Triple Negative Breast Neoplasms
|
0.030 |
Biomarker
|
disease |
BEFREE |
Outlined in previous publications, we identified a series of potent, dual TTK/CLK2 inhibitors with strong efficacy in TNBC xenograft models.
|
30998356 |
2019 |
Triple-Negative Breast Carcinoma
|
0.030 |
Biomarker
|
disease |
BEFREE |
Outlined in previous publications, we identified a series of potent, dual TTK/CLK2 inhibitors with strong efficacy in TNBC xenograft models.
|
30998356 |
2019 |
Triple Negative Breast Neoplasms
|
0.030 |
Biomarker
|
disease |
BEFREE |
On the basis of these data, CC-671 was moved forward for clinical development as a potent and selective TTK/CLK2 inhibitor in a subset of patients with TNBC.<i></i>.
|
29866747 |
2018 |
Triple-Negative Breast Carcinoma
|
0.030 |
Biomarker
|
disease |
BEFREE |
On the basis of these data, CC-671 was moved forward for clinical development as a potent and selective TTK/CLK2 inhibitor in a subset of patients with TNBC.<i></i>.
|
29866747 |
2018 |
Triple Negative Breast Neoplasms
|
0.030 |
Biomarker
|
disease |
BEFREE |
These compounds were discovered from a TNBC phenotypic screen and possess a unique dual inhibition profile targeting TTK (mitotic exit) and CLK2 (mRNA splicing).
|
28991472 |
2017 |
Triple-Negative Breast Carcinoma
|
0.030 |
Biomarker
|
disease |
BEFREE |
These compounds were discovered from a TNBC phenotypic screen and possess a unique dual inhibition profile targeting TTK (mitotic exit) and CLK2 (mRNA splicing).
|
28991472 |
2017 |
Persistent Mullerian duct syndrome
|
0.020 |
Biomarker
|
disease |
BEFREE |
CLK2 inhibition has been proposed as a potential mechanism to improve autism and neuronal functions in Phelan-McDermid syndrome (PMDS).
|
29985556 |
2018 |
Persistent Mullerian duct syndrome
|
0.020 |
Biomarker
|
disease |
BEFREE |
Pharmacological and genetic activation of Akt or inhibition of CLK2 relieved synaptic deficits in Shank3-deficient and PMDS patient-derived neurons.
|
26847545 |
2016 |
Malignant neoplasm of prostate
|
0.010 |
Biomarker
|
disease |
BEFREE |
These interactions give rise to repeated transitions between (high HIPK1-PAGE4, low CLK2-PAGE4) and (low HIPK1-PAGE4, high CLK2-PAGE4) cell phenotypes, which possess differing sensitivities to the standard PCa therapies, such as androgen deprivation therapy (ADT).
|
30813315 |
2019 |
Prostate carcinoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
These interactions give rise to repeated transitions between (high HIPK1-PAGE4, low CLK2-PAGE4) and (low HIPK1-PAGE4, high CLK2-PAGE4) cell phenotypes, which possess differing sensitivities to the standard PCa therapies, such as androgen deprivation therapy (ADT).
|
30813315 |
2019 |
Autistic Disorder
|
0.010 |
Biomarker
|
disease |
BEFREE |
CLK2 inhibition has been proposed as a potential mechanism to improve autism and neuronal functions in Phelan-McDermid syndrome (PMDS).
|
29985556 |
2018 |
Diabetes Mellitus, Non-Insulin-Dependent
|
0.010 |
Biomarker
|
disease |
BEFREE |
More studies can evidence the negative role of CLK2 in the control of liver metabolism, contributing to the improvement of insulin resistance, obesity, and type 2 diabetes.
|
29575149 |
2018 |
22q13.3 Deletion Syndrome
|
0.010 |
Biomarker
|
disease |
BEFREE |
X-ray Structures and Feasibility Assessment of CLK2 Inhibitors for Phelan-McDermid Syndrome.
|
29985556 |
2018 |
Diabetes
|
0.010 |
Biomarker
|
disease |
BEFREE |
Thus, our results suggest that protein CLK2 integrates some important hypothalamic pathways, and may be a promising molecule for new therapeutic approaches for obesity and diabetes.
|
27733761 |
2017 |
Diabetes Mellitus
|
0.010 |
Biomarker
|
group |
BEFREE |
Thus, our results suggest that protein CLK2 integrates some important hypothalamic pathways, and may be a promising molecule for new therapeutic approaches for obesity and diabetes.
|
27733761 |
2017 |
Obesity
|
0.010 |
Biomarker
|
disease |
BEFREE |
Thus, our results suggest that protein CLK2 integrates some important hypothalamic pathways, and may be a promising molecule for new therapeutic approaches for obesity and diabetes.
|
27733761 |
2017 |
androgen independent prostate cancer
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
We demonstrate that HIPK1 is expressed in both androgen-dependent and androgen-independent prostate cancer (PCa) cells, whereas CLK2 and PAGE4 are expressed only in androgen-dependent cells.
|
28289210 |
2017 |
Glioblastoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
However, the function of CLK2 in glioblastoma progression has not been described.
|
27050366 |
2016 |
Neoplasms
|
0.010 |
Biomarker
|
group |
BEFREE |
In two glioblastoma xenograft models, the survival duration of mice with CLK2-knockdown GSCs was significantly longer than mice with control tumors.
|
27050366 |
2016 |
Adult Glioblastoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
However, the function of CLK2 in glioblastoma progression has not been described.
|
27050366 |
2016 |
Childhood Glioblastoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
However, the function of CLK2 in glioblastoma progression has not been described.
|
27050366 |
2016 |
Glioblastoma Multiforme
|
0.010 |
Biomarker
|
disease |
BEFREE |
However, the function of CLK2 in glioblastoma progression has not been described.
|
27050366 |
2016 |
Malignant neoplasm of breast
|
0.010 |
Biomarker
|
disease |
BEFREE |
Loss of CLK2 in luminal breast cancer cells leads to the upregulation of epithelial-to-mesenchymal transition (EMT)-related genes and a switch to mesenchymal splice variants of several genes, including ENAH (MENA).
|
25670169 |
2015 |
Breast Carcinoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Loss of CLK2 in luminal breast cancer cells leads to the upregulation of epithelial-to-mesenchymal transition (EMT)-related genes and a switch to mesenchymal splice variants of several genes, including ENAH (MENA).
|
25670169 |
2015 |
Tumor Cell Invasion
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
Downregulation of CLK2 inhibits breast cancer growth in cell culture and in xenograft models and it enhances cell migration and invasion.
|
25670169 |
2015 |