scholarly journals Gene Expression Signature Associated with Clinical Outcome in ALK-Positive Anaplastic Large Cell Lymphoma

Cancers ◽  
2021 ◽  
Vol 13 (21) ◽  
pp. 5523
Author(s):  
Daugrois Camille ◽  
Bessiere Chloé ◽  
Dejean Sébastien ◽  
Anton Leberre Véronique ◽  
Commes Thérèse ◽  
...  
Keyword(s):  
Gene Expression ◽  
T Cell Activation ◽  
Cell Activation ◽  
Predictive Power ◽  
Gene Expression Signature ◽  
Large Cell ◽  
Gene Signature ◽  
Sequencing Data ◽  
Microarray Gene Expression ◽  
Alk Positive

Anaplastic large cell lymphomas associated with ALK translocation have a good outcome after CHOP treatment; however, the 2-year relapse rate remains at 30%. Microarray gene-expression profiling of 48 samples obtained at diagnosis was used to identify 47 genes that were differentially expressed between patients with early relapse/progression and no relapse. In the relapsing group, the most significant overrepresented genes were related to the regulation of the immune response and T-cell activation while those in the non-relapsing group were involved in the extracellular matrix. Fluidigm technology gave concordant results for 29 genes, of which FN1, FAM179A, and SLC40A1 had the strongest predictive power after logistic regression and two classification algorithms. In parallel with 39 samples, we used a Kallisto/Sleuth pipeline to analyze RNA sequencing data and identified 20 genes common to the 28 genes validated by Fluidigm technology—notably, the FAM179A and FN1 genes. Interestingly, FN1 also belongs to the gene signature predicting longer survival in diffuse large B-cell lymphomas treated with CHOP. Thus, our molecular signatures indicate that the FN1 gene, a matrix key regulator, might also be involved in the prognosis and the therapeutic response in anaplastic lymphomas.

Changes in the Immune System and Gene Expression in Bipolar Disorder

2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
H.A. Drexhage
Keyword(s):  
Gene Expression ◽  
Bipolar Disorder ◽  
Environmental Factors ◽  
Inflammatory Response ◽  
T Cell Activation ◽  
Twin Study ◽  
Cell Activation ◽  
Gene Expression Signature ◽  
Inflammatory Gene Expression ◽  
Response System

The etiology of bipolar disorder is thought to involve multiple genes and environmental factors. Recently the immune system has been implicated in the pathogenesis. Various abnormalities indicate the presence of an activated inflammatory response system. In this presentation evidence will be presented on:1.A higher susceptibility for autoimmune diseases (thyroiditis, gastritis, type 1 diabetes), not only in patients but also in first degree relatives independent from mood disturbances.2.An inflammatory gene-expression signature comprising of 19 pro-inflammatory genes in monocytes, the monocyte (and its descendent cells) being important in the activation of the inflammatory response. The inflammatory gene-expression profile was also found in the monocytes of bipolar offspring, especially in those developing a mood disorder (prognostic value of the test?).3.Common environmental factors (infection, stress and dietary components?) as the factors causing the inflammatory monocyte gene-expression signature (evidenced in a twin study).4.A general T cell activation not only linked to the trait of the disorder, but also to the state of the disorder (i.e. with mania) and in part due to genetic factors (evidenced in a twin study). Also T cell activation is not linked to monocyte activation.5.A poor T regulator activation which is genetically determined and correlates with the presence of above-described autoimmune diseases.In sum, there is clear evidence for an activated inflammatory response system in bipolar disorder, yet different components are separately activated in a complex fashion linked to the phenotype of the disorder and involving both genes and environmental factors.

Abstract 647: Identification of Platelet Derived Growth Factors A, B, C and D Specific Role in Vascular Remodeling

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Maria Gonzalez Diez ◽  
Anton Razuvaev ◽  
Ulf Hedin ◽  
Anders Hamsten
Keyword(s):  
Gene Expression ◽  
Cell Differentiation ◽  
Blood Vessel ◽  
Platelet Activation ◽  
T Cell Activation ◽  
Vascular Remodeling ◽  
Cell Activation ◽  
Opposite Effect ◽  
Specific Role ◽  
Biological Processes

Restenosis is a major complication after coronary angioplasty and stenting. The major cause of restenosis is neointimal hyperplasia, which results from an excessive proliferative response of vascular smooth muscle cells (VSMC) to mechanical injury. Platelet derived growth factor (PDGF) family members (A, B, C, D) are known to be related to vascular remodeling. However whether this role is specific for each one or overlapping remains to be elucidated. Aim: To assess the specific role of PDGF family members (A, B, C, D) in vascular remodeling after injury. Methods: We used an established model of balloon injury in rat carotid artery. The endothelium of the intima is mechanically removed. The animals (n=10/group) were sacrificed at different time points after injury (0-2-20 hours, 2-5-15 days, 6-12 weeks). mRNA from carotid arteries were isolated for gene expression studies using microarray gene expression. Results: PDGFs are differentially expressed in vascular remodeling (mRNA, A adj P val=3.28E-06, B adj P val=4.52E-8, C adj P val=5,91E-15, D adj P val=2,64E-18). Also the expression profile differs among them. We selected the genes highly correlated with each of the PDGFs (Spearman correlation, │rs >0.7│) and identified the most preeminent biological pathways associated to each one. PDGF-A positively correlates with program cell death. On the other hand, PDGF-B and C have some overlapping biological processes. There is positive correlation with blood vessel morphogenesis and angiogenesis (B), cell differentiation (B and C), DNA replication (B and C), antigen presentation and T-cell activation/differentiation (B and C). However, there is negative correlation with platelet activation (B) and cell adhesion (B and C). PDGF-D positively correlates with blood vessel morphogenesis and angiogenesis (like B) and cell differentiation (B, C), but is negatively correlated with T-cell activation/proliferation (opposite effect to B and C), apoptosis (opposite effect to A) and platelet activation (B). Conclusion: We identified specific biological processes for PDGF- A, B, C and D. Despite some overlapping, each one plays a specific role within vascular remodeling.

