|
Malignant Neoplasms
|
0.090 |
Biomarker
|
group |
BEFREE |
Uveal melanoma (UM) is the most common intraocular cancer with a high mortality rate that requires new research in the field of prevention and treatment. c-REL is a member of the nuclear factor κB (NF-κB) transcription factor family and an emerging regulator of tumorigenesis.
|
31768922 |
2019 |
|
Primary malignant neoplasm
|
0.050 |
Biomarker
|
group |
BEFREE |
Uveal melanoma (UM) is the most common intraocular cancer with a high mortality rate that requires new research in the field of prevention and treatment. c-REL is a member of the nuclear factor κB (NF-κB) transcription factor family and an emerging regulator of tumorigenesis.
|
31768922 |
2019 |
|
Carcinogenesis
|
0.040 |
AlteredExpression
|
phenotype |
BEFREE |
Uveal melanoma (UM) is the most common intraocular cancer with a high mortality rate that requires new research in the field of prevention and treatment. c-REL is a member of the nuclear factor κB (NF-κB) transcription factor family and an emerging regulator of tumorigenesis.
|
31768922 |
2019 |
|
Uveal melanoma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
On multivariate analysis, scleral invasion and c-REL nuclear expression found to be an independent prognostic factor (p < 0.05) CONCLUSIONS: To the best of our knowledge, this was the first study reporting the expression of the c-REL protein in uveal melanoma.
|
31768922 |
2019 |
|
Eczema
|
0.100 |
GeneticVariation
|
disease |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
|
Rheumatoid Arthritis
|
0.460 |
GeneticVariation
|
disease |
GWASCAT |
Genetic influences on susceptibility to rheumatoid arthritis in African-Americans.
|
30423114 |
2019 |
|
Multiple Sclerosis
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
We found that miR-455-5p expression was highly correlated with disease severity in MS patients. miR-455-5p expression inversely correlates with its inflammatory-predicted targets (MyD88 and REL) in relapse- and remitting-phase patients.
|
30310937 |
2019 |
|
Malignant Neoplasms
|
0.090 |
Biomarker
|
group |
BEFREE |
In nearly all MYD88-wild-type DLBCL-LT, we found cancer-promoting mutations that either activate the NF-κB pathway through alternative genes (NFKBIE or REL) or activate other canonical cancer pathways (BRAF, MED12, PIK3R1, and STAT3).
|
29857068 |
2018 |
|
Primary malignant neoplasm
|
0.050 |
Biomarker
|
group |
BEFREE |
In nearly all MYD88-wild-type DLBCL-LT, we found cancer-promoting mutations that either activate the NF-κB pathway through alternative genes (NFKBIE or REL) or activate other canonical cancer pathways (BRAF, MED12, PIK3R1, and STAT3).
|
29857068 |
2018 |
|
heavy drinking
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
Non-treatment-seeking underage drinkers who reported past-month heavy drinking (N = 167; ages 17 to 20; 42% female; 59% non-Hispanic White) were randomly assigned to receive a single session of BMI or REL.
|
29750362 |
2018 |
|
Adult T-Cell Lymphoma/Leukemia
|
0.010 |
Biomarker
|
disease |
BEFREE |
Interferon regulatory factor (IRF) 4 and the proto-oncogene c-Rel cooperate in growth and antiviral drug resistance of adult T-cell leukemia/lymphoma (ATLL).
|
29684346 |
2018 |
|
respiratory compensation
|
0.010 |
Biomarker
|
disease |
BEFREE |
Three dimensional kinetic and kinematic data were collected from all participants running at relative (REL: 1.5 km·h<sup>-1</sup> below respiratory compensation point) and absolute (ABS: 4.5 m·s<sup>-1</sup>) speeds.
|
29334675 |
2018 |
|
cervical cancer
|
0.010 |
Biomarker
|
disease |
BEFREE |
Here, we applied CRISPR/Cas9n-mediated genome editing to successfully knockout the NF-κB subunit c-REL in HeLa Kyoto cells as a model system for cervical cancers.
