|
Tumor Progression
|
0.030 |
AlteredExpression
|
phenotype |
BEFREE |
Altogether our data indicate that MICAL2 over-expression is associated with cancer progression and metastatic disease.
|
26689989 |
2016 |
|
Carcinogenesis
|
0.010 |
AlteredExpression
|
phenotype |
BEFREE |
<b>Results:</b> MICAL2 was found to be highly expressed in CRC tissues, and its expression was associated with CRC carcinogenesis and poor patient outcome.
|
30555547 |
2018 |
|
Tumor Cell Invasion
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
MICAL2 is a novel human cancer gene controlling mesenchymal to epithelial transition involved in cancer growth and invasion.
|
26689989 |
2016 |
|
Cerebrovascular accident
|
0.100 |
GeneticVariation
|
group |
GWASCAT |
Meta-Analysis of Genome-Wide Association Studies Identifies Genetic Risk Factors for Stroke in African Americans.
|
26089329 |
2015 |
|
Malignant Neoplasms
|
0.030 |
AlteredExpression
|
group |
BEFREE |
MICAL2 is expressed in cancer associated neo-angiogenic capillary endothelia and it is required for endothelial cell viability, motility and VEGF response.
|
31004710 |
2019 |
|
Malignant Neoplasms
|
0.030 |
AlteredExpression
|
group |
BEFREE |
Molecule interacting with CasL2 (MICAL2), a microtubule-associated monooxygenase, is highly expressed in various cancers and is involved in cancer pathogenesis, but the mechanisms underlying its regulation in carcinogenesis are unclear.
|
30555547 |
2018 |
|
Malignant Neoplasms
|
0.030 |
Biomarker
|
group |
BEFREE |
Immunohistochemistry showed MICAL2-positive cells on the cancer invasive front and in metastasizing cancer cells inside emboli, but not at sites of metastasis, suggesting MICAL2 expression was 'on' in a subpopulation of primary cancer cells seemingly detaching from the tissue of origin, enter emboli and travel to distant sites, and was turned 'off' upon homing at metastatic sites.
|
26689989 |
2016 |
|
Primary malignant neoplasm
|
0.030 |
AlteredExpression
|
group |
BEFREE |
Molecule interacting with CasL2 (MICAL2), a microtubule-associated monooxygenase, is highly expressed in various cancers and is involved in cancer pathogenesis, but the mechanisms underlying its regulation in carcinogenesis are unclear.
|
30555547 |
2018 |
|
Primary malignant neoplasm
|
0.030 |
AlteredExpression
|
group |
BEFREE |
MICAL2 is expressed in cancer associated neo-angiogenic capillary endothelia and it is required for endothelial cell viability, motility and VEGF response.
|
31004710 |
2019 |
|
Primary malignant neoplasm
|
0.030 |
Biomarker
|
group |
BEFREE |
Immunohistochemistry showed MICAL2-positive cells on the cancer invasive front and in metastasizing cancer cells inside emboli, but not at sites of metastasis, suggesting MICAL2 expression was 'on' in a subpopulation of primary cancer cells seemingly detaching from the tissue of origin, enter emboli and travel to distant sites, and was turned 'off' upon homing at metastatic sites.
|
26689989 |
2016 |
|
Neoplasms
|
0.020 |
Biomarker
|
group |
BEFREE |
The challenges and perspectives for MICAL2 in tumor are also discussed.
|
29483957 |
2018 |
|
Neoplasms
|
0.020 |
AlteredExpression
|
group |
BEFREE |
Interestingly, immunohistochemical analysis of 105 prostate cancer specimens on the tissue microarray indicated that MICAL2-PV expression status was strongly correlated with Gleason scores (P < 0.0001) or tumor classification (P < 0.0001).
|
16675569 |
2006 |
|
Prostatic Neoplasms
|
0.010 |
Biomarker
|
group |
LHGDN |
Expression of novel molecules, MICAL2-PV (MICAL2 prostate cancer variants), increases with high Gleason score and prostate cancer progression.
|
16675569 |
2006 |