Microvasculature and VEGF expression in cartilaginous tumors

Ayala, Gustavo; Liu, Chen; Nicosia, Roberto F.; Horowitz, Steven H.; Lackman, Richard D.

doi:10.1016/s0046-8177(00)80248-8

Cited by 68 publications

(64 citation statements)

References 14 publications

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“…In 1 series of 26 cartilage-derived tumors, pericartilage microvessels were observed in all of the tumors, including enchondroma and all grades of chondrosarcoma. 43 Intracartilage microvessels were not seen in any of the enchondroma samples, whereas intracartilage microvessel counts were much higher in grade 2 and 3 chondrosarcoma than in grade 1 chondrosarcoma. Similarly, chondrocyte VEGF expression measured by immunohistochemistry increased with increasing tumor grade.…”

Section: Skeletal Sarcomasmentioning

confidence: 79%

“…Similarly, chondrocyte VEGF expression measured by immunohistochemistry increased with increasing tumor grade. 43 Based on preclinical data indicating a role for PDGF in chondrocyte proliferation, another group evaluated 67 chondrosarcoma tumor samples for PDGF-AA homodimer and PDGFR-a expression by immunohistochemistry. 44 PDGFR-a expression increased with increasing tumor grade.…”

Section: Skeletal Sarcomasmentioning

confidence: 99%

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Markers of angiogenesis and clinical features in patients with sarcoma

DuBois

Demetri

2007

Cancer

128

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Objective: Patient outcome after traumatic brain injury (TBI) is highly variable. The underlying pathophysiology of this is poorly understood, but inflammation is potentially an important factor. Microglia orchestrate many aspects of this response. Their activation can be studied in vivo using the positron emission tomography (PET) ligand [11C](R)PK11195 (PK). In this study, we investigate whether an inflammatory response to TBI persists, and whether this response relates to structural brain abnormalities and cognitive function. Methods: Ten patients, studied at least 11 months after moderate to severe TBI, underwent PK PET and structural magnetic resonance imaging (including diffusion tensor imaging). PK binding potentials were calculated in and around the site of focal brain damage, and in selected distant and subcortical brain regions. Standardized neuropsychological tests were administered. Results: PK binding was significantly raised in the thalami, putamen, occipital cortices, and posterior limb of the internal capsules after TBI. There was no increase in PK binding at the original site of focal brain injury. High PK binding in the thalamus was associated with more severe cognitive impairment, although binding was not correlated with either the time since the injury or the extent of structural brain damage. Interpretation: We demonstrate that increased microglial activation can be present up to 17 years after TBI. This suggests that TBI triggers a chronic inflammatory response particularly in subcortical regions. This highlights the importance of considering the response to TBI as evolving over time and suggests interventions may be beneficial for longer intervals after trauma than previously assumed. ANN NEUROL 2011;

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Section: Skeletal Sarcomasmentioning

confidence: 79%

Section: Skeletal Sarcomasmentioning

confidence: 99%

Markers of angiogenesis and clinical features in patients with sarcoma

DuBois

Demetri

2007

Cancer

128

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“…The regulation, however, is disorganized in chondrosarcoma because of its oncogenicity. Ayala et al 23 suggested that upregulation of VEGF expression and neovascularization led to a high grade of human chondrosarcoma. The present study demonstrated that the VEGF 165 protein is the active angiogenic stimulator in human chondrosarcoma.…”

Section: Discussionmentioning

confidence: 99%

“…In fact, the upregulation of VEGF and bFGF in many tumors has been observed in recent years. 22 Ayala et al 23 demonstrated, by immunohistochemical analysis, that VEGF expression was to a greater extent detected in higher-grade chondrosarcomas and associated with the number of intratumoral microvessels. The efficacy of anti-bFGF immunotherapy in rat chondrosarcoma was reported by Coppola et al 24 The mechanism or molecular events of angiogenesis in chondrosarcoma, however, have not been clarified yet.…”

mentioning

confidence: 99%

Human chondrosarcoma secretes vascular endothelial growth factor to induce tumor angiogenesis and stores basic fibroblast growth factor for regulation of its own growth

Furumatsu

Nishida

Kawai

et al. 2001

Intl Journal of Cancer

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“…The benign counterpart of CS is enchondroma, which by its nature grows during infancy and typically has little clinical importance in adulthood [8,21]. The differential diagnosis between enchondroma and Grades I and II CS is a challenge for the anatomic pathologist and is often the object of studies to determine certain parameters such as permeative infiltration with encapsulation of host bone trabeculae as proposed by Mirra et al [16] and Schiller [21] or the presence of hypercellularity combined with cellular atypia and myxoid areas [1,3,10,16,19,20]. Furthermore, this tumor can have different histologic grades in different areas of the tumor [19].…”

Section: Introductionmentioning

confidence: 99%

Surgical Treatment of Grade I Central Chondrosarcoma

Donati

Colangeli

et al. 2010

Clinical Orthopaedics &Amp; Related Research

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The grade of chondrosarcoma relates to the likelihood of local recurrence and metastases. Many Grade I chondrosarcomas behave benignly if aggressively, and the question arises regarding whether wide resection is essential to control the disease. We therefore asked whether intralesional surgery also could be extended to Grade I chondrosarcomas without an increase in recurrence. We retrospectively reviewed 31 patients with Grade I chondrosarcomas of the limbs. The minimum followup was 66 months (mean, 157 months; range, 66-296 months

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Microvasculature and VEGF expression in cartilaginous tumors

Cited by 68 publications

References 14 publications

Markers of angiogenesis and clinical features in patients with sarcoma

Markers of angiogenesis and clinical features in patients with sarcoma

Human chondrosarcoma secretes vascular endothelial growth factor to induce tumor angiogenesis and stores basic fibroblast growth factor for regulation of its own growth

Surgical Treatment of Grade I Central Chondrosarcoma

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