Characterization of human breast cancer tissues by infrared imaging

The Analyst ◽  
2016 ◽  
Vol 141 (2) ◽  
pp. 606-619 ◽  
Author(s):  
M. Verdonck ◽  
A. Denayer ◽  
B. Delvaux ◽  
S. Garaud ◽  
R. De Wind ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Cells ◽  
Breast Tumor ◽  
Human Breast Cancer ◽  
Infrared Imaging ◽  
Human Breast ◽  
Automated Identification ◽  
Breast Tumor Cells ◽  
Cancer Tissues

FTIR imaging allows automated identification and quantification of breast tumor cells as well as investigating tumor-related stroma alterations.

scholarly journals Productive Infection of Human Breast Cancer Cell Lines with Human Cytomegalovirus (HCMV)

Pathogens ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 641
Author(s):  
Kaitlin M. Branch ◽  
Erica C. Garcia ◽  
Yin Maggie Chen ◽  
Matthew McGregor ◽  
Mikayla Min ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Tumor ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Human Breast ◽  
Breast Tumor Cells

Breast cancer is the leading cause of cancer deaths among women worldwide. There are many known risk factors for breast cancer, but the role of infectious disease remains unclear. Human cytomegalovirus (HCMV) is a widespread herpesvirus that usually causes little disease. Because HCMV has been detected in breast tumor biopsy samples and is frequently transmitted via human breast milk, we investigated HCMV replication in breast tumor cells. Four human breast cancer cell lines with different expression profiles for the key diagnostic markers of the estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2), were infected with a bacterial artificial chromosome-derived HCMV clinical strain TB40/E tagged with green fluorescent protein (GFP). Fluorescence microscopy confirmed that all four breast cancer cell lines supported virus entry. RNA was isolated from infected cells and the expression of immediate early (UL123), early (UL54), and late (UL111A) genes was confirmed using PCR. Viral proteins were detected by immunoblotting, and viral progeny were produced during the infection of breast tumor cells, as evidenced by subsequent infection of fibroblasts with culture supernatants. These results demonstrate that breast tumor cells support productive HCMV infection and could indicate that HCMV replication may play a role in breast cancer progression.

scholarly journals Characterization of p53-mediated Up-regulation of CD95 Gene Expression upon Genotoxic Treatment in Human Breast Tumor Cells

2003 ◽  
Vol 278 (34) ◽  
pp. 31667-31675 ◽  
Author(s):  
Carmen Ruiz-Ruiz ◽  
Gema Robledo ◽  
Eva Cano ◽  
Juan Miguel Redondo ◽  
Abelardo Lopez-Rivas
Keyword(s):  
Gene Expression ◽  
Tumor Cells ◽  
Breast Tumor ◽  
Human Breast ◽  
Human Breast Tumor ◽  
Breast Tumor Cells

Abstract A34: Characterization of tumor infiltrating lymphocytes in human breast cancer by infrared imaging

2015 ◽  
Author(s):  
Magali Verdonck ◽  
Soizic Garaud ◽  
Laurence Buisseret ◽  
Hugues Duvillier ◽  
Christine Desmedt ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
Infrared Imaging ◽  
Tumor Infiltrating Lymphocytes ◽  
Human Breast ◽  
Infiltrating Lymphocytes

scholarly journals Interactions between estrogen and insulin-like growth factor signaling pathways in human breast tumor cells.

2003 ◽  
pp. 331-345 ◽  
Author(s):  
I H L Hamelers ◽  
P H Steenbergh
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Signaling Pathways ◽  
Breast Tumor ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Synergistic Effects ◽  
Human Breast ◽  
Breast Tumor Cells ◽  
Igf I

Estrogens and insulin-like growth factors (IGFs) act as mitogens promoting cell proliferation in normal breast tissue as well as in breast carcinomas. Both hormones have been shown to play a role in the development of breast cancer and were found to activate multiple signaling pathways leading to proliferation of human breast cancer cell lines in vitro. Originally, it was considered that these agents manifest their mitogenic actions through separate pathways, but a growing body of evidence suggests that the IGF- and estrogen-mediated signaling pathways are intertwined. 17beta-Estradiol (E2) has been shown to enhance IGF signaling at multiple levels. E2 treatment of breast cancer cells alters expression of nearly all of the IGF family members including IGF-I, IGF-II, IGF-binding proteins, IGF type I receptor (IGF-RI), and insulin receptor substrate 1. The ligand-bound estrogen receptor has been reported to bind to and to activate the IGF-RI directly. Vice versa, IGF signaling has been reported to enhance estrogen receptor activation in human breast cancer cells by inducing phosphorylation of the estrogen receptor. Finally, several groups have described synergistic effects of the combination of E2 and IGF-I on S phase entry in breast tumor cell lines. Here, we review recent, often contradictory, reports describing the effects of E2 and IGFs on the proliferation of breast tumor cells, with special emphasis on the synergistic effects of the two hormones.

scholarly journals Atorvastatin Inhibits Breast Cancer Cells by Downregulating PTEN/AKT Pathway via Promoting Ras Homolog Family Member B (RhoB)

2019 ◽  
Vol 2019 ◽  
pp. 1-15 ◽  
Author(s):  
Qing Ma ◽  
Yang Gao ◽  
Pei Xu ◽  
Kai Li ◽  
Xiaolong Xu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Family Member ◽  
Tumor Cells ◽  
Breast Tumor ◽  
Breast Cancer Cells ◽  
Akt Pathway ◽  
Altered Expression ◽  
Breast Tumor Cells ◽  
Cancer Tissues

Background. Breast cancer (BC) is one of the most common malignant tumors in women around the world. Atorvastatin (ATO) was found to be associated with a decreased risk of recurrence and mortality in cancer. But the exact mechanism of its carcinostatic effects is unclear. The expression level of Ras homolog family member B (RhoB) in breast cancer cells was found to be upregulated after being treated with ATO. Thus, we conjecture that altered expression of RhoB induced by ATO may be decisive for the migration and progression of breast cancer. Methods. The effects of ATO on breast tumor cells in vivo and in vitro were detected by clone formation assay, CCK-8 assay, flow cytometry, wound healing, transwell assays, tumor xenograft model, and immunohistochemistry. Distribution of RhoB in different breast cancer tissues and its influence on prognosis were analyzed using the data from TCGA or GEO databases. The relationship between RhoB and PTEN/AKT pathway was detected by Western blotting and RT-qPCR. Results. ATO inhibits proliferation, invasion, EMT, and PTEN/AKT pathway and promotes apoptosis in breast tumor cells. In addition, ATO inhibits the volume and weight of breast tumor in tumor-bearing mice and upregulated RhoB in tumor tissues. The expression of RhoB in mRNA and protein level was upregulated in statin-treated breast cancer cells and downregulated in cancer tissues. Low expression of RhoB links with poor prognosis in patients with breast cancer (HR = 0.74[0.66–0.83], p =7e−8, log-rank test). Further research found that RhoB inhibits the proliferation, invasion, EMT, and PTEN/AKT signal pathway in breast tumor cells. Conclusions. The exact mechanism of ATO’s carcinostatic effects in breast cancer is related to downregulating PTEN/AKT pathway via promoting RhoB. Our study also demonstrates the potential applicability of RhoB as a therapeutic target for breast cancer.

Expression of thyroid-stimulating hormone receptor, octamer-binding transcription factor 4, and intracisternal A particle-promoted polypeptide in human breast cancer tissues

2012 ◽  
Vol 9 (3) ◽  
Author(s):  
Vijayakumar Govindaraj ◽  
Nirmala Singh Yaduvanshi ◽  
Harish Krishnamachar ◽  
A. Jagannadha Rao
Keyword(s):  
Breast Cancer ◽  
Hormone Receptor ◽  
Breast Tumor ◽  
Human Breast Cancer ◽  
Thyroid Stimulating Hormone ◽  
Normal Breast ◽  
Human Breast ◽  
Glycoprotein Hormone ◽  
Cancer Tissues ◽  
Stimulating Hormone

