B stage breast cancer IIA–IIIB. The presence and frequency of various populations of cancer stem cells (CSC) and somatic stem cells were assessed in the blood, breast tumor tissue, and normal breast tissue. Our results suggest that patients with BC can be divided into two distinct groups based on the frequency of aldehyde dehydrogenase positive cells (ALDH1+ cells) in the blood (ALDH1hi and ALDH1low). In the ALDH1hi cells group, the tumor is dominated by epithelial tumor cells CD44+CD24low, CD326+CD44+CD24−, and CD326−CD49f+, while in the ALDH1low cells group, CSCs of mesenchymal origin and epithelial tumor cells (CD227+CD44+CD24− and CD44+CD24−CD49f+) are predominant. In vitro CSCs of the ALDH1low cells group expressing CD326 showed high resistance to cytostatics, CD227+ CSCs of the ALDH1hi cells group are sensitive to cytostatics. Epithelial precursors of a healthy mammary gland were revealed in normal breast tissue of patients with BC from both groups. The cells were associated with a positive effect of chemotherapy and remission in BC patients. Thus, dynamic control of their presence in blood and assessment of the sensitivity of CSCs to cytostatics in vitro can improve the effectiveness of chemotherapy in BC.

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