GalNAc glycoprotein expression by breast cell lines, primary breast cancer and normal breast epithelial membrane

Nine malignant breast epithelial cell lines and 3 normal breast cell lines were examined for stress fiber formation and expression of TPM1 isoform-specific RNAs and proteins. Stress fiber formation was strong (++++) in the normal cell lines and varied among the malignant cell lines (negative to +++). Although TPM1γand TPM1δwere the dominant transcripts ofTPM1, there was no clear evidence for TPM1δprotein expression. Four novel human TPM1 gene RNA isoforms were discovered (λ,μ,ν, andξ), which were not identified in adult and fetal human cardiac tissues. TPM1λwas the most frequent isoform expressed in the malignant breast cell lines, and it was absent in normal breast epithelial cell lines. By western blotting, we were unable to distinguish between TPM1γ,λ, andνprotein expression, which were the only TPM1 gene protein isoforms potentially expressed. Some malignant cell lines demonstrated increased or decreased expression of these isoforms relative to the normal breast cell lines. Stress fiber formation did not correlate with TPM1γRNA expression but significantly and inversely correlated with TPM1δand TPM1λexpression, respectively. The exact differences in expression of these novel isoforms and their functional properties in breast epithelial cells will require further study.

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bFGF and aFGF induce membrane ruffling in breast cancer cells but not in normal breast epithelial cells: FGFR-4 involvement

Biochemical Journal ◽

10.1042/bj3060609 ◽

1995 ◽

Vol 306 (2) ◽

pp. 609-616 ◽

Cited By ~ 29

Author(s):

C L Johnston ◽

H C Cox ◽

J J Gomm ◽

R C Coombes

Keyword(s):

Breast Cancer ◽

Growth Factors ◽

Epithelial Cells ◽

Cell Lines ◽

Physiological Role ◽

Normal Breast ◽

Breast Cancer Cell Lines ◽

Breast Epithelial Cells ◽

Membrane Ruffling ◽

Breast Epithelial

Acidic and basic fibroblast growth factors (aFGF and bFGF) are growth factors which may have a physiological role in the normal breast and in breast cancer. A study of the effects of aFGF and bFGF on a variety of breast cell lines and epithelial cells purified from normal breast organoids showed that whereas normal breast cells did not exhibit membrane ruffling in response to either of these growth factors, some breast cancer cell lines did. This difference was not due to lack of receptor since all the cell lines tested were mitogenically stimulated by bFGF. Dominant negative mutations of FGF receptor 3 (FGFR-3) and the small GTP-binding protein p21rac inhibited membrane ruffling, showing that receptor dimerization and phosphorylation and p21rac activation are prerequisites for membrane ruffling in response to aFGF and bFGF. Transient transfection of individual FGFRs into cos-7 cells showed that FGFR-1, FGFR-2 and FGFR-3 could not mediate a membrane ruffling response whereas FGFR-4 could. These studies elucidate one signalling mechanism of FGF and point to differences in the response of normal and cancer breast epithelial cells which may be important in cell motility.

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Ezrin expression in primary breast cancer, metastatic lymph nodes and normal breast tissue

Geburtshilfe und Frauenheilkunde ◽

10.1055/s-0030-1254964 ◽

2010 ◽

Vol 70 (05) ◽

Author(s):

D Gschwantler-Kaulich ◽

C Natter ◽

S Steurer ◽

I Walter ◽

C Singer

Keyword(s):

Breast Cancer ◽

Lymph Nodes ◽

Primary Breast Cancer ◽

Breast Tissue ◽

Normal Breast Tissue ◽

Normal Breast ◽

Metastatic Lymph Nodes ◽

Metastatic Lymph ◽

Ezrin Expression

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

Oncogene ◽

10.1038/sj.onc.1207100 ◽

2003 ◽

Vol 22 (48) ◽

pp. 7600-7606 ◽

Cited By ~ 108

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

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Growth inhibition and induction of phenotypic alterations by tiazofurin: Differential effects on MCF-7 breast cancer and HBL-100 breast cell lines

European Journal of Cancer and Clinical Oncology ◽

10.1016/0277-5379(89)90136-3 ◽

1989 ◽

Vol 25 (5) ◽

pp. 883-889 ◽

Cited By ~ 10

Author(s):

Y. Sidi ◽

E. Beery ◽

C. Panet ◽

L. Wasserman ◽

A. Novogrodsky ◽

...

