Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
The VEGFC/VEGFR3 pathway is regarded as the principal inducer of lymphangiogenesis and it contributes to metastases; however, no data are available regarding its role during primary colorectal cancer development.
|
31239267 |
2019 |
Secondary Neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Lymphatic vessel density and VEGF-C expression as independent predictors of melanoma metastases.
|
28756123 |
2017 |
Secondary Neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
While no significant differences in expression levels among the different modes of metastases were noted for VEGF-A and -D, VEGF-C expression was significantly higher in the group of predominantly retroperitoneal metastases compared to the group with extensive intraperitoneal metastases.
|
28591727 |
2017 |
Secondary Neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Strong VEGF-C expression was found in patients with distant metastases (p = .008).
|
25900716 |
2016 |
Secondary Neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
KITENIN silencing did not inhibit either HLEC invasion or tube formation in all tested cells, but it resulted in decreased expression of the lymphangiogenic inducer VEGF-C. KITENIN expression was significantly associated with tumor stage, depth of invasion, lymph node and distant metastases and poor survival.
|
26496979 |
2016 |
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Mice were given injections of an antibody against VEGFR3 or an adenovirus encoding human VEGFC before orthotopic tumors and metastases formed.
|
25754161 |
2015 |
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
In conclusion, the expression of HGF‑α or c‑Met was closely correlated with VEGF‑C, LMVD and metastases of lymph nodes, indicating that HGF‑α, c‑Met and VEGF‑C may perform important and collaborative actions in lymphangiogenesis and lymphatic metastasis of primary NSCLC.
|
25504327 |
2015 |
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
In metastatic breast cancers, NFAT5 promotes epithelial-mesenchymal transition (EMT) and invasion of cells by switching on the expression of the calcium binding protein S100A4, and facilitates the angiogenesis of breast epithelial cells and thus the development of metastases by transcriptionally activating vascular endothelial growth factor C (VEGF-C).
|
25311085 |
2014 |
Secondary Neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The association of VEGFR-3 expression with VEGF-C mRNA and MLC suggested that the poor prognosis and tumor metastasis associated with VEGFR-3 expression may be due, in part, to its role in promoting angiogenesis.
|
24858271 |
2014 |
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
The aim of the current study is to identify relationships between VEGF-A and VEGF-C, and their impact in angiogenesis and metastases in thyroid cancers.
|
23845470 |
2013 |
Secondary Neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
We found no correlation of VEGF-C expression with tumor grade, FIGO stage, lymph node, or distant metastases.
|
19911196 |
2009 |
Secondary Neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Although the level of VEGF-C was high, it does not seem to have a direct influence on tumor metastasis in osteosarcomas.
|
18440723 |
2008 |
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
To confirm the role of lymphangiogenesis in mediating metastasis, the low-metastatic LAPC-9 tumor cells were engineered to overexpress VEGF-C, and the development of metastases was evaluated.
|
17583576 |
2007 |
Secondary Neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The inhibition of tumor-derived VEGF-C with a soluble VEGFR3 decoy receptor, sVEGFR3-Fc, expressed via a recombinant adeno-associated viral vector, potently blocks tumor-associated lymphangiogenesis and tumor metastasis to the lymph nodes, when the treatment was initiated before the tumor implantation.
|
16061674 |
2005 |
Secondary Neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Primary and local recurrences expressed a relatively low level of VEGF-C, as did negative lymph nodes and distant metastases.
|
14676121 |
2003 |
Secondary Neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
One might expect a different pattern of VEGF-C expression in the various types of thyroid cancer because of their different means of metastases.
|
12915657 |
2003 |
Secondary Neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In addition, analysis of 10 patients, from whom specimens of both the primary skin melanoma and melanoma metastases were available, indicated a correlation between VEGF-C expression in the primary tumor and lymph node localization of metastases.
|
12910524 |
2003 |
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Vascular endothelial growth factor C (VEGF-C) is a critical activator of tumor lymphangiogenesis that recently has been strongly implicated in the tumor metastasis process.
|
12471041 |
2003 |
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Our data suggest that VEGF-C facilitates tumor metastasis via the lymphatic vessels and that tumor spread can be inhibited by blocking the interaction between VEGF-C and its receptor.
|
11280723 |
2001 |
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Vascular endothelial growth factor-C-mediated lymphangiogenesis promotes tumour metastasis.
|
11179212 |
2001 |
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Thus, VEGF-C induces selective hyperplasia of the lymphatic vasculature, which is involved in the draining of interstitial fluid and in immune function, inflammation, and tumor metastasis.
|
9162011 |
1997 |