|
Adult T-Cell Lymphoma/Leukemia
|
0.300 |
Biomarker
|
disease |
CTD_human |
Integrated molecular analysis of adult T cell leukemia/lymphoma.
|
26437031 |
2015 |
|
Craniofacial Abnormalities
|
0.300 |
Biomarker
|
group |
CTD_human |
A zebrafish screen for craniofacial mutants identifies wdr68 as a highly conserved gene required for endothelin-1 expression.
|
16759393 |
2006 |
|
Esophageal Neoplasms
|
0.100 |
GeneticVariation
|
group |
GWASCAT |
Genome-wide association study identifies three new susceptibility loci for esophageal squamous-cell carcinoma in Chinese populations.
|
21642993 |
2011 |
|
Malignant neoplasm of esophagus
|
0.100 |
GeneticVariation
|
disease |
GWASDB |
Genome-wide association study identifies three new susceptibility loci for esophageal squamous-cell carcinoma in Chinese populations.
|
21642993 |
2011 |
|
MYELODYSPLASTIC SYNDROME
|
0.040 |
GeneticVariation
|
group |
BEFREE |
Somatic missense mutations of the CSNK1A1 gene encoding casein kinase 1 alpha (CK1α) occur in a subset of myelodysplastic syndrome (MDS) with del(5q) karyotype.
|
31462704 |
2020 |
|
MYELODYSPLASTIC SYNDROME
|
0.040 |
Biomarker
|
group |
BEFREE |
Newer genomic technologies, such as single-nucleotide polymorphism array and next-generation sequencing, revealed the heterozygous deletions resulting in haploinsufficient gene expression (e.g., CSNK1A1, DDX41 on chromosome 5, CUX1, LUC7L2, EZH2 on chromosome 7) involved in the pathogenesis of MDS.
|
31093808 |
2019 |
|
MYELODYSPLASTIC SYNDROME
|
0.040 |
Biomarker
|
group |
BEFREE |
Identification of commonly deleted genes such as RPS14, miRNA-145, HSPA9, CD78, and CSNK1a1 have elucidated the precise biological changes responsible for the anemia, leukopenia, and thrombocytosis that characterizes del(5q) MDS and highlighted the importance of allelic haploinsufficiency in the hematological phenotype.
|
30578738 |
2019 |
|
MYELODYSPLASTIC SYNDROME
|
0.040 |
GeneticVariation
|
group |
BEFREE |
Between June 1, 2004, and May 31, 2014, in King's College (London, UK), we did whole-exome sequencing of five patients with isolated del(5q) followed by targeted screening for CSNK1A1 mutations and 20 myelodysplastic syndrome-associated mutations in 245 additional patients with myeloid neoplasms.
|
26688096 |
2015 |
|
Neoplasms
|
0.020 |
Biomarker
|
group |
BEFREE |
An anomaly in the active-site peptide from CSNK1A1 was observed in a tumor sample that was consistent with an altered catalytic aspartic acid.
|
27031502 |
2016 |
|
Neoplasms
|
0.020 |
GeneticVariation
|
group |
BEFREE |
39 (16%) of 250 patients with myeloid neoplasms had isolated del(5q), of whom seven (18%) had CSNK1A1 mutations.
|
26688096 |
2015 |
|
Neoplasm Metastasis
|
0.020 |
Biomarker
|
phenotype |
BEFREE |
In addition, because capping protein Z-line α1, PP1CB, and CSNK1A1 are involved in cell motility, which underlies invasion and metastasis of human cancer; they may be novel targets for antimetastatic therapies as well.
|
21566537 |
2011 |
|
Neoplasm Metastasis
|
0.020 |
AlteredExpression
|
phenotype |
LHGDN |
Wnt-5a/Ca2+-induced NFAT activity is counteracted by Wnt-5a/Yes-Cdc42-casein kinase 1alpha signaling in human mammary epithelial cells.
|
16880514 |
2006 |
|
Anemia
|
0.010 |
Biomarker
|
disease |
BEFREE |
Identification of commonly deleted genes such as RPS14, miRNA-145, HSPA9, CD78, and CSNK1a1 have elucidated the precise biological changes responsible for the anemia, leukopenia, and thrombocytosis that characterizes del(5q) MDS and highlighted the importance of allelic haploinsufficiency in the hematological phenotype.
