Effects of lymphocytes and fibroblasts on the growth of human mammary carcinoma cells studied in short-term primary cultures

Ögmundsdóttir, Helga M.; Pétursdóttir, Ingibjörg; Guðmundsdóttir, Ingibjörg; Ámundadóttir, Laufey T.; Rønnov‐Jessen, Lone; Petersen, Ole W.

doi:10.1007/bf02634232

Cited by 18 publications

(9 citation statements)

References 28 publications

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“…Yashiro et al (2005) demonstrated that tumor size is significantly increased in mice when breast cancer cells are co-inoculated with breast fibroblasts. In other experiments, it was shown that fibroblasts cultured from normal healthy tissue tend to have inhibitory effects on cell growth, whereas fibroblasts cultured from tumors stimulate the growth of several cell types, including mammary carcinoma cells and myofibroblasts (Hooff, 1988;Adams et al, 1988;Ronnov-Jessen et al, 1990;Ogmundsdottir et al, 1993;Ronnov-Jessen et al, 1995;Horgan et al, 1987;Mueller and Fusenig, 2004;Bhowmick et al, 2004;Tsukada et al, 1987).…”

Section: Introductionmentioning

confidence: 94%

Interaction of Tumor with Its Micro-environment: A Mathematical Model

Kim

Friedman

2009

Bull. Math. Biol.

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This paper is concerned with early development of transformed epithelial cells (TECs) in the presence of fibroblasts in the tumor micro-environment. These two types of cells interact by means of cytokines such as transforming growth factor (TGF-beta) and epidermal growth factor (EGF) secreted, respectively, by the TECs and the fibroblasts. As this interaction proceeds, TGF-beta induces fibroblasts to differentiate into myofibroblasts which secrete EGF at a larger rate than fibroblasts. We monitor the entire process in silico, in a setup which mimics experiments in a Tumor Chamber Invasion Assay, where a semi-permeable membrane coated by extracellular matrix (ECM) is placed between two chambers, one containing TECs and another containing fibroblasts. We develop a mathematical model, based on a system of PDEs, that includes the interaction between TECs, fibroblasts, myofibroblasts, TGF-beta, and EGF, and we show how model parameters affect tumor progression. The model is used to generate several hypotheses on how to slow tumor growth and invasion. In an Appendix, it is proved that the mathematical model has a unique global in-time solution.

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Section: Introductionmentioning

confidence: 94%

Interaction of Tumor with Its Micro-environment: A Mathematical Model

Kim

Friedman

2009

Bull. Math. Biol.

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“…It has been proposed that, in vivo, tumour epithelial cells may have an absolute dependence on paracrine signals from neighbouring cells (Lippmann et al, 1989;Osborne and Arteaga, 1990). This is reinforced by in vitro studies that showed paracrine factors secreted by breast tumour-derived fibroblasts or lymphocytes stimulated proliferation of breast cancer cell lines (Adams et al, 1988b;van Roozendaal et al, 1992) and primary cultures of breast cancer epithelial (Ogmundsdottir et al, 1993;Hofland et al, 1995;Emerman et al, 1996). Thus, paracrine-autocrine interactions are likely to be important factors in determining the biological behaviour of a tumour.…”

Section: Genetic Analysismentioning

confidence: 99%

Short-term primary culture of epithelial cells derived from human breast tumours

Speirs

Green²,

Walton³

et al. 1998

Br J Cancer

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Summary As experimental models for breast cancer, most studies rely on established human breast cancer cell lines. However, many of these lines were established over 20 years ago, many from pleural effusions rather than the primary tumour, so the validity of using them as representative models is questionable. This paper describes our experiences, over a 3-year period, in establishing short-term epithelial-cellenriched preparations from primary breast tumours based on differential centrifugation followed by culture in selective media. Epithelial cells were successfully cultured from 55% of samples, but culture success did not appear to be correlated with tumour histology, stage, grade or node status. Epithelial cell-enriched cultures were immunopositive for broad-spectrum cytokeratin and epithelial membrane antigen (EMA). Positivity for keratin 19 confirmed that the cultures contained tumour-derived cells, which additionally showed significantly higher activity of the reductive pathway of the steroid-converting enzyme 17p-hydroxysteroid dehydrogenase type 1. That the cultures contained tumour and not normal epithelial cells was further substantiated by the complete absence of the calmodulin-like gene NB-1 in tumour-derived cultures; this is only associated with normal breast epithelia. Eighty-five per cent of cultures established from oestrogen receptor (ER)-positive tumours expressed ER in vitro; this was functional in 66% of cultures, although ER-positive phenotype was gradually lost over time. In conclusion, epithelial cells can be isolated and maintained as short-term cultures from primary breast tumours irrespective of histopathological or clinical details, providing a model system with a greater biological and clinical relevance than breast cancer cell lines.

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“…In our previous studies, we demonstrated that lymphocytes stimulate the growth of mammary carcinoma cells in primary cultures (Ögmundsdóttir et al, 1993, 1995). This growth stimulation was associated with tumor‐cell expression of MHC class I antigens (Ögmundsdóttir et al, 1995).…”

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confidence: 91%

Altered expression of HLA class I antigens in breast cancer: Association with prognosis

et al. 2000

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Loss of surface expression of class I major histocompatibility antigens is commonly observed in malignant tumors and has been considered one of the mechanisms for escape from cytotoxic T cells. However, natural killer cells kill cells lacking HLA class I antigens. In the present study, we characterized by immunohistochemistry the HLA class I expression of breast carcinomas from 187 patients with TNM stages I and II, diagnosed 1981–1984, using β2‐microglobulin as a marker and evaluated the effect on survival with a follow‐up of up to 14 years. The largest group (48%) consisted of HLA class I–negative tumors (≤10% of cells stained), mixed expression (>10% and <80% of cells stained) was seen in 36% and only 15% were classified as HLA class I–positive (≥80% cells stained). No associations could be established with various clinicopathological parameters, such as tumor size, presence of lymph node metastases, histological grade, expression of hormone receptors, S phase and p53 mutations. There was no effect on recurrence‐free survival in the whole group; but among node‐negative patients (n = 86), those who had tumors with mixed HLA class I expression had a significantly higher probability of disease recurrence (OR = 3.42, p = 0.014) than patients with either HLA class I–positive or –negative tumors, particularly after more than 5 years. In node‐positive patients who received adjuvant therapy, this phenotype was not associated with disease recurrence. Int. J. Cancer 89:500–505, 2000. © 2000 Wiley‐Liss, Inc.

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Effects of lymphocytes and fibroblasts on the growth of human mammary carcinoma cells studied in short-term primary cultures

Cited by 18 publications

References 28 publications

Interaction of Tumor with Its Micro-environment: A Mathematical Model

Interaction of Tumor with Its Micro-environment: A Mathematical Model

Short-term primary culture of epithelial cells derived from human breast tumours

Altered expression of HLA class I antigens in breast cancer: Association with prognosis

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