Vascular endothelial growth factor (VEGF)-C - a potent risk factor in children diagnosed with stadium 4 neuroblastoma.

Nowicki, Michał; Konwerska, Aneta; Ostalska‐Nowicka, Danuta; Derwich, Katarzyna; B, Miśkowiak; Kondraciuk, Beata; Samulak, Dariusz; Witt, Martin

doi:10.2478/v10042-008-0067-7

Cited by 14 publications

(19 citation statements)

References 52 publications

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“…Early and late forms of circulating EPCs are characterized by the gradual decrease in CD133 expression, with an increase in CD105, CD31 and von Willebrand's factor expression [4]. Of note, late EPCs no longer express CD133, while the presence of CD34 is variable [21][22][23].…”

Section: Discussionmentioning

confidence: 99%

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Evaluation of cardiac muscle microvessel density in children diagnosed with cyanotic heart defects

Jankowska

Malińska²,

Nowicki

et al. 2014

Folia Histochem Cytobiol.

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Abstract:Angiogenesis is largely an adaptive response to tissue hypoxia, which occurs in a wide variety of situations. Interestingly, the extent of hypoxia-induces angiogenesis in the cardiac muscle of children diagnosed with congenital cyanotic heart defects is not well established. Thus, the aim of this study was to 1) estimate the cardiac muscle microvessel density (MVD) in children diagnosed with cyanotic (study group) and non-cyanotic (control group) heart defects and to 2) evaluate the prognostic significance of MVD value in the development of ventricular dysfunction in the postoperative period. The study group included 42 children diagnosed with cyanotic heart defects. The control group comprised 33 patients with a diagnosis of non-cyanotic heart failure. The collected tissue included cardiac muscle sections from the right atrium and interventricular or interatrial wall during surgical correction of the defect. Immunocytochemistry with monoclonal mouse anti-human antibodies against CD31, CD34 and CD105 was employed to estimate the MVD value. The mean cardiac muscle MVD, defined by CD34 expression, was 596.7 ± 32.6 microvessels per 1 mm 2 in the study group, which was not significantly different from the mean MVD in the control group (461.2 ± 30.5). Interestingly, in non-cyanotic heart defects, an inner area of subendocardial meshwork was estimated to have 75.3 ± 7.0 microvessels per 1 mm 2 , compared to 92.8 ± 10.9 microvessels per 1 mm 2 (p = 0.0082) in patients with cyanotic heart defects. No significant correlations between MVD value and ventricular dysfunction were found. Cyanotic heart defects resulting in chronic hypoxia might provoke angiogenesis in the subendocardial meshwork of the heart wall. The process seems to be independent of the type of cyanotic heart disease and most likely takes place during antenatal development. A ventricular dysfunction observed in some cases of cyanotic heart defects could not be predicted by the estimation of MVD.

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Section: Discussionmentioning

confidence: 99%

“…Angiogenesis is largely an adaptive response to tissue hypoxia, which occurs in a wide variety of situations [3,4]. Interestingly, the extent of hypoxia-induces angiogenesis in the cardiac muscle of children diagnosed with congenital cyanotic heart defects is not yet well established [2,5].…”

Section: Introductionmentioning

confidence: 99%

Evaluation of cardiac muscle microvessel density in children diagnosed with cyanotic heart defects

Jankowska

Malińska²,

Nowicki

et al. 2014

Folia Histochem Cytobiol.

