Canine mammary cancer tumour behaviour and patient survival time are associated with collagen fibre characteristics

AbstractPrecise diagnosis and prognosis are key in prevention and reduction of morbidity and mortality in all types of cancers. Here we show that changes in the collagen fibres in the main histological subtypes of canine mammary gland carcinomas are directly associated with the tumour behaviour and the animal survival time and could become a useful tool in helping with diagnosis. Imaging by second harmonic generation and multiphoton excited fluorescence microscopy were performed to evaluate the collagen and cellular segment parameters in cancer biopsies. We present a retrospective study of 45 cases of canine mammary cancer analysing 836 biopsies regions including normal mammary gland tissue, benign mixed tumours, carcinoma in mixed tumour, carcinosarcoma, micropapillary carcinoma and solid carcinoma. The image analyses and the comparison between the tumour types allowed to assess the collagen fibre changes during tumour progression. We demonstrate that the collagen parameters correlate with the clinical and pathological data, the results show that in neoplastic tissues, the collagen fibres are more aligned and shorter as compared to the normal tissues. There is a clear association of the mean fibre length with the dogs survival times, the carcinomas presenting shorter collagen fibres indicate a worse survival rate.

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Malignancy Associated MicroRNA Expression Changes in Canine Mammary Cancer of Different Malignancies

ISRN Veterinary Science ◽

10.1155/2014/148597 ◽

2014 ◽

Vol 2014 ◽

pp. 1-5 ◽

Cited By ~ 9

Author(s):

Marie-Charlotte von Deetzen ◽

Bernd T. Schmeck ◽

Achim D. Gruber ◽

Robert Klopfleisch

Keyword(s):

Mammary Gland ◽

Lymph Node ◽

Mirna Expression ◽

Mammary Cancer ◽

Normal Mammary Gland ◽

Primary Tumors ◽

Normal Gland ◽

Metastatic Cells ◽

Node Metastases ◽

Nucleolar Rna

MicroRNA has been suspected to be generally involved in carcinogenesis since their first description. A first study supported this assumption for canine mammary tumors when miRNA expression was compared to normal gland. The present study extends these results by comparing the expression of 16 microRNA (miRNA) and 4 small nucleolar RNA (snoRNA) in tumors of different malignancy, for example, adenomas, nonmetastasizing and metastasizing carcinomas as well as lymph node metastases, with each other and with normal mammary gland. All neoplastic tissues differed in their miR-210 expression levels from normal gland. While metastatic cells differed in their expression of mir-29b, miR-101, mir-125a, miR-143, and miR-145 from primary tumors, the comparison of miRNA expression in primary tumors of different malignancy failed to reveal significant differences except for a significant downregulation of mir-125a in metastasizing carcinomas when compared to adenomas.

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Cadherin Cell Adhesion System in Canine Mammary Cancer: A Review

Veterinary Medicine International ◽

10.1155/2012/357187 ◽

2012 ◽

Vol 2012 ◽

pp. 1-8 ◽

Cited By ~ 10

Author(s):

Adelina Gama ◽

Fernando Schmitt

Keyword(s):

Cell Adhesion ◽

Adhesion Molecules ◽

Mammary Cancer ◽

Current Knowledge ◽

Tumour Progression ◽

Biological Functions ◽

Canine Mammary Cancer ◽

Organ Systems ◽

Adhesion System

Cadherin-catenin adhesion complexes play important roles by providing cell-cell adhesion and communication in different organ systems. Abnormal expression of cadherin adhesion molecules constitutes a common phenomenon in canine mammary cancer and has been frequently implicated in tumour progression. This paper summarizes the current knowledge on cadherin/catenin adhesion molecules (E-cadherin,β-catenin, and P-cadherin) in canine mammary cancer, focusing on the putative biological functions and clinical significance of these molecules in this disease. This paper highlights the need for further research studies in this setting in order to elucidate the role of these adhesion molecules during tumour progression and metastasis.

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Dual recombinase action in the normal and neoplastic mammary gland epithelium

Scientific Reports ◽

10.1038/s41598-021-00231-8 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Patrick D. Rädler ◽

Kerry Vistisen ◽

Aleata A. Triplett ◽

Rayane Dennaoui ◽

Yong Li ◽

...

Keyword(s):

Mammary Gland ◽

Epithelial Cells ◽

Cancer Cells ◽

Mammary Cancer ◽

Gene Activation ◽

Metastatic Tumor ◽

Mammary Tumors ◽

Lineage Tracing ◽

Normal Mammary Gland ◽

Transgenic Mouse Line

AbstractWe developed a transgenic mouse line that expresses the codon-optimized Flp recombinase under the control of the MMTV promoter in luminal epithelial cells of the mammary gland. In this report, we demonstrate the versatile applicability of the new MMTV-Flp strain to manipulate genes in a temporally and spatially controlled manner in the normal mammary gland, in luminal-type mammary tumors that overexpress ERBB2, and in a new KRAS-associated mammary cancer model. Although the MMTV-Flp is expressed in a mosaic pattern in the luminal epithelium, the Flp-mediated activation of a mutant KrasG12D allele resulted in basal-like mammary tumors that progressively acquired mesenchymal features. Besides its applicability as a tool for gene activation and cell lineage tracing to validate the cellular origin of primary and metastatic tumor cells, we employed the MMTV-Flp transgene together with the tamoxifen-inducible Cre recombinase to demonstrate that the combinatorial action of both recombinases can be used to delete or to activate genes in established tumors. In a proof-of-principle experiment, we conditionally deleted the JAK1 tyrosine kinase in KRAS-transformed mammary cancer cells using the dual recombinase approach and found that lack of JAK1 was sufficient to block the constitutive activation of STAT3. The collective results from the various lines of investigation showed that it is, in principle, feasible to manipulate genes in a ligand-controlled manner in neoplastic mammary epithelial cells, even when cancer cells acquire a state of cellular plasticity that may no longer support the expression of the MMTV-Flp transgene.

