Progression of mycosis fungoides is associated with changes in angiogenesis and expression of the matrix metalloproteinases 2 and 9

Vacca, Angelo; Moretti, Sonia; Ribatti, Doménico; Pellegrino, A.; Pimpinelli, Nicola; Bianchi, Beatrice; Bonifazi, E.; Ria, Roberto; Serio, Gabriella; Dammacco, Franco

doi:10.1016/s0959-8049(97)00186-x

Cited by 90 publications

(89 citation statements)

References 25 publications

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“…3 Our results indicate that VEGF production is an early event in CTCL progression. Indeed, a very high frequency of VEGF-positive cells (490%) was seen in five of 11 patients with early disease, suggesting that VEGF is involved in the early stages of angiogenesis in CTCL.…”

Section: Discussionmentioning

confidence: 54%

“…28 AP-2 activity is also inversely correlated with the expression of matrix metalloproteinase-2 (MMP-2), and like VEGF production, MMP-2 expression increases with the progression of CTCL. 3,39 Hence, loss of AP-2 might not only contribute to the VEGF production, but could be important in several aspects of CTCL progression.…”

Section: Discussionmentioning

confidence: 99%

“…Interstage comparisons show that the microvessel area increases in parallel with disease progression; that is, the value of the mean microvessel area in the plaque stage is significantly higher than the value for the patch stage, and the value for the tumor stage is significantly higher than that of the plaque stage. 3,4 Thus, increased angiogenesis is likely to be important for the pathophysiology and progression of CTCL. However, the molecular mechanisms responsible for increased angiogenesis in CTCL are unknown.…”

Section: Introductionmentioning

confidence: 99%

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Jak3- and JNK-dependent vascular endothelial growth factor expression in cutaneous T-cell lymphoma

et al. 2006

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Section: Discussionmentioning

confidence: 54%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Jak3- and JNK-dependent vascular endothelial growth factor expression in cutaneous T-cell lymphoma

et al. 2006

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Section: To the Editormentioning

confidence: 99%

“…4 We have previously demonstrated that angiogenesis is correlated with tumor growth (S-phase fraction) in monoclonal gammopathies of undetermined significance (MGUS) and MM grouped according to a pathway of progression, and with progression stages both in B cell NHL and mycosis fungoides. [5][6][7][8] Correspondence Bunworasate et al's paper 1 opens the question about the effective role played by EPO in the transformation of MDS in an acute myeloblastic leukemia: EPO might promote an angiogenic response in the bone marrow of patients with MDS and favor tumor progression. If this hypothesis is confirmed by experimental and clinical data, a further question is the necessity of reconsidering the therapeutic role of EPO in the treatment of anemia associated with MDS.…”

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A potential role of erythropoietin in angiogenesis associated with myelodysplastic syndromes

Ribatti

2002

Leukemia

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Bunworasate et al 1 have recently published a brief report in which they described a transformation of a myelodysplastic syndrome (MDS) in an acute monoblastic leukemia in a patient 6 weeks after the initiation of erythropoietin (EPO) therapy for refractory anemia with ringed sideroblasts. Multiparameter flow cytometric analysis of bone marrow cells demonstrated coexpression of the EPO receptor with CD45 and CD13 on the surface of blasts.The incubation of marrow cells with EPO, compared to without, resulted in 1.3-and 1.6-fold increases, respectively, in tritiated thymidine incorporation and bromodeoxyuridine incorporation into CD13 + cells. The authors concluded that leukemic transformation in patients with EPO may be EPO-dependent and that management should consist of the discontinuation of EPO followed by observation, if clinically feasible.In 1999 we published a paper in which we demonstrated a proangiogenic activity of EPO both in vitro and in vivo. 2 We showed that an endothelial cell line expressed EPO receptors (EPORs) by Western blot analysis. Also EPO stimulated Janus kinase-2 (JAK-2) phosphorylation, cell proliferation, and matrix metalloproteinase-2 production in the endothelial cells and significantly enhanced their differentiation into vascular structures when seeded on Matrigel. In vivo, EPO induced a potent angiogenic response in the chick embryo chorioallantoic membrane (CAM) assay. Accordingly, endothelial cells of the CAM vasculature expressed EPORs and the angiogenic response of CAM blood vessels to EPO was comparable to that elicited by the prototypic angiogenic cyokine fibroblast growth factor-2 (FGF-2). Taken together, these data demonstrated the ability of EPO to interact directly with endothelial cells and to elicit an angiogenic response in vitro and in vivo and thus act as a bona fide direct angiogenic factor.Angiogenesis is a critical event for the progression and prognosis of tumors. 3 Tumor growth consists of an avascular and subsequent vascular phase. Assuming that it is dependent on angiogenesis which, in turn, depends on the release of angiogenic factors, acquisition of an angiogenic capability can be seen as an expression of progression from neoplastic transformation to tumor growth and metastasis. While the role of angiogenesis in the growth, progression and metastasis spread of solid tumors is well established, more recently, it has been demonstrated that the progression of several cancers of hematopoietic lineage, including non-Hodgkin's lymphomas (NHL), lymphoblastic leukemia, B cell chronic lymphocytic leukemia, acute myeloid leukemia, multiple myeloma (MM), and MDS are also clearly related to the degree of angiogenesis. 4 We have previously demonstrated that angiogenesis is correlated with tumor growth (S-phase fraction) in monoclonal gammopathies of undetermined significance (MGUS) and MM grouped according to a pathway of progression, and with progression stages both in B cell NHL and mycosis fungoides. [5][6][7][8] Correspondence Bunworasate et al's paper 1 opens the q...

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ETS-1 converts endothelial cells to the angiogenic phenotype by inducing the expression of matrix metalloproteinases and integrin ?3

1999

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The transcription factor ETS-1 is induced in endothelial cells (ECs) by angiogenic growth factors and the specific elimination of ETS-1 synthesis by antisense oligodeoxynucleotide inhibited angiogenesis in vitro (Iwasaka et al., 1996, J Cell Physiol 169:522-531). To understand the precise role of ETS-1 in angiogenesis, we established both high and low ETS-1 expression EC lines and compared angiogenic properties of these cell lines with those of the parental murine EC line, MSS-31. Although growth rate was almost identical for each cell line, the invasiveness was markedly enhanced in high ETS-1 expression cells and reduced in low ETS-1 expression cells compared with that of parental cells. The gene expressions of matrix metalloproteinases (MMP-1, MMP-3, and MMP-9) and gelatinolytic activity of MMP-9 were significantly increased in high ETS-1 expression cells. Low ETS-1 expression cells could not spread on a vitronectin substratum, and the phosphorylation of focal adhesion kinase was markedly impaired because of the reduced expression of integrin ␤ 3 . These results indicate that ETS-1 is a principal regulator that converts ECs to the angiogenic phenotype.

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Progression of mycosis fungoides is associated with changes in angiogenesis and expression of the matrix metalloproteinases 2 and 9

Cited by 90 publications

References 25 publications

Jak3- and JNK-dependent vascular endothelial growth factor expression in cutaneous T-cell lymphoma

Jak3- and JNK-dependent vascular endothelial growth factor expression in cutaneous T-cell lymphoma

A potential role of erythropoietin in angiogenesis associated with myelodysplastic syndromes

ETS-1 converts endothelial cells to the angiogenic phenotype by inducing the expression of matrix metalloproteinases and integrin ?3

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