Self Cite

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“…The majority of patients with NBs have widespread lymphatic and/or haematogenous metastases at diagnosis. Whereas angiogenesis has been studied extensively (reviewed by Rossler) [4], few reports have examined lymphangiogenesis in NBs [5][6][7][8][9][10][11].…”

Section: Introductionmentioning

confidence: 99%

LYVE-1 upregulation and lymphatic invasion correlate with adverse prognostic factors and lymph node metastasis in neuroblastoma

2012

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Neuroblastoma (NB) accounts for 15% of all childhood cancer deaths. The majority of patients have widespread lymphatic and/or haematogenous metastases at diagnosis, but lymphangiogenesis has not been well documented. Sixty-seven NBs were immunostained for the lymphatic endothelial marker, LYVE-1, and the lymphatic density (LD) and lymphatic invasion (LI), were counted in LYVE-1-expressing lymphatics. LYVE-1-stained lymphatic vessels and LI were present in 26/67 (39%) and 14/67 (21%) of the NBs, respectively. Central LD (CLD) and LI were higher in NBs from stage 4 (p = 0.012, p = 0.004, respectively), high-risk group (p = 0.030, p = 0.002), NBs with high mitosis karyorrhexis index (MKI) (p = 0.011, p = 0.005), unfavourable histology group (p = 0.040, p = 0.017) and distant lymph node metastasis (LNM) (p < 0.001 for each). Marginal LD (MLD) was higher in patients with LNM (p < 0.001). CLD and MLD correlated with LI (p < 0.001 each). Total LYVE-1 protein levels, quantified by a sensitive enzyme-linked immunosorbent assay (n = 55), were also higher in NBs from patients with stage 4 disease (p = 0.046), high-risk group (p = 0.028), MYCN-amplified NBs (p = 0.034) and LNM (p = 0.038). Kaplan-Meier analysis showed that the presence of CLD was associated with both worse OS at 5 years (77% [95% CI: 62-87%] versus 60% [95% CI: 32-80%], p = 0.062) and EFS (74% [95% CI: 58-85%] versus 43% [95% CI: 15-69%], p = 0.070) and LI with OS (71% [95% CI: 57-81%] versus 56% [95% CI: 26-78%], p = 0.055). Significant upregulation of LYVE-1 and the presence of LI in patients with stage 4 and high-risk disease, MYCN-amplification and LNM suggests that LYVE-1 may have value as predictors of outcome.

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“…136 VEGF isoforms have been found in both neuroblastoma cell lines and in primary tumors 137 , and the mRNA abundance 124,138 and protein expression were associated with higher stage tumors. 138,139 Vascular endothelial growth factor receptors (VEFGR) have been identified on neuroblastoma cells 140,141,142 as well as in primary tumor specimens. 143,138 Both VEGF and VEGFR are involved in promoting neuroblastoma cell survival.…”

Section: Neuroblastoma and Growth Factorsmentioning

confidence: 99%

Cell Survival Signaling in Neuroblastoma

Megison¹,

Gillory²,

Beierle³

2013

ACAMC

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Neuroblastoma is the most common extracranial solid tumor of childhood and is responsible for over 15% of pediatric cancer deaths. Neuroblastoma tumorigenesis and malignant transformation is driven by overexpression and dominance of cell survival pathways and a lack of normal cellular senescence or apoptosis. Therefore, manipulation of cell survival pathways may decrease the malignant potential of these tumors and provide avenues for the development of novel therapeutics. This review focuses on several facets of cell survival pathways including protein kinases (PI3K, AKT, ALK, and FAK), transcription factors (NF-κB, MYCN and p53), and growth factors (IGF, EGF, PDGF, and VEGF). Modulation of each of these factors decreases the growth or otherwise hinders the malignant potential of neuroblastoma, and many therapeutics targeting these pathways are already in the clinical trial phase of development. Continued research and discovery of effective modulators of these pathways will revolutionize the treatment of neuroblastoma.

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Vascular endothelial growth factor (VEGF)-C - a potent risk factor in children diagnosed with stadium 4 neuroblastoma.

Cited by 14 publications

References 52 publications

Evaluation of cardiac muscle microvessel density in children diagnosed with cyanotic heart defects

Evaluation of cardiac muscle microvessel density in children diagnosed with cyanotic heart defects

LYVE-1 upregulation and lymphatic invasion correlate with adverse prognostic factors and lymph node metastasis in neuroblastoma

Cell Survival Signaling in Neuroblastoma

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