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Antineoplastic effect of iodine and iodide in dimethylbenz[a]anthracene-induced mammary tumors: association between lactoperoxidase and estrogen-adduct production

Endocrine Related Cancer ◽

10.1530/erc-11-0065 ◽

2011 ◽

Vol 18 (4) ◽

pp. 529-539 ◽

Cited By ~ 13

Author(s):

Ofelia Soriano ◽

Guadalupe Delgado ◽

Brenda Anguiano ◽

Pavel Petrosyan ◽

Edith D Molina-Servín ◽

...

Keyword(s):

Mammary Gland ◽

Dna Adducts ◽

Mammary Cancer ◽

Mammary Tumors ◽

Molecular Iodine ◽

Mammary Tissue ◽

Normal Mammary Gland ◽

Peroxisome Proliferator ◽

Peroxisome Proliferator Activated Receptor ◽

Antineoplastic Effect

Several groups, including ours, have reported that iodine exhibited antiproliferative and apoptotic effects in various cancer cells only if this element is supplemented as molecular iodine, or as iodide, to cells that are able to oxidize it with the enzyme thyroperoxidase. In this study, we analyzed the effect of various concentrations of iodine and/or iodide in the dimethylbenz[a]anthracene (DMBA) mammary cancer model in rats. The results show that 0.1% iodine or iodide increases the expression of peroxisome proliferator-activated receptor type γ (PPARγ), triggering caspase-mediated apoptosis pathways in damaged mammary tissue (DMBA-treated mammary gland) as well as in frank mammary tumors, but not in normal mammary gland. DMBA treatment induces the expression of lactoperoxidase, which participates in the antineoplastic effect of iodide and could be involved in the pro-neoplastic effect of estrogens, increasing the formation of DNA adducts. In conclusion, our results show that a supplement of 0.1% molecular iodine/potassium iodide (0.05/0.05%) exert antineoplastic effects, preventing estrogen-induced DNA adducts and inducing apoptosis through PPARγ/caspases in pre-cancer and cancerous cells. Since this iodine concentration does not modify the cytology (histology, apoptosis rate) or physiology (triiodothyronine and thyrotropin) of the thyroid gland, we propose that it be considered as an adjuvant treatment for premenopausal mammary cancer.

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T2* relaxation times of intraductal murine mammary cancer, invasive mammary cancer, and normal mammary gland

Medical Physics ◽

10.1118/1.3684950 ◽

2012 ◽

Vol 39 (3) ◽

pp. 1309-1313 ◽

Cited By ~ 3

Author(s):

Elizabeth Hipp ◽

Xiaobing Fan ◽

Sanaz A. Jansen ◽

Erica J. Markiewicz ◽

James Vosicky ◽

...

Keyword(s):

Mammary Gland ◽

Mammary Cancer ◽

Relaxation Times ◽

Normal Mammary Gland ◽

T2 Relaxation

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THE UPTAKE OF OESTRADIOL IN THE NORMAL MAMMARY GLAND. AN EXPERIMENTAL STUDY IN RATS

Acta Endocrinologica ◽

10.1530/acta.0.056s228 ◽

1967 ◽

Vol 56 (1_Suppl) ◽

pp. S228

Author(s):

Sten Sander

Keyword(s):

Experimental Study ◽

Mammary Gland ◽

Normal Mammary Gland

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The Contribution of Hypoxia-Inducible Factor (HIF) -1 Alpha to Normal Mammary Gland Development and Mammary Tumorigenesis

10.21236/ada422423 ◽

2003 ◽

Author(s):

Tiffany N. Seagroves

Keyword(s):

Mammary Gland ◽

Mammary Gland Development ◽

Hypoxia Inducible Factor ◽

Mammary Tumorigenesis ◽

Normal Mammary Gland ◽

Gland Development

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P2X7 Receptor Promotes Mouse Mammary Cancer Cell Invasiveness and Tumour Progression, and Is a Target for Anticancer Treatment

Cancers ◽

10.3390/cancers12092342 ◽

2020 ◽

Vol 12 (9) ◽

pp. 2342 ◽

Cited By ~ 3

Author(s):

Lucie Brisson ◽

Stéphanie Chadet ◽

Osbaldo Lopez-Charcas ◽

Bilel Jelassi ◽

David Ternant ◽

...

Keyword(s):

Cancer Cells ◽

Cancer Cell ◽

Cancer Progression ◽

P2x7 Receptor ◽

Mammary Cancer ◽

Tumour Progression ◽

Mammary Cancer Cell ◽

Cell Invasiveness ◽

Cancer Cell Invasiveness

The P2X7 receptor is an ATP-gated cation channel with a still ambiguous role in cancer progression, proposed to be either pro- or anti-cancerous, depending on the cancer or cell type in the tumour. Its role in mammary cancer progression is not yet defined. Here, we show that P2X7 receptor is functional in highly aggressive mammary cancer cells, and induces a change in cell morphology with fast F-actin reorganization and formation of filopodia, and promotes cancer cell invasiveness through both 2- and 3-dimensional extracellular matrices in vitro. Furthermore, P2X7 receptor sustains Cdc42 activity and the acquisition of a mesenchymal phenotype. In an immunocompetent mouse mammary cancer model, we reveal that the expression of P2X7 receptor in cancer cells, but not in the host mice, promotes tumour growth and metastasis development, which were reduced by treatment with specific P2X7 antagonists. Our results demonstrate that P2X7 receptor drives mammary tumour progression and represents a pertinent target for mammary cancer treatment.

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