|
30578738 |
2019 |
|
Medulloblastoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Using a newly described small-molecule, SSTC3, we show that CK1a activators could address a significant unmet clinical need for patients with SMO inhibitor-resistant medulloblastoma, including those harboring mutations in TRP53.
|
30487124 |
2019 |
|
Childhood Medulloblastoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Using a newly described small-molecule, SSTC3, we show that CK1a activators could address a significant unmet clinical need for patients with SMO inhibitor-resistant medulloblastoma, including those harboring mutations in TRP53.
|
30487124 |
2019 |
|
Adult Medulloblastoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Using a newly described small-molecule, SSTC3, we show that CK1a activators could address a significant unmet clinical need for patients with SMO inhibitor-resistant medulloblastoma, including those harboring mutations in TRP53.
|
30487124 |
2019 |
|
5q-syndrome
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Rps14, Csnk1a1 and miRNA145/miRNA146a deficiency cooperate in the clinical phenotype and activation of the innate immune system in the 5q- syndrome.
|
30651631 |
2019 |
|
Thrombocytosis
|
0.010 |
Biomarker
|
disease |
BEFREE |
Identification of commonly deleted genes such as RPS14, miRNA-145, HSPA9, CD78, and CSNK1a1 have elucidated the precise biological changes responsible for the anemia, leukopenia, and thrombocytosis that characterizes del(5q) MDS and highlighted the importance of allelic haploinsufficiency in the hematological phenotype.
|
30578738 |
2019 |
|
Myelodysplastic Syndrome with Isolated del(5q)
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Rps14, Csnk1a1 and miRNA145/miRNA146a deficiency cooperate in the clinical phenotype and activation of the innate immune system in the 5q- syndrome.
|
30651631 |
2019 |
|
Chromosome 5, trisomy 5q
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Rps14, Csnk1a1 and miRNA145/miRNA146a deficiency cooperate in the clinical phenotype and activation of the innate immune system in the 5q- syndrome.
|
30651631 |
2019 |
|
Adrenal gland hypofunction
|
0.010 |
AlteredExpression
|
phenotype |
BEFREE |
Compared with healthy controls, 19 of the 68 genes were found modulated in patients with AI at baseline, 18 of which were restored to control levels 12 weeks after therapy was switched: ARNTL [BMAL] (P = 0.024), CLOCK (P = 0.016), AANAT (P = 0.021), CREB1 (P = 0.010), CREB3 (P = 0.037), MAT2A (P = 0.013); PRKAR1A, PRKAR2A, and PRKCB (all P < 0.010) and PER3, TIMELESS, CAMK2D, MAPK1, SP1, WEE1, CSNK1A1, ONP3, and PRF1 (all P < 0.001).
|
29846607 |
2018 |
|
Acute monocytic leukemia
|
0.010 |
Biomarker
|
disease |
BEFREE |
Small Molecules Co-targeting CKIα and the Transcriptional Kinases CDK7/9 Control AML in Preclinical Models.
|
30146162 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.010 |
Biomarker
|
disease |
BEFREE |
Small Molecules Co-targeting CKIα and the Transcriptional Kinases CDK7/9 Control AML in Preclinical Models.
|
30146162 |
2018 |
|
Adrenal cortical hypofunction
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Compared with healthy controls, 19 of the 68 genes were found modulated in patients with AI at baseline, 18 of which were restored to control levels 12 weeks after therapy was switched: ARNTL [BMAL] (P = 0.024), CLOCK (P = 0.016), AANAT (P = 0.021), CREB1 (P = 0.010), CREB3 (P = 0.037), MAT2A (P = 0.013); PRKAR1A, PRKAR2A, and PRKCB (all P < 0.010) and PER3, TIMELESS, CAMK2D, MAPK1, SP1, WEE1, CSNK1A1, ONP3, and PRF1 (all P < 0.001).
|
29846607 |
2018 |
|
Hematologic Neoplasms
|
0.010 |
Biomarker
|
group |
BEFREE |
The phylogenetically related Ser/Thr kinases CSNK1A1 (CK1α) and CSNK2 (CK2) have recently gained a growing importance in hematologic malignancies arising both from precursors and from mature blood cells.
|
28969692 |
2017 |