T.69. T Cell Activation and Th2-related Gene Expression Correlate with Disease Activity in Glatiramer Acetate-treated Multiple Sclerosis

2009 ◽  
Vol 131 ◽  
pp. S70
Author(s):  
Finn Sellebjerg ◽  
Martin Krakauer ◽  
Dan Hesse ◽  
Henrik Lund ◽  
Signe Limborg ◽  
...  
Keyword(s):  
Gene Expression ◽  
Multiple Sclerosis ◽  
T Cell ◽  
Disease Activity ◽  
Glatiramer Acetate ◽  
T Cell Activation ◽  
Cell Activation ◽  
Related Gene

scholarly journals Nanoconfinement of Microvilli Alters Gene Expression and Boosts T cell Activation

2021 ◽  
Author(s):  
Morteza Aramesh ◽  
Diana Stoycheva ◽  
Ioana Sandu ◽  
Stephan J. Ihle ◽  
Tamara Zund ◽  
...  
Keyword(s):  
Gene Expression ◽  
T Cells ◽  
T Cell ◽  
Cell Signaling ◽  
T Cell Activation ◽  
Cell Activation ◽  
Local Environment ◽  
T Cell Signaling ◽  
Sense And Respond ◽  
Altered Gene

T cells sense and respond to their local environment at the nanoscale by forming small actin-rich protrusions, called microvilli, which play critical roles in signaling and antigen recognition, particularly at the interface with the antigen presenting cells. However, the mechanisms by which microvilli contribute to cell signaling and activation is largely unknown. Here, we present a tunable engineered system that promotes microvilli formation and T cell signaling via physical stimuli. We discovered that nanoporous surfaces favored microvilli formation, and markedly altered gene expression in T cells and promoted their activation. Mechanistically, confinement of microvilli inside of nanopores leads to size-dependent sorting of membrane-anchored proteins, specifically segregating CD45 phosphatases and T cell receptors (TCR) from the tip of the protrusions when microvilli are confined in 200 nm pores, but not in 400 nm pores. Consequently, formation of TCR nanoclustered hotspots within 200 nm pores, allows sustained and augmented signaling that prompts T cell activation even in the absence of TCR agonists. The synergistic combination of mechanical and biochemical signals on porous surfaces presents a straightforward strategy to investigate the role of microvilli in T cell signaling as well as to boost T cell activation and expansion for application in the growing field of adoptive immunotherapy.

Abstract 3987: Predicting MCL1 inhibitor sensitivity in large cell line panels using a gene expression signature

2019 ◽  
Author(s):  
Andreas Wernitznig ◽  
Dorothea Rudolph ◽  
Matthias Samwer ◽  
Norbert Schweifer ◽  
Francesca Trapani ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Line ◽  
Gene Expression Signature ◽  
Large Cell ◽  
Expression Signature

Abstract 3987: Predicting MCL1 inhibitor sensitivity in large cell line panels using a gene expression signature

2019 ◽  
Author(s):  
Andreas Wernitznig ◽  
Dorothea Rudolph ◽  
Matthias Samwer ◽  
Norbert Schweifer ◽  
Francesca Trapani ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Line ◽  
Gene Expression Signature ◽  
Large Cell ◽  
Expression Signature

scholarly journals Induction of c-ets and c-fos gene expression upon antigenic stimulation of a T cell hybridoma with inducible cytolytic capacity.

1987 ◽  
Vol 166 (3) ◽  
pp. 810-815 ◽  
Author(s):  
Y Kaufmann ◽  
T Silverman ◽  
B Z Levi ◽  
K Ozato
Keyword(s):  
Gene Expression ◽  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Specific Antigen ◽  
Functional Differentiation ◽  
Mrna Levels ◽  
Cellular Oncogenes ◽  
Differentiation Of Lymphocytes ◽  
Stimulation Of

Expression of cellular oncogenes was studied in a T cell hybridoma that undergoes cytolytic activation when stimulated by specific antigen or by anti-Thy-1 antibody. The activation occurs without induction of hybridoma proliferation, providing a model to examine oncogene expression during functional differentiation of lymphocytes. We found that c-fos and c-ets-1 mRNAs were transiently induced at high levels in the hybridoma 30 min and 4 h after stimulation, respectively. c-myc and c-ets-2 oncogenes were constitutively expressed in the hