Multiple Sclerosis
|
0.110 |
GeneticVariation
|
disease |
BEFREE |
Nevertheless, we found suggestive evidence for an association of MS with variants in two new genes, the VAV2 gene and the gene for ZNF433.
|
20598377 |
2010 |
Malignant neoplasm of breast
|
0.060 |
Biomarker
|
disease |
BEFREE |
Finally, we confirmed that a dual targeting strategy is a viable and efficient therapeutic approach to hinder the metastasis of breast cancer in xenograft models, showcasing the important need for further clinical evaluation of this regimen to impede the spread of disease and improve patient survival.<b>Implications:</b> This study provides new insight into the therapeutic benefit of combining NEDD9 depletion with ROCK inhibition to reduce tumor cell dissemination and discovers a new regulatory role of NEDD9 in the modulation of VAV2-dependent activation of Rac1 and actin polymerization.<i></i>.
|
28235899 |
2017 |
Malignant neoplasm of breast
|
0.060 |
Biomarker
|
disease |
BEFREE |
Our laboratory has demonstrated that MST3 promotes tumorigenicity through the VAV2/Rac1 signal axis in breast cancer.
|
30416862 |
2018 |
Malignant neoplasm of breast
|
0.060 |
Biomarker
|
disease |
BEFREE |
New evidence suggests that the exchange factors Vav2 and Vav3 play synergistic roles in breast cancer by sustaining tumor growth, neoangiogenesis, and metastasis.
|
23033535 |
2012 |
Malignant neoplasm of breast
|
0.060 |
Biomarker
|
disease |
BEFREE |
Conversely, the ectopic expression of an active version of Vav2 promotes mesenchymal-epithelial transitions using E-cadherin-dependent and independent mechanisms depending on the mesenchymal breast cancer cell line used.
|
30087437 |
2019 |
Malignant neoplasm of breast
|
0.060 |
Biomarker
|
disease |
BEFREE |
These results indicate that MST3 interacts with VAV2 to activate Rac1 and promote the tumorigenicity of breast cancer.
|
26910843 |
2016 |
Malignant neoplasm of breast
|
0.060 |
AlteredExpression
|
disease |
BEFREE |
Microarray analyses revealed that Vav2 and Vav3 controlled a vast transcriptional program in breast cancer cells through mechanisms that were shared between the two proteins, isoform-specific or synergistic.
|
23033540 |
2012 |
Breast Carcinoma
|
0.060 |
Biomarker
|
disease |
BEFREE |
New evidence suggests that the exchange factors Vav2 and Vav3 play synergistic roles in breast cancer by sustaining tumor growth, neoangiogenesis, and metastasis.
|
23033535 |
2012 |
Breast Carcinoma
|
0.060 |
Biomarker
|
disease |
BEFREE |
Our laboratory has demonstrated that MST3 promotes tumorigenicity through the VAV2/Rac1 signal axis in breast cancer.
|
30416862 |
2018 |
Breast Carcinoma
|
0.060 |
Biomarker
|
disease |
BEFREE |
These results indicate that MST3 interacts with VAV2 to activate Rac1 and promote the tumorigenicity of breast cancer.
|
26910843 |
2016 |
Breast Carcinoma
|
0.060 |
Biomarker
|
disease |
BEFREE |
Conversely, the ectopic expression of an active version of Vav2 promotes mesenchymal-epithelial transitions using E-cadherin-dependent and independent mechanisms depending on the mesenchymal breast cancer cell line used.
|
30087437 |
2019 |
Breast Carcinoma
|
0.060 |
Biomarker
|
disease |
BEFREE |
Finally, we confirmed that a dual targeting strategy is a viable and efficient therapeutic approach to hinder the metastasis of breast cancer in xenograft models, showcasing the important need for further clinical evaluation of this regimen to impede the spread of disease and improve patient survival.<b>Implications:</b> This study provides new insight into the therapeutic benefit of combining NEDD9 depletion with ROCK inhibition to reduce tumor cell dissemination and discovers a new regulatory role of NEDD9 in the modulation of VAV2-dependent activation of Rac1 and actin polymerization.<i></i>.
|
28235899 |
2017 |
Breast Carcinoma
|
0.060 |
AlteredExpression
|
disease |
BEFREE |
Microarray analyses revealed that Vav2 and Vav3 controlled a vast transcriptional program in breast cancer cells through mechanisms that were shared between the two proteins, isoform-specific or synergistic.
