Stromal Involvement In Malignant Growth

Hooff, A. van den

doi:10.1016/s0065-230x(08)60437-6

Cited by 201 publications

(71 citation statements)

References 191 publications

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“…Several lines of studies indicate that the growth and invasive potential of carcinoma cells are influenced through interaction with host stromal cells (van den Hooff, 1988;Matsumoto et al, 1989;Camps et al, 1990;Wernert, 1997). Indeed, the in vitro invasion of various human oral squamous carcinoma cells into collagen gel matrix was specifically induced by co-cultivation with stromal fibroblasts (Matsumoto et al, 1989) and the fibroblast-derived factor responsible for invasion of oral carcinoma cells proved to be HGF (Matsumoto et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

“…Establishment of an autocrine loop of growth factors is involved in tumorigenic transformation and progression to malignant cancer cells (Sporn and Roberts, 1985;Ullrich and Schlessinger, 1990;Wright et al, 1993;Levine et al, 1995;Silletti and Raz, 1996;Chicoine and Silbergeld, 1997). In addition to these factors, participation of paracrine factors have been implicated in tumour invasion and malignant progression, as based on the notion that growth and invasive potentials of carcinoma cells are influenced through interactions with host stromal cells (van den Hooff, 1988;Matsumoto et al, 1989;Camps et al, 1990;Wernert, 1997). HGF is a mesenchymal-(or stromal-)derived paracrine factor which affects cell growth, cell motility and morphogenesis of a wide variety of cells, including malignant ones (Jiang et al, 1993;Matsumoto and Nakamura, 1997;Birchmeier and Gherardi, 1998).…”

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confidence: 99%

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Autocrine and paracrine motility factors and their involvement in invasiveness in a human oral carcinoma cell line

et al. 1999

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Summary Invasive potentials of malignant cancer cells are regulated by cell motility factors. To examine the regulation of motility and invasiveness in oral squamous carcinoma, we investigated autocrine-and/or paracrine-acting cell motility factors, using a newly established human cell line (IF cells) from oral squamous cell carcinoma, which has highly invasive and metastatic characteristics. Conditioned medium derived from IF cells stimulated cell scattering and migration of GB-d1 gallbladder carcinoma cells, indicating that IF cells secreted cell motility factors. Using antibodies, IF-derived cell motility factors proved to be transforming growth factor (TGF)-α and TGF-β1. Antibodies against TGF-α and TGF-β1 inhibited autonomous migration of the IF cells. On the other hand, in vitro invasion of IF cells was strongly enhanced by hepatocyte growth factor (HGF) but only slightly by TGF-α and TGF-β1. The conditioned medium from fibroblasts enhanced in vitro invasion of IF cells, an event abrogated by anti-HGF antibody, but not by antibodies against TGF-α and TGF-β1. Importantly, IF cells secreted a factor inducing HGF production in fibroblasts and the factor was identified as interleukin-1, which means that a mutual interaction exists between tumour cells and fibroblasts, as mediated by the HGF/HGF-inducer loop. These results indicate that IF cells utilize TGF-α and TGF-β1 as autocrine-acting motility factors and HGF as a paracrine-acting motility factor, and that invasiveness of IF cells is particularly stimulated by HGF derived from stromal fibroblasts. Utilization of multiple cell motility/invasion factors that act in distinct pathways may confer highly invasive and metastatic potentials in IF oral squamous carcinoma cells.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Autocrine and paracrine motility factors and their involvement in invasiveness in a human oral carcinoma cell line

et al. 1999

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“…It was noted long time ago that changes in the microenvironment accompany tumor formation [8][9][10]. Increased fibroblast proliferation and ECM remodeling are often found adjacent to cancer cells.…”

Section: The Tumor Microenvironment: From Reactive Neighborhood To Acmentioning

confidence: 99%

Microenvironmental regulation of cancer development

Polyák

2008

Current Opinion in Genetics & Development

294

213

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Numerous studies have demonstrated that the tumor microenvironment not only responds to and supports carcinogenesis, but actively contributes to tumor initiation, progression, and metastasis. During tumor progression all cells composing the tumor undergo phenotypic and epigenetic changes. Paracrine signaling between epithelial and stromal cells is important for the regulation of the proliferation, invasive, angiogenic, and metastatic behavior of cancer cells. Better understanding the molecular mechanisms by which stromal cells exert these effects may open up new venues for cancer therapeutic and preventative interventions.

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“…57,58 Whether fibrosis is accompanied with tumor or not depends on the types of collagen it produces. 59 Tumor-associated fibrosis is characterized by increased collagen Type III content; such fibrotic lesions are mostly in the early immature stage. On the other hand, fibrosis unaccompanied with tumor contains decreased content of Type III and increased contents of Types I and IV collagen; such fibrotic lesions are mostly in the late mature stage.…”

Section: Medical Devicesmentioning

confidence: 99%

Beyond foreign‐body‐induced carcinogenesis: Impact of reactive oxygen species derived from inflammatory cells in tumorigenic conversion and tumor progression

Okada

2007

Intl Journal of Cancer

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Foreign-body-induced carcinogenesis is a traditional, maybe old, way of understanding cancer development. A number of novel approaches are available today to elucidate cancer development. However, there are things we learn from the old, and thus I bring out some examples of various clinical cases and experimental models of foreign-body-induced tumorigenesis. What is notable is that the foreign bodies themselves are unrelated to each other, whereas commonly underlying in them is to induce inflammatory reaction, especially stromal proliferation, where those exogenous materials are incorporated and undigested. Such foreign-body-induced carcinogenesis is also recognized in the step of tumor progression, the final step of carcinogenesis that tumor cells acquire malignant phenotypes including metastatic properties. And the phenomenon is universally observed in several cell lines of different origins. In this review I would like to show the evidence that tumor development and progression are accelerated inevitably by inflammation caused from foreign bodies, and that reactive oxygen species derived from inflammatory cells are one of the most important genotoxic mediators to accelerate the process. ' 2007 Wiley-Liss, Inc.

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Stromal Involvement In Malignant Growth

Cited by 201 publications

References 191 publications

Autocrine and paracrine motility factors and their involvement in invasiveness in a human oral carcinoma cell line

Autocrine and paracrine motility factors and their involvement in invasiveness in a human oral carcinoma cell line

Microenvironmental regulation of cancer development

Beyond foreign‐body‐induced carcinogenesis: Impact of reactive oxygen species derived from inflammatory cells in tumorigenic conversion and tumor progression

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