Keyword(s):

Breast Cancer ◽

Growth Inhibition ◽

Cell Lines ◽

Differential Effects ◽

Breast Cell Lines ◽

Mcf 7

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Targeted next-generation sequencing assays using triplet samples of normal breast tissue, primary breast cancer, and recurrent/metastatic lesions

10.21203/rs.2.16536/v3 ◽

2020 ◽

Author(s):

Toshiaki Akahane ◽

Naoki Kanomata ◽

Oi Harada ◽

Tetsumasa Yamashita ◽

Junichi Kurebayashi ◽

...

Keyword(s):

Breast Cancer ◽

Primary Tumor ◽

Primary Breast Cancer ◽

Breast Tissue ◽

Normal Breast Tissue ◽

Metastatic Breast ◽

Normal Breast ◽

Human Breast ◽

Metastatic Lesions ◽

Generation Sequencing

Abstract Background: Next-generation sequencing (NGS) has shown that recurrent/metastatic breast cancer lesions may have additional genetic changes compared with the primary tumor. These additional changes may be related to tumor progression and/or drug resistance. However, breast cancer-targeted NGS is not still widely used in clinical practice to compare the genomic profiles of primary breast cancer and recurrent/metastatic lesions.Methods: Triplet samples of genomic DNA were extracted from each patient’s normal breast tissue, primary breast cancer, and recurrent/metastatic lesion(s). A DNA library was constructed using the QIAseq Human Breast Cancer Panel (93 genes, Qiagen) and then sequenced using MiSeq (Illumina). The Qiagen web portal was utilized for data analysis.Results: Successful results for three or four samples (normal breast tissue, primary tumor, and at least one metastatic/recurrent lesion) were obtained for 11 of 35 breast cancer patients with recurrence/metastases (36 samples). We detected shared somatic mutations in all but one patient, who had a germline mutation in TP53. Additional mutations that were detected in recurrent/metastatic lesions compared with primary tumor were in genes including TP53 (three patients) and one case each of ATR, BLM, CBFB, EP300, ERBB2, MUC16, PBRM1, and PIK3CA. Actionable mutations and/or copy number variations (CNVs) were detected in 73% (8/11) of recurrent/metastatic breast cancer lesions.Conclusions: The QIAseq Human Breast Cancer Panel assay showed that recurrent/metastatic breast cancers sometimes acquired additional mutations and CNV. Such additional genomic changes could provide therapeutic target.

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The role of low keV virtual monochromatic imaging in increasing the conspicuity of primary breast cancer in dual-energy spectral thoracic CT examination for staging purposes

Acta Radiologica ◽

10.1177/0284185119858040 ◽

2019 ◽

Vol 61 (2) ◽

pp. 168-174 ◽

Cited By ~ 3

Author(s):

Yavuz Metin ◽

Nurgül Orhan Metin ◽

Oğuzhan Özdemir ◽

Filiz Taşçı ◽

Sibel Kul

Keyword(s):

Breast Cancer ◽

Primary Breast Cancer ◽

Breast Tissue ◽

Normal Breast Tissue ◽

Energy Levels ◽

Iodine Content ◽

Pectoral Muscle ◽

Dual Energy ◽

Normal Breast

Background The additive value of dual-energy spectral computerized tomography (DESCT) in breast cancer imaging is still unknown. Purpose To investigate the role of DESCT in improving the conspicuity of primary breast cancer. Material and Methods Twenty-nine patients who were histopathologically diagnosed with breast cancer and underwent DESCT for staging of lung metastasis were evaluated retrospectively. The visual conspicuity of breast cancer was scored by two readers separately in reconstructed virtual monochromatic images obtained at 40, 60, 80, and 100 keV. A circular region of interest slightly smaller than the maximum contrasted portion of the primary breast cancer was manually placed. Iodine enhancement (HU) and iodine content (mg/mL) values of tumor, normal breast tissue and pectoral muscle, and contrast-to-noise values of images at four different energy levels were calculated. Results The lesion conspicuity score peaked at 40-keV series for both readers and was significantly higher than those at other energy levels (all P < 0.001). Lesion iodine enhancement was highest at 40-keV virtual monochromatic image reconstructions ( P < 0.001). The iodine content was significantly higher in tumor than normal breast tissue, and pectoral muscle ( P < 0.001). The highest contrast-to-noise value was obtained at 60 keV (4.0 ± 2.5), followed by 40 keV (3.9 ± 2.2), without a significant difference ( P = 0.33). Conclusion The conspicuity of primary breast cancer was significantly higher in low keV virtual monochromatic images obtained by DESCT. This gives us hope that DESCT may play an effective role in detecting incidental breast lesions. It also raises the question of whether quantitative values obtained by DESCT can be used for characterization of primary breast lesion.