|
23033540 |
2012 |
Tumor Cell Invasion
|
0.040 |
Biomarker
|
phenotype |
BEFREE |
Manipulating SF-1 and VAV2 abundance in cultured ACC cells revealed that VAV2 was a critical factor for SF-1-induced cytoskeletal remodeling and invasion in culture (Matrigel) and in vivo (chicken chorioallantoic membrane) models.
|
28270555 |
2017 |
Tumor Cell Invasion
|
0.040 |
Biomarker
|
phenotype |
BEFREE |
Expression of constitutively active Vav2 and RhoA in cells depleted for RIAM partially rescued their invasion, indicating that Vav2 and RhoA mediate RIAM function.
|
21454517 |
2011 |
Tumor Cell Invasion
|
0.040 |
Biomarker
|
phenotype |
BEFREE |
We concluded that Vav2 might promote invasion and metastasis of gastric cancer by regulating some invasion and metastasis-related genes.
|
28459214 |
2017 |
Tumor Cell Invasion
|
0.040 |
Biomarker
|
phenotype |
BEFREE |
Given the regulatory role of Vav2, the function of Nek3 in PRL-mediated motility and invasion was examined.
|
17297458 |
2007 |
Neoplasm Metastasis
|
0.030 |
Biomarker
|
phenotype |
BEFREE |
Finally, we confirmed that a dual targeting strategy is a viable and efficient therapeutic approach to hinder the metastasis of breast cancer in xenograft models, showcasing the important need for further clinical evaluation of this regimen to impede the spread of disease and improve patient survival.<b>Implications:</b> This study provides new insight into the therapeutic benefit of combining NEDD9 depletion with ROCK inhibition to reduce tumor cell dissemination and discovers a new regulatory role of NEDD9 in the modulation of VAV2-dependent activation of Rac1 and actin polymerization.<i></i>.
|
28235899 |
2017 |
Neoplasm Metastasis
|
0.030 |
Biomarker
|
phenotype |
BEFREE |
We concluded that Vav2 might promote invasion and metastasis of gastric cancer by regulating some invasion and metastasis-related genes.
|
28459214 |
2017 |
Neoplasm Metastasis
|
0.030 |
Biomarker
|
phenotype |
BEFREE |
Altogether, our work suggested that EphB3 acted as a tumor promoter in PTC by increasing the in vitro migration as well as the in vivo metastasis of PTC cells through regulating the activities of Vav2 and Rho GTPases in a kinase-dependent manner.
|
27986811 |
2017 |
Neoplasms
|
0.030 |
Biomarker
|
group |
BEFREE |
Altogether, our work suggested that EphB3 acted as a tumor promoter in PTC by increasing the in vitro migration as well as the in vivo metastasis of PTC cells through regulating the activities of Vav2 and Rho GTPases in a kinase-dependent manner.
|
27986811 |
2017 |
Neoplasms
|
0.030 |
Biomarker
|
group |
BEFREE |
Finally, we confirmed that a dual targeting strategy is a viable and efficient therapeutic approach to hinder the metastasis of breast cancer in xenograft models, showcasing the important need for further clinical evaluation of this regimen to impede the spread of disease and improve patient survival.<b>Implications:</b> This study provides new insight into the therapeutic benefit of combining NEDD9 depletion with ROCK inhibition to reduce tumor cell dissemination and discovers a new regulatory role of NEDD9 in the modulation of VAV2-dependent activation of Rac1 and actin polymerization.<i></i>.
|
28235899 |
2017 |
Neoplasms
|
0.030 |
AlteredExpression
|
group |
BEFREE |
Expression of Vav2 protein in gastric cancer tissues was related to degree of tumor differentiation, lymph node metastasis, and clinical stages.
|
28459214 |
2017 |
Agenesis of corpus callosum
|
0.020 |
Biomarker
|
disease |
BEFREE |
Because VAV2 is a druggable target, our findings suggest that blocking VAV2 may be a new therapeutic approach to inhibit metastatic progression in ACC patients.
|
28270555 |
2017 |
Agenesis of corpus callosum
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
To assess the prognostic role of VAV2 expression in ACC by investigation of a large cohort of patients.
|
28911143 |
2017 |