|
Prostatic Neoplasms
|
0.320 |
AlteredExpression
|
group |
BEFREE |
Since viral infection was not blocked by epigenetic modifiers, and these compounds may independently-induce anti-tumor effects, we propose that epigenetic modifiers and virotherapy are compatible in treatment of prostate tumors defective in JAK1 expression and IFN signaling.
|
27366948 |
2016 |
|
Prostatic Neoplasms
|
0.320 |
GeneticVariation
|
group |
LHGDN |
Identification of inactivating mutations in the JAK1, SYNJ2, and CLPTM1 genes in prostate cancer cells using inhibition of nonsense-mediated decay and microarray analysis.
|
16102578 |
2005 |
|
Malignant neoplasm of prostate
|
0.320 |
GeneticVariation
|
disease |
BEFREE |
Two different heterozygous mutations in the Janus kinase 1 (JAK1) gene result in complete loss of the protein in several different prostate cancer cell lines.
|
16102578 |
2005 |
|
Malignant neoplasm of prostate
|
0.320 |
Biomarker
|
disease |
BEFREE |
Because the activation of STAT3 is mediated by the action of an upstream Janus kinase (JAK) kinase, usually JAK1 or JAK2, the activation step for STAT3 might itself be a target for therapy in prostate cancer.
|
14749471 |
2004 |
|
Hypereosinophilic syndrome
|
0.300 |
Biomarker
|
disease |
GENOMICS_ENGLAND |
JAK1 gain-of-function causes an autosomal dominant immune dysregulatory and hypereosinophilic syndrome.
|
28111307 |
2017 |
|
Lupus Erythematosus, Systemic
|
0.240 |
Biomarker
|
disease |
BEFREE |
Ex-vivo studies of human SLE have demonstrated the effect of JAK1/2 inhibition on the activation of the STAT proteins and autoantibody production from B cells.
|
30462559 |
2019 |
|
Lupus Erythematosus, Systemic
|
0.240 |
Biomarker
|
disease |
BEFREE |
This study provides the foundation for future phase 3 trials of JAK1/2 inhibition with baricitinib as a new potential oral therapy for systemic lupus erythematosus.
|
30043749 |
2018 |
|
Lupus Erythematosus, Systemic
|
0.240 |
Biomarker
|
disease |
BEFREE |
Safety, tolerability, efficacy and pharmacodynamics of the selective JAK1 inhibitor GSK2586184 in patients with systemic lupus erythematosus.
|
27055521 |
2016 |
|
Lupus Erythematosus, Systemic
|
0.240 |
Biomarker
|
disease |
BEFREE |
In conclusion, the deficiency in Jak1‑Stat3 signal transduction in NZW IL‑10R1 cells induces a loss in the inhibition ability of proliferation and activation as well as a migration tendency of B lymphocytes, which is hypothesized to be associated with the occurrence and development of the autoimmune disease systemic lupus erythematosus (SLE).
|
24737344 |
2014 |
|
Lupus Erythematosus, Systemic
|
0.240 |
Biomarker
|
disease |
MGD |
Taken together, Jak1(S645P+/-) mice showed an increased activation of the IL-6-JAK-STAT pathway leading to a systemic lupus erythematosus-like phenotype and offering a new valuable tool to study the role of the JAK/STAT pathway in disease development.
|
23791841 |
2013 |
|
Autoimmune Diseases
|
0.160 |
GeneticVariation
|
group |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
|
Autoimmune Diseases
|
0.160 |
Biomarker
|
group |
BEFREE |
Upadacitinib is a novel selective Janus kinase 1 inhibitor developed for treatment of rheumatoid arthritis and other autoimmune diseases.
|
30633369 |
2019 |
|
Autoimmune Diseases
|
0.160 |
Biomarker
|
group |
BEFREE |
After demonstrating efficacy in a rat adjuvant-induced arthritis (rAIA) model, PF-04965842 (25) was nominated as a clinical candidate for the treatment of JAK1-mediated autoimmune diseases.
|
29298069 |
2018 |
|
Autoimmune Diseases
|
0.160 |
Biomarker
|
group |
BEFREE |
Dual Inhibition of TYK2 and JAK1 for the Treatment of Autoimmune Diseases: Discovery of (( S)-2,2-Difluorocyclopropyl)((1 R,5 S)-3-(2-((1-methyl-1 H-pyrazol-4-yl)amino)pyrimidin-4-yl)-3,8-diazabicyclo[3.2.1]octan-8-yl)methanone (PF-06700841).
|
30113844 |
2018 |
|
Autoimmune Diseases
|
0.160 |
Biomarker
|
group |
BEFREE |
In conclusion, the deficiency in Jak1‑Stat3 signal transduction in NZW IL‑10R1 cells induces a loss in the inhibition ability of proliferation and activation as well as a migration tendency of B lymphocytes, which is hypothesized to be associated with the occurrence and development of the autoimmune disease systemic lupus erythematosus (SLE).
|
24737344 |
2014 |
|
Autoimmune Diseases
|
0.160 |
GeneticVariation
|
group |
BEFREE |
Janus kinase 1 (JAK1), JAK2, and signal transducer and activator of transcription 3 (STAT3) play an important role in Th1 and Th17 differentiation and gene polymorphisms of these factors have been demonstrated to be associated with certain autoimmune diseases.
|
23611997 |
2013 |
|
Autoimmune Diseases
|
0.160 |
GeneticVariation
|
group |
LHGDN |
We suggest that mutations in the JAK1 and Tyk2 genes may be identified as initial molecular defects in human cancers and autoimmune diseases.
|
16239216 |
2005 |
|
Autoimmune Diseases
|
0.160 |
GeneticVariation
|
group |
BEFREE |
We suggest that mutations in the JAK1 and Tyk2 genes may be identified as initial molecular defects in human cancers and autoimmune diseases.
|
16239216 |
2005 |
|
Eczema
|
0.150 |
Biomarker
|
disease |
BEFREE |
This study evaluated the safety and efficacy of multiple doses of the selective Janus kinase 1 inhibitor upadacitinib in patients with moderate-to-severe atopic dermatitis.
|
31786154 |
2020 |
|
Eczema
|
0.150 |
Biomarker
|
disease |
BEFREE |
Treatment of atopic dermatitis with ruxolitinib cream (JAK1/JAK2 inhibitor) or triamcinolone cream.
|
31629805 |
2020 |
|
Eczema
|
0.150 |
Biomarker
|
disease |
BEFREE |
Our aim was to address the direct impact of kinase inhibition of the JAK1/3 pathways by tofacitinib on keratinocyte immune function and barrier formation in atopic dermatitis (AD) and psoriasis.
|
30357932 |
2019 |
|
Eczema
|
0.150 |
Biomarker
|
disease |
BEFREE |
Abrocitinib (PF-04965842) is an oral Janus kinase 1 selective inhibitor under investigation for the treatment of atopic dermatitis.
|
31577341 |
2019 |
|
Eczema
|
0.150 |
GeneticVariation
|
disease |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
|
Eczema
|
0.150 |
AlteredExpression
|
disease |
BEFREE |
Taken together, results of this investigation reveal that IL-4 signals through the Jak1, 2/Stat6 pathway in keratinocytes to stimulate CCL26 expression and this may provide an explanation for the pathogenesis of AD.
|
22226123 |
2012 |
|
Diabetic Nephropathy
|
0.130 |
Biomarker
|
disease |
BEFREE |
Hence, inhibition of these changes by treatment with a JAK1/2 inhibitor suggests that such treatment may help retard progression of early diabetic kidney disease in patients.
|
28554737 |
2017 |