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Quantification of prolactin receptor mRNA in multiple human tissues and cancer cell lines by real time RT-PCR

Journal of Endocrinology ◽

10.1677/joe.0.171r001 ◽

2001 ◽

Vol 171 (1) ◽

pp. R1-R4 ◽

Cited By ~ 62

Author(s):

SK Peirce ◽

WY Chen ◽

WY Chen

Keyword(s):

Breast Cancer ◽

Prostate Cancer ◽

Cell Lines ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Cancer Cell Lines ◽

Normal Breast ◽

Breast Cancer Cell Lines ◽

Human Tissues ◽

Normal Human

Human prolactin (hPRL) has been reported to be involved in breast and prostate cancer development. The hPRL receptor (hPRLR) is expressed in a wide variety of tissues in at least three isoforms. In this study, a one-step real time reverse transcription PCR technique was used to determine relative expression levels of hPRLR mRNA in eleven human breast cancer cell lines, HeLa cells, three prostate cancer cell lines and nine normal human tissues. The housekeeping gene beta-actin was used for internal normalization. We demonstrate that hPRLR mRNA is up-regulated in six of the eleven breast cancer cell lines tested when compared with normal breast tissue. Of the cancer cell lines tested, we found that T-47D cells have the highest level of hPRLR mRNA, followed by MDA-MB-134, BT-483, BT-474, MCF-7 and MDA-MB-453 cells. In two breast cancer cell lines (MDA-MB-468 and BT-549), the hPRLR levels were found to be comparable to that of normal breast tissue. Three breast cancer cell lines (MDA-MB-436, MDA-MB-157 and MDA-MB-231) expressed hPRLR mRNA at levels lower than that of normal tissue. In contrast, in all three commonly used prostate cancer cell lines (LNCaP, PC-3 and DU 145), the levels of hPRLR mRNA were found to be down-regulated relative to that of normal prostate tissue. Of nine normal human tissues tested, we found that the uterus and the breast have the highest levels of hPRLR mRNA, followed by the kidney, the liver, the prostate and the ovary. The levels of hPRLR mRNA were the lowest among the trachea, the brain and the lung.

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Bringing androgens up a NOTCH in breast cancer

Endocrine Related Cancer ◽

10.1530/erc-14-0248 ◽

2014 ◽

Vol 21 (4) ◽

pp. T183-T202 ◽

Cited By ~ 19

Author(s):

Gerard A Tarulli ◽

Lisa M Butler ◽

Wayne D Tilley ◽

Theresa E Hickey

Keyword(s):

Breast Cancer ◽

Epithelial Cells ◽

Normal Breast ◽

Notch Signalling ◽

Breast Development ◽

Breast Epithelium ◽

Breast Epithelial Cells ◽

Androgen Action ◽

Breast Epithelial

While it has been known for decades that androgen hormones influence normal breast development and breast carcinogenesis, the underlying mechanisms have only been recently elucidated. To date, most studies have focused on androgen action in breast cancer cell lines, yet these studies represent artificial systems that often do not faithfully replicate/recapitulate the cellular, molecular and hormonal environments of breast tumoursin vivo. It is critical to have a better understanding of how androgens act in the normal mammary gland as well as inin vivosystems that maintain a relevant tumour microenvironment to gain insights into the role of androgens in the modulation of breast cancer development. This in turn will facilitate application of androgen-modulation therapy in breast cancer. This is particularly relevant as current clinical trials focus on inhibiting androgen action as breast cancer therapy but, depending on the steroid receptor profile of the tumour, certain individuals may be better served by selectively stimulating androgen action. Androgen receptor (AR) protein is primarily expressed by the hormone-sensing compartment of normal breast epithelium, commonly referred to as oestrogen receptor alpha (ERa (ESR1))-positive breast epithelial cells, which also express progesterone receptors (PRs) and prolactin receptors and exert powerful developmental influences on adjacent breast epithelial cells. Recent lineage-tracing studies, particularly those focussed on NOTCH signalling, and genetic analysis of cancer risk in the normal breast highlight how signalling via the hormone-sensing compartment can influence normal breast development and breast cancer susceptibility. This provides an impetus to focus on the relationship between androgens, AR and NOTCH signalling and the crosstalk between ERa and PR signalling in the hormone-sensing component of breast epithelium in order to unravel the mechanisms behind the ability of androgens to modulate breast cancer initiation and growth.

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