|
28767691 |
2017 |
|
Carcinogenesis
|
0.040 |
Biomarker
|
phenotype |
BEFREE |
Analysis of the genes harboring these loci revealed two genes (ARID1B and REL) and two significantly enriched pathways (chromatin organization and cellular stress response) suggesting that the process of lung carcinogenesis is linked to chromatin remodeling, inflammation, and tumor microenvironment restructuring.
|
28759038 |
2017 |
|
Composite Lymphoma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Of the NF-κB genes analyzed, c-REL was overexpressed in g.i.MZBL. c-REL amplification was limited to 6/22 large cell MZBL including the large cell component of 2/9 composite small cell/large cell lymphomas, and c-Rel protein expression was found in the large cell compartment of composite lymphomas.
|
28729720 |
2017 |
|
Tuberculosis
|
0.010 |
Biomarker
|
disease |
BEFREE |
Crystallographic and solution structure of the N-terminal domain of the Rel protein from Mycobacterium tuberculosis.
|
28672070 |
2017 |
|
Autoimmune Diseases
|
0.120 |
AlteredExpression
|
group |
BEFREE |
However, despite the highly reduced Treg compartment, double-deficient mice did not develop autoimmunity even when aged to more than 1 y, suggesting that c-REL and IκB<sub>NS</sub> are required for T cell effector function as well.
|
28652399 |
2017 |
|
Malignant Neoplasms
|
0.090 |
Biomarker
|
group |
BEFREE |
Foxp3-expressing regulatory T cells (Tregs) are essential regulators of immune homeostasis and, thus, are prime targets for therapeutic interventions of diseases such as cancer and autoimmunity. c-REL and IκB<sub>NS</sub> are important regulators of Foxp3 induction in Treg precursors upon γ-chain cytokine stimulation.
|
28652399 |
2017 |
|
Primary malignant neoplasm
|
0.050 |
Biomarker
|
group |
BEFREE |
Foxp3-expressing regulatory T cells (Tregs) are essential regulators of immune homeostasis and, thus, are prime targets for therapeutic interventions of diseases such as cancer and autoimmunity. c-REL and IκB<sub>NS</sub> are important regulators of Foxp3 induction in Treg precursors upon γ-chain cytokine stimulation.
|
28652399 |
2017 |
|
Neoplasms
|
0.090 |
Biomarker
|
group |
BEFREE |
In addition to DNA damage repair genes such as ATM and BRCA1, anti-apoptotic BCL2 was significantly elevated in REL-high FL and tFL tumors.
|
28095352 |
2017 |
|
Carcinogenesis
|
0.040 |
Biomarker
|
phenotype |
BEFREE |
REL, a proto-oncogene located on frequently amplified 2p16.1-p15 locus, promotes tumorigenesis in many cancer types through deregulation of the NF-κB pathway; however, its role in FL pathobiology or chemoresistance has not been addressed.
|
28095352 |
2017 |
|
Lymphoma, Follicular
|
0.020 |
Biomarker
|
disease |
BEFREE |
Altogether these data suggest that other genes located in amplified 2p16.1-p15 locus may have more oncogenic role in FL etiology; however, high REL expression may be useful as a predictive biomarker of response to immunochemotherapy, and inhibition of c-REL may potentially sensitize resistant FL or tFL cells to chemotherapy.
|
28095352 |
2017 |
|
Dengue Fever
|
0.010 |
Biomarker
|
disease |
BEFREE |
We propose a model in which AaHMGB1 bends NF-kB/Rel target DNA to recruit and allow more efficient AaRel1A binding to activate transcription of effector genes, culminating in a stronger Toll pathway-mediated response against DENV infection.
|
27867076 |
2017 |
|
Malignant Neoplasms
|
0.090 |
Biomarker
|
group |
BEFREE |
Our literature search found that miR‑574 is regulated in cancer stem cells (CSCs), and next we used the microRNA (miRNA) database (www.mirdb.org) to find REL as a target of miR‑574.
|
27779701 |
2016 |
|
Primary malignant neoplasm
|
0.050 |
Biomarker
|
group |
BEFREE |
Our literature search found that miR‑574 is regulated in cancer stem cells (CSCs), and next we used the microRNA (miRNA) database (www.mirdb.org) to find REL as a target of miR‑574.
|
27779701 |
2016 |