Fibroblast stimulation of breast cancer cell growth in a serum-free system

Ryan, MC; Orr, David; Horgan, Kieran

doi:10.1038/bjc.1993.237

Cited by 27 publications

(14 citation statements)

References 23 publications

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“…7 Multiple studies have demonstrated that CAFs have a stronger growth-promoting effect on normal or cancerous breast epithelial cells than NAFs. [31][32][33][34][35][36] Overall, these previous results support our findings indicating that NAFs inhibit the growth of normal or hyperplastic epithelium, but are, in general, less able to alter the growth of cancer epithelial cells.…”

Section: Discussionsupporting

confidence: 90%

Human Breast Fibroblasts Inhibit Growth of the MCF10AT Xenograft Model of Proliferative Breast Disease

Sadlonova

Mukherjee

Bowe

et al. 2007

The American Journal of Pathology

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Stromal fibroblasts are important for normal breast homeostasis and regulation of epithelial growth; however, this regulatory function is altered during carcinogenesis. To study the role of fibroblasts in the development of breast cancer, fibroblasts derived from normal breast (NAFs) were incorporated into the MCF10AT xenograft model of progressive proliferative breast disease. The persistence of human NAFs in xenografts was established by intracellular labeling and tyramide-coupled fluorescent in situ hybridization. Overall, the number of MCF10AT epithelial structures was decreased, and the rate of epithelial cell apoptosis was increased in xenografts containing NAFs. However, these changes were primarily in low-grade epithelial structures, corresponding to normal or mildly hyperplastic ductal epithelium. The level and rate of apoptosis of high-grade epithelial structures, corresponding to in situ and invasive carcinoma, were not consistently altered by NAFs. In addition, there was variability in the growth-inhibitory capacity of NAFs derived from different individuals. NAFs induced changes in the morphology of high-grade MCF10AT structures and in xenograft stroma, including the composition of extracellular matrix, and increased angiogenesis and lymphocytic infiltration. These findings imply that NAFs can inhibit the growth of normal and hyperplastic epithelium but are less able to regulate the more transformed epithelial cells that arise during carcinogenesis. (Am J Pathol 2007, 170

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Section: Discussionsupporting

confidence: 90%

Human Breast Fibroblasts Inhibit Growth of the MCF10AT Xenograft Model of Proliferative Breast Disease

Sadlonova

Mukherjee

Bowe

et al. 2007

The American Journal of Pathology

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“…Recently, it was shown that CM prepared from parenchymal or endothelial cells or fi broblasts from the target organ stimulated the growth of metastatic sublines that specifically metastasize to these organs [20][21][22], In our model CM from lung, the target metastasizing organ, enhanced the proliferation of M3 cells, even in serum-free culture, indicating the presence of mitogenic factor(s). Some authors [23,24] have found that lung factors preferen tially enhanced the in vitro proliferation of cells with high metastatic ability.…”

Section: Discussionmentioning

confidence: 61%

Effect of Host-Organ Environment on the in vivo and in vitro Behavior of a Murine Mammary Adenocarcinoma

Puricelli¹,

Gómez²,

Vidal³

et al. 1994

Tumor Biol

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We investigated the role that organ environment may play in determining the homing of disseminated cells from a murine mammary adenocarcinoma moderately metastatic to lung (M3). Conditioned medium (CM) from normal lung was able to enhance both local and metastatic growth. It increased the number of lung colonies when inoculated together with tumor cells via intravenous or separately via intraperitoneal route. Several in vitro studies were performed in order to elucidate possible mechanisms. It was shown that lung CM stimulated the in vitro growth and the migration of M3 cells. Normal kidney and liver CM lacked all these capacities.

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“…Conditioned media from human breast cancer-derived fibroblasts stimulate the growth of breast cancer cells (van Roozendaal et al, 1992;Ryan et al, 1993;Singer et al, 1995). Co-culture experiments in which breast cancer cells and fibroblasts are separated by a microporous membrane have shown that factors secreted by fibroblasts stimulate the growth of breast cancer cells with reciprocal stimulation of fibroblast growth by the breast cancer cells (Hofland et al, 1995).…”

Section: Proliferative Effect Of Kgf On Breast Cancer Cell Linesmentioning

confidence: 99%

Expression of keratinocyte growth factor and its receptor in human breast cancer

Bansal

Cox²,

Marsh³

et al. 1997

Br J Cancer

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Summary The level of expression of keratinocyte growth factor (KGF) mRNA has been measured in human breast cell lines, purified populations of epithelial cells, myoepithelial cells and fibroblasts from reduction mammoplasty tissue and a panel of 42 breast cancers and 30 non-malignant human breast tissues using a semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR) procedure. We found similar levels of KGF mRNA in malignant and non-malignant breast tissues. The study of the amount of KGF mRNA in breast cell lines and purified populations of cells revealed that fibroblasts are the predominant source of KGF with malignant and non-malignant epithelial cells containing very low levels of KGF mRNA. We have examined the distribution of fibroblast growth factor receptor (FGFR)-2-lllb, which is a highaffinity receptor for KGF and find that it is present on malignant and non-malignant epithelial cells. The level of FGFR-2-lllb present on breast cancer cell lines was sufficient for KGF stimulation of breast cancer cell proliferation. Other members of the fibroblast growth factor family have been either not expressed in the human breast (FGF3, FGF4) or have been found at much reduced levels in breast cancer (FGF1, FGF2) and this is the first member of the family to potentially influence the progression of breast cancer through stimulation of cell division.

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Fibroblast stimulation of breast cancer cell growth in a serum-free system

Cited by 27 publications

References 23 publications

Human Breast Fibroblasts Inhibit Growth of the MCF10AT Xenograft Model of Proliferative Breast Disease

Human Breast Fibroblasts Inhibit Growth of the MCF10AT Xenograft Model of Proliferative Breast Disease

Effect of Host-Organ Environment on the in vivo and in vitro Behavior of a Murine Mammary Adenocarcinoma

Expression of keratinocyte growth factor and its receptor in human breast cancer

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