“…Myofibroblasts produced lytic enzymes able to degrade the BM surrounding tumour glands, and also participated in the synthesis of the ECM components of the tumour stroma, which subsequently altered the adhesive and migratory properties of the epithelial colon cancer cells. 16 In prostate cancer reactive stroma is mainly composed of myofibroblast and fibroblast what has been clearly shown in some previous investigation. 2,3 Our current study confirmed appearance of myofibroblasts in prostate cancer reactive stroma, especially in Gleason pattern 3 tumours, but not in adjacent peritumourous tissue and stroma in BPH.…”
Section: Discussionmentioning
confidence: 69%
“…15 Newest concepts which point out the importance of tumourous stroma in tumour development and progression intensified investigation of stroma in many tumours, including prostate adenocarcinoma. 2,3,[16][17][18][19][20] Reactive stroma in breast and colon carcinoma has been described and in these cancers reactive stroma is composed of mixture of myofibroblasts, fibroblasts, endothelial cells and immune cells. Although all of these cells could be potentially involved in cancerogenesis, myofibroblasts were of special interest.…”
Section: Discussionmentioning
confidence: 99%
“…Although all of these cells could be potentially involved in cancerogenesis, myofibroblasts were of special interest. [16][17][18] Using a coimplantation tumour xenograft model, Orimo et al 18 demonstrated that carcinoma-associated fibroblasts (CAFs) extracted from human breast carcinomas promoted the growth of admixed breast carcinoma cells significantly more than do normal mammary fibroblasts derived from the same patients. The CAFs, which exhibited the traits of myofibroblasts, played a central role in promoting the growth of tumour cells through their ability to secrete stromal cell-derived factor 1 (SDF-1), which stimulated tumour growth directly, acting through the cognate receptor, CXCR4 that is expressed by carcinoma cells.…”
Section: Discussionmentioning
confidence: 99%
“…The CAFs also promoted angiogenesis by recruiting endothelial progenitor cells into carcinomas. 18 Martin et al 16 showed that myofibroblasts were accumulated at the invasive front of the colorectal carcinomas. Myofibroblasts produced lytic enzymes able to degrade the BM surrounding tumour glands, and also participated in the synthesis of the ECM components of the tumour stroma, which subsequently altered the adhesive and migratory properties of the epithelial colon cancer cells.…”
The aim of this study was to analyse relationship between changes of the stroma and expression of tenascin-C (TN-C) and laminin in prostate carcinoma. Tenascin-C immunostaining was increased, and laminin decreased in carcinomas compared with peritumoural tissue and benign prostate hyperplasia (Po0.05). Statistical analysis confirmed connection between stromal changes and TN-C expression in prostate carcinoma (Po0.05). Gleason pattern 3 carcinomas showed more pronounced stromal reaction and TN-C expression compared with Gleason pattern 4 carcinomas (Po0.05). The main cells in prostate cancer stroma are myofibroblasts that are also responsible for tenascin production. Degradation of laminin was not connected with myofibroblastic stromal changes.
“…Myofibroblasts produced lytic enzymes able to degrade the BM surrounding tumour glands, and also participated in the synthesis of the ECM components of the tumour stroma, which subsequently altered the adhesive and migratory properties of the epithelial colon cancer cells. 16 In prostate cancer reactive stroma is mainly composed of myofibroblast and fibroblast what has been clearly shown in some previous investigation. 2,3 Our current study confirmed appearance of myofibroblasts in prostate cancer reactive stroma, especially in Gleason pattern 3 tumours, but not in adjacent peritumourous tissue and stroma in BPH.…”
Section: Discussionmentioning
confidence: 69%
“…15 Newest concepts which point out the importance of tumourous stroma in tumour development and progression intensified investigation of stroma in many tumours, including prostate adenocarcinoma. 2,3,[16][17][18][19][20] Reactive stroma in breast and colon carcinoma has been described and in these cancers reactive stroma is composed of mixture of myofibroblasts, fibroblasts, endothelial cells and immune cells. Although all of these cells could be potentially involved in cancerogenesis, myofibroblasts were of special interest.…”
Section: Discussionmentioning
confidence: 99%
“…Although all of these cells could be potentially involved in cancerogenesis, myofibroblasts were of special interest. [16][17][18] Using a coimplantation tumour xenograft model, Orimo et al 18 demonstrated that carcinoma-associated fibroblasts (CAFs) extracted from human breast carcinomas promoted the growth of admixed breast carcinoma cells significantly more than do normal mammary fibroblasts derived from the same patients. The CAFs, which exhibited the traits of myofibroblasts, played a central role in promoting the growth of tumour cells through their ability to secrete stromal cell-derived factor 1 (SDF-1), which stimulated tumour growth directly, acting through the cognate receptor, CXCR4 that is expressed by carcinoma cells.…”
Section: Discussionmentioning
confidence: 99%
“…The CAFs also promoted angiogenesis by recruiting endothelial progenitor cells into carcinomas. 18 Martin et al 16 showed that myofibroblasts were accumulated at the invasive front of the colorectal carcinomas. Myofibroblasts produced lytic enzymes able to degrade the BM surrounding tumour glands, and also participated in the synthesis of the ECM components of the tumour stroma, which subsequently altered the adhesive and migratory properties of the epithelial colon cancer cells.…”
The aim of this study was to analyse relationship between changes of the stroma and expression of tenascin-C (TN-C) and laminin in prostate carcinoma. Tenascin-C immunostaining was increased, and laminin decreased in carcinomas compared with peritumoural tissue and benign prostate hyperplasia (Po0.05). Statistical analysis confirmed connection between stromal changes and TN-C expression in prostate carcinoma (Po0.05). Gleason pattern 3 carcinomas showed more pronounced stromal reaction and TN-C expression compared with Gleason pattern 4 carcinomas (Po0.05). The main cells in prostate cancer stroma are myofibroblasts that are also responsible for tenascin production. Degradation of laminin was not connected with myofibroblastic stromal changes.
“…Accumulation of fibroblast-like cells, including myofibroblasts, is frequently observed associated with the edge of an actively expanding tumour mass (Martin et al, 1996;Emura et al, 2000). Such a phenomenon has been demonstrated, to different extents, in a variety of tumours and there is increasing evidence that tumour stroma may promote tumour progression (Liotta and Kohn, 2001;Pupa et al, 2002).…”
The development of an altered stromal microenvironment is a common feature of many tumours including squamous cell carcinoma (SCC), and there is increasing evidence that these changes in the stroma, which include increased expression of proteases and cytokines, may actually promote tumour progression. A common finding is that stromal fibroblasts become 'activated' myofibroblasts, expressing smooth muscle actin and secreting cytokines, proteases and matrix proteins. We show that myofibroblasts are commonly found in the stroma of oral SCC and are often concentrated at the invasive margin of the tumour. Using oral SCC cells and primary oral fibroblasts, we demonstrate that tumour cells directly induce a myofibroblastic phenotype, and that this transdifferentiation is dependent on SCC-derived TGF-b1. In turn, myofibroblasts secrete significantly higher levels of hepatocyte growth factor/scatter factor compared with fibroblast controls, and this cytokine promotes SCC invasion through Matrigel, a mixture of basement membrane proteins. This is the first time that this double paracrine mechanism has been demonstrated between squamous carcinoma cells and fibroblasts, and emphasises that cancer invasion can be promoted indirectly by the release of tumour-induced host factors from stroma.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.