A review and meta-analysis of gene expression profiles in suicide

2022 ◽  
Vol 56 ◽  
pp. 39-49
Author(s):  
Ignazio S Piras ◽  
Matthew J. Huentelman ◽  
Federica Pinna ◽  
Pasquale Paribello ◽  
Marco Solmi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Expression Profiles ◽  
Meta Analysis ◽  
Gene Expression Profiles

Gene Expression Profiles as Predictors of Poor Outcomes in Stage II Colorectal Cancer: A Systematic Review and Meta-analysis

2009 ◽  
Vol 8 (4) ◽  
pp. 207-214 ◽  
Author(s):  
An-Ting T. Lu ◽  
Shelley R. Salpeter ◽  
Anthony E. Reeve ◽  
Steven Eschrich ◽  
Patrick G. Johnston ◽  
...  
Keyword(s):  
Gene Expression ◽  
Colorectal Cancer ◽  
Systematic Review ◽  
Expression Profiles ◽  
Meta Analysis ◽  
Gene Expression Profiles ◽  
Stage Ii ◽  
Stage Ii Colorectal Cancer ◽  
Poor Outcomes

scholarly journals Gene Expression Comparison between Sézary Syndrome and Lymphocytic-Variant Hypereosinophilic Syndrome Refines Biomarkers for Sézary Syndrome

Cells ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 1992
Author(s):  
Andrea Moerman-Herzog ◽  
Syed J. Mehdi ◽  
Henry K. Wong
Keyword(s):  
Gene Expression ◽  
T Cell ◽  
Expression Profiles ◽  
Meta Analysis ◽  
Hypereosinophilic Syndrome ◽  
Diagnostic Delay ◽  
Gene Expression Profiles ◽  
Sézary Syndrome ◽  
Sezary Syndrome ◽  
Gene Expression Studies

Sézary syndrome (SS), an aggressive cutaneous T-cell lymphoma (CTCL) with poor prognosis, is characterized by the clinical hallmarks of circulating malignant T cells, erythroderma and lymphadenopathy. However, highly variable clinical skin manifestations and similarities with benign mimickers can lead to significant diagnostic delay and inappropriate therapy that can lead to disease progression and mortality. SS has been the focus of numerous transcriptomic-profiling studies to identify sensitive and specific diagnostic and prognostic biomarkers. Benign inflammatory disease controls (e.g., psoriasis, atopic dermatitis) have served to identify chronic inflammatory phenotypes in gene expression profiles, but provide limited insight into the lymphoproliferative and oncogenic roles of abnormal gene expression in SS. This perspective was recently clarified by a transcriptome meta-analysis comparing SS and lymphocytic-variant hypereosinophilic syndrome, a benign yet often clonal T-cell lymphoproliferation, with clinical features similar to SS. Here we review the rationale for selecting lymphocytic-variant hypereosinophilic syndrome (L-HES) as a disease control for SS, and discuss differentially expressed genes that may distinguish benign from malignant lymphoproliferative phenotypes, including additional context from prior gene expression studies to improve understanding of genes important in SS.

scholarly journals Meta-analysis of gene expression profiles in long-term non-progressors infected with HIV-1

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Sun Young Lee ◽  
Yong Kwang Park ◽  
Cheol-Hee Yoon ◽  
Kisoon Kim ◽  
Kyung-Chang Kim
Keyword(s):  
Gene Expression ◽  
Expression Profiles ◽  
Meta Analysis ◽  
Gene Expression Profiles ◽  
Hiv 1

scholarly journals Correcting differential gene expression analysis for cyto-architectural alterations in substantia nigra of Parkinson's disease patients reveals known and potential novel disease-associated genes and pathways

2021 ◽  
Author(s):  
Federico Ferraro ◽  
Christina Fevga ◽  
Vincenzo Bonifati ◽  
Wim Mandemakers ◽  
Ahmed Mahfouz ◽  
...  
Keyword(s):  
Gene Expression ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Substantia Nigra ◽  
Expression Profiles ◽  
Meta Analysis ◽  
Gene Expression Profiles ◽  
Substantia Nigra Pars Compacta ◽  
Ammonium Transport ◽  
Protein Interaction Data

Several studies have analyzed gene expression profiles in the substantia nigra to better understand the pathological mechanisms causing Parkinson's disease (PD). However, the concordance between the identified gene signatures in these individual studies was generally low. This might be caused by a change in cell type composition as loss of dopaminergic neurons in the substantia nigra pars compacta is a hallmark of PD. Through an extensive meta-analysis of nine previously published microarray studies, we demonstrated that a big proportion of the detected differentially expressed genes was indeed caused by cyto-architectural alterations due to the heterogeneity in the neurodegenerative stage and/or technical artifacts. After correcting for cell composition, we identified a common signature that deregulated the previously unreported ammonium transport, as well as known biological processes including bioenergetic pathways, response to proteotoxic stress, and immune response. By integrating with protein-interaction data, we shortlisted a set of key genes, such as LRRK2, PINK1, and PRKN known to be related to PD; others with compelling evidence for their role in neurodegeneration, such as GSK3β, WWOX, and VPC; as well as novel potential players in the PD pathogenesis, including NTRK1, TRIM25, ELAVL1. Together, these data showed the importance of accounting for cyto-architecture in these analyses and highlight the contribution of multiple cell types and novel processes to PD pathology providing potential new targets for drug development.

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