Chronic fatigue syndrome: identification of transcription factor (TFs) associated with gene expression for drug signature prediction

2019 ◽  
Vol 8 (1) ◽  
Author(s):  
Jyoti Kant Choudhari ◽  
Mukesh Kumar Verma ◽  
Biju Prava Sahariah
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Chronic Fatigue Syndrome ◽  
Chronic Fatigue ◽  
Fatigue Syndrome

Post-exertion malaise in chronic fatigue syndrome: symptoms and gene expression

2013 ◽  
Vol 1 (4) ◽  
pp. 190-209 ◽  
Author(s):  
Jacob D. Meyer ◽  
Alan R. Light ◽  
Sanjay K. Shukla ◽  
Derek Clevidence ◽  
Steven Yale ◽  
...  
Keyword(s):  
Gene Expression ◽  
Chronic Fatigue Syndrome ◽  
Chronic Fatigue ◽  
Fatigue Syndrome

scholarly journals Utility of the Blood for Gene Expression Profiling and Biomarker Discovery in Chronic Fatigue Syndrome

2002 ◽  
Vol 18 (4) ◽  
pp. 193-199 ◽  
Author(s):  
Suzanne D. Vernon ◽  
Elizabeth R. Unger ◽  
Irina M. Dimulescu ◽  
Mangalathu Rajeevan ◽  
William C. Reeves
Keyword(s):  
Gene Expression ◽  
Chronic Fatigue Syndrome ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Biomarker Discovery ◽  
Chronic Fatigue ◽  
Classification Algorithms ◽  
Control Analysis ◽  
Healthy Controls ◽  
Fatigue Syndrome

Chronic fatigue syndrome (CFS) is a debilitating illness lacking consistent anatomic lesions and eluding conventional laboratory diagnosis. Demonstration of the utility of the blood for gene expression profiling and biomarker discovery would have implications into the pathophysiology of CFS. The objective of this study was to determine if gene expression profiles of peripheral blood mononuclear cells (PMBCs) could distinguish between subjects with CFS and healthy controls. Total RNA from PBMCs of five CFS cases and seventeen controls was labeled and hybridized to 1764 genes on filter arrays. Gene intensity values were analyzed by various classification algorithms and nonparametric statistical methods. The classification algorithms grouped the majority of the CFS cases together, and distinguished them from the healthy controls. Eight genes were differentially expressed in both an age-matched case-control analysis and when comparing all CFS cases to all controls. Several of the diffrentially expressed genes are associated with immunologic functions (e.g., CMRF35 antigen, IL-8, HD protein) and implicate immune dysfunction in the pathophysiology of CFS. These results successfully demonstrate the utility of the blood for gene expression profiling to distinguish subjects with CFS from healthy controls and for identifying genes that could serve as CFS biomarkers.

scholarly journals Gene Expression Subtypes in Patients with Chronic Fatigue Syndrome/Myalgic Encephalomyelitis

2008 ◽  
Vol 197 (8) ◽  
pp. 1171-1184 ◽  
Author(s):  
Jonathan R. Kerr ◽  
Robert Petty ◽  
Beverley Burke ◽  
John Gough ◽  
David Fear ◽  
...  
Keyword(s):  
Gene Expression ◽  
Chronic Fatigue Syndrome ◽  
Chronic Fatigue ◽  
Myalgic Encephalomyelitis ◽  
Fatigue Syndrome

scholarly journals Genetics and Gene Expression Involving Stress and Distress Pathways in Fibromyalgia with and without Comorbid Chronic Fatigue Syndrome

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Kathleen C. Light ◽  
Andrea T. White ◽  
Scott Tadler ◽  
Eli Iacob ◽  
Alan R. Light
Keyword(s):  
Gene Expression ◽  
Chronic Fatigue Syndrome ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Chronic Fatigue ◽  
Future Research ◽  
Sensory Receptor ◽  
Methyl Transferase ◽  
Fatigue Syndrome ◽  
Inherited Susceptibility

In complex multisymptom disorders like fibromyalgia syndrome (FMS) and chronic fatigue syndrome (CFS) that are defined primarily by subjective symptoms, genetic and gene expression profiles can provide very useful objective information. This paper summarizes research on genes that may be linked to increased susceptibility in developing and maintaining these disorders, and research on resting and stressor-evoked changes in leukocyte gene expression, highlighting physiological pathways linked to stress and distress. These include the adrenergic nervous system, the hypothalamic-pituitary-adrenal axis and serotonergic pathways, and exercise responsive metabolite-detecting ion channels. The findings to date provide some support for both inherited susceptibility and/or physiological dysregulation in all three systems, particularly for catechol-O-methyl transferase (COMT) genes, the glucocorticoid and the related mineralocorticoid receptors (NR3C1, NR3C2), and the purinergic 2X4 (P2X4) ion channel involved as a sensory receptor for muscle pain and fatigue and also in upregulation of spinal microglia in chronic pain models. Methodological concerns for future research, including potential influences of comorbid clinical depression and antidepressants and other medications, on gene expression are also addressed.

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