AbstractThyroid-stimulating hormone receptor (TSHR) is one of the members of glycoprotein hormone receptor family; activation of TSHR by thyroid-stimulating hormone (TSH) regulates thyroid function, proliferation, and differentiation. The other family members of glycoprotein hormone receptors, such as leutinizing hormone receptor (LHR), human chorionic gonadotropin (hCG), and follicle-stimulating hormone (FSH) are known to be expressed in nonendocrine tissues including human breast cancer and regulate proliferation and differentiation. The involvement of thyroid hormones in the growth and differentiation of normal breast tissue is well documented. However, the presence of TSHR in breast cancer has not been demonstrated. The aim of the present study was to establish the expression pattern of TSHR along with transcription factors, such as octamer 4 (OCT4) and intracisternal A particle-promoted polypeptide (IPP) in human breast tumor.For this study, patients with stages I–III breast cancers and adjacent noncancerous tissues were prospectively accrued and analyzed. We employed semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analysis to determine the expression levels of TSHR in normal and human breast cancer tissues.The results indicated that a significant increase in TSHR expression was observed in tumor tissues compared to normal breast tissues. RT-PCR analysis of OCT4 and IPP also revealed a significant increase in breast tumor tissues over the controls.To our knowledge, this is the first report demonstrating expression of TSHR and IPP in normal breast and breast tumors. The expression of TSHR, IPP, and OCT4 increased in the human breast tumor samples over the noncancer tissues. However, further studies are needed to establish an unequivocal role for TSHR in breast tumor progression.

scholarly journals Characterization of Tumor Infiltrating Lymphocytes in Human Breast Cancer by Infrared Imaging

2014 ◽  
Vol 25 ◽  
pp. i19
Author(s):  
M. Verdonck ◽  
S. Garaud ◽  
L. Buisseret ◽  
H. Duvillier ◽  
C. Desmedt ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
Infrared Imaging ◽  
Tumor Infiltrating Lymphocytes ◽  
Human Breast ◽  
Infiltrating Lymphocytes

On the Cytotoxicity of Chiral Ruthenium Complexes Containing Sulfur Amino Acids Against Breast Tumor Cells (MDA-231 and MCF-7)

2020 ◽  
Vol 20 ◽  
Author(s):  
Celisnolia M. Leite ◽  
João Honorato de Araujo-Neto ◽  
Rodrigo S. Corrêa ◽  
Legna Colina-Vegas ◽  
Diego Martínez-Otero ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Amino Acids ◽  
Tumor Cells ◽  
Cell Lines ◽  
Breast Tumor ◽  
Human Breast Cancer ◽  
Ruthenium Complexes ◽  
Sulfur Amino Acids ◽  
Human Breast ◽  
Mcf 7

Background: Breast cancer is one of the most common types among women. Its incidence progressively increases with age, especially after age 50. Platinum compounds are not efficient in the treatment of breast cancer, highlighting the use of other metals for the development of new chemotherapeutic agents. Objective: This paper aims to obtain three new ruthenium compounds that incorporate sulfur amino acids in their structures and to investigate their cytotoxic activity in breast tumor cell lines. Methods: Complexes with general formula [Ru(AA)(dppb)(bipy)] (complexes 1 and 2) or [Ru(AA)(dppb)(bipy)]PF6 (complex 3), where AA = L-cysteinate (1), D-penicillaminate (2), and L-deoxyalliinate (3), dppb = 1,4- bis(diphenylphosphino)butane and 2,2´-bipyridine, were obtained from the cis-[RuCl2(dppb)(bipy)] precursor. The cytotoxicity of the complexes on MDA-MB-231 (triple negative human breast cancer); MCF-7 (double positive human breast cancer) and V79 (hamster lung fibroblast) were performed by the MTT (4,5-dimethylthiazol-2-yl-2,5- diphenyltetrazolium bromide) method. The control agent was the cisplatin, which is a commercially available drug for cancer treatment. Results: In complexes (1) and (2), the ligands are coordinated to the metal center by nitrogen and sulfur atoms, while in complex (3) coordination is through the oxygen and nitrogen atoms. These suggestions are based on the infrared and 31P1H NMR data. For complexes (1) and (2), their X-ray structures were determined confirming this suggestion. The three complexes are stable in a mixture of DMSO (80 %) and biological medium (20 %) for at least 48 h and presented cytotoxicity against the MDA-MB-231 and MCF-7 tumor cells with reasonable selectivity indexes. Conclusion: Our work demonstrated that ruthenium complexes containing sulfur amino acids, bipyridines and bisphosphines showed cytotoxicity against the MDA-MB-231 and MCF-7 cancer cell lines, in vitro, and that they interact weakly with the DNA (Deoxyribonucleic Acid) and the HSA (Human Serum Albumin) biomolecules.

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