|
Colorectal Carcinoma
|
0.320 |
AlteredExpression
|
disease |
BEFREE |
We found that ACS5 expression was upregulated in CRC cells and CRC tissues and that high ACS5 expression was more frequent in CRC patients with excess muscular layer and with poor tumor differentiation.
|
28808653 |
2017 |
|
Colorectal Carcinoma
|
0.320 |
Biomarker
|
disease |
BEFREE |
The results suggest the involvement of ACS5 in the early genesis of colorectal cancer, most likely by modification of the transport and pool formation of long-chain acyl-CoA thioesters, as recently demonstrated for other isoforms of the ACS family.
|
16110457 |
2005 |
|
Colorectal Carcinoma
|
0.320 |
GeneticVariation
|
disease |
UNIPROT |
|
|
|
|
Arthritis, Adjuvant-Induced
|
0.300 |
Biomarker
|
disease |
CTD_human |
Impaired intrinsic chiral inversion activity of ibuprofen in rats with adjuvant-induced arthritis.
|
18988084 |
2008 |
|
Arthritis, Collagen-Induced
|
0.300 |
Biomarker
|
disease |
CTD_human |
Impaired intrinsic chiral inversion activity of ibuprofen in rats with adjuvant-induced arthritis.
|
18988084 |
2008 |
|
Arthritis, Experimental
|
0.300 |
Biomarker
|
disease |
CTD_human |
Impaired intrinsic chiral inversion activity of ibuprofen in rats with adjuvant-induced arthritis.
|
18988084 |
2008 |
|
mathematical ability
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Gene discovery and polygenic prediction from a genome-wide association study of educational attainment in 1.1 million individuals.
|
30038396 |
2018 |
|
Platelet mean volume determination (procedure)
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
The Allelic Landscape of Human Blood Cell Trait Variation and Links to Common Complex Disease.
|
27863252 |
2016 |
|
Neoplasms
|
0.070 |
Biomarker
|
group |
BEFREE |
RNA sequencing identified a novel FGFR2-ACSL5 fusion in the resistant tumor that was absent from the matched pre-treatment tumor.
|
28122360 |
2017 |
|
Neoplasms
|
0.070 |
Biomarker
|
group |
BEFREE |
This integrative proteomic and lipidomic study from mouse to human and from liver to blood identified the following disease signatures: (i) an HCC signature: upregulated hepatic scd1/scd2, fads2, and acsl5:acsl1 ratio, elevated vaccenic and erucic acids, and reduced margaric and linoleic acids in both liver and plasma; (ii) a NASH signature that correlates with tumor burden: upregulated hepatic elovl6, elevated oleic, adrenic, and osbond acids, and reduced cervonic acid in liver and plasma; and (iii) a NASH signature: reduced hepatic and circulating lignoceric and eicosapentaenoic acids.
|
23749645 |
2013 |
|
Neoplasms
|
0.070 |
Biomarker
|
group |
BEFREE |
ACS-1 also inhibited matrix metalloproteinase-9 activity, cellular migration, and invasion, and ACS-2 reduced tumor burden and resulted in increased tumor host interactions.
|
22436383 |
2012 |
|
Neoplasms
|
0.070 |
Biomarker
|
group |
BEFREE |
Immunohistochemistry was performed for LGALS4 (Galectin 4), ACS5 (Acyl-CoA synthetase) and CLU (Clusterin) proteins: LGALS4 was highly up-regulated, particularly in the most differentiated tumors, while CLU was lost in all tumors.
|
19903339 |
2009 |
|
Neoplasms
|
0.070 |
Biomarker
|
group |
BEFREE |
These results indicate that ACSL5 is a critical factor for survival of glioma cells under acidic tumor microenvironment, thus providing novel molecular basis for cancer therapy.
|
18806831 |
2009 |
|
Neoplasms
|
0.070 |
Biomarker
|
group |
BEFREE |
Deregulation of the ACSL5-fl/ACSL5-Delta 20 homeostasis in the maturation and shedding of cells along the CVA might also be of relevance for the development of intestinal neoplasia.
|
17681178 |
2007 |
|
Neoplasms
|
0.070 |
AlteredExpression
|
group |
BEFREE |
With regard to its value for histopathological diagnosis, immunohistochemical characterization of endometrioid adenocarcinomas shows that a decrease in ACS5 expression correlates with tumour dedifferentiation.
|
16241998 |
2005 |
|
Adenocarcinoma
|
0.030 |
AlteredExpression
|
group |
BEFREE |
Using a standardized immunohistochemical approach, colorectal adenocarcinomas with low (n=41; group 1) or high (n=31; group 2) ACSL5 levels were identified.
|
28153554 |
2017 |
|
Carcinogenesis
|
0.030 |
Biomarker
|
phenotype |
BEFREE |
Whilst impaired expression of ACSL5 has been associated with sporadic colorectal carcinogenesis, little is known about ACSL5 as a prognostic factor.
|
28153554 |
2017 |
|
Adenocarcinoma
|
0.030 |
Biomarker
|
group |
BEFREE |
ACSL5-related pathways were characterized in normal mucosa and sporadic adenocarcinomas of the human intestine.
|
24770931 |
2014 |
|
Carcinogenesis
|
0.030 |
Biomarker
|
phenotype |
BEFREE |
Uncoupling of ACSL5 and mitochondrial mortalin by mutated TP53 could be important in colorectal carcinogenesis.
|
24770931 |
2014 |
|
Adenocarcinoma
|
0.030 |
AlteredExpression
|
group |
BEFREE |
However, basal ACS5 enzymatic activity was increased as a percentage of the total activity of ACSs in both groups, arguing for an absolute (group 1) or relative (group 2) increase in ACS5 enzymatic activity in all adenocarcinomas investigated.
|
16110457 |
2005 |
|
Carcinogenesis
|
0.030 |
Biomarker
|
phenotype |
BEFREE |
Whilst an increase in ACS4 expression has been associated with colorectal carcinogenesis, little is known about possible pathogenetic functions of other ACS isoforms, such as ACS5, in tumourigenesis.
|
16110457 |
2005 |
|
Myocardial Infarction
|
0.020 |
Biomarker
|
disease |
BEFREE |
ATLAS-ACS-2 Thrombolysis in Myocardial Infarction-51 was a double-blind, multicenter, phase 3 clinical trial that randomized patients within 7 days of an ACS event to standard of care plus either rivaroxaban 2.5 mg BID, 5 mg BID, or placebo (n = 15,526).
|
30340765 |
2018 |
|
Myocardial Infarction
|
0.020 |
GeneticVariation
|
disease |
BEFREE |
Evidence from Anti-Xa Therapy to Lower Cardiovascular Events in Addition to Standard Therapy in Subjects with Acute Coronary Syndrome-Thrombolysis In Myocardial Infarction-51 (ATLAS-ACS 2-TIMI 51) supports the use of the direct, oral, factor Xa inhibitor rivaroxaban (2.5 mg twice-daily [bid] and 5 mg bid) in reducing mortality and morbidity in patients with acute coronary syndrome, when combined with antiplatelets.
|
29566413 |
2018 |
|
Acute Coronary Syndrome
|
0.020 |
Biomarker
|
disease |
BEFREE |
Evidence from Anti-Xa Therapy to Lower Cardiovascular Events in Addition to Standard Therapy in Subjects with Acute Coronary Syndrome-Thrombolysis In Myocardial Infarction-51 (ATLAS-ACS 2-TIMI 51) supports the use of the direct, oral, factor Xa inhibitor rivaroxaban (2.5 mg twice-daily [bid] and 5 mg bid) in reducing mortality and morbidity in patients with acute coronary syndrome, when combined with antiplatelets.
|
29566413 |
2018 |
|
Acute Coronary Syndrome
|
0.020 |
GeneticVariation
|
disease |
BEFREE |
Usefulness of Rivaroxaban for Secondary Prevention of Acute Coronary Syndrome in Patients With History of Congestive Heart Failure (from the ATLAS-ACS-2 TIMI-51 Trial).
|
30340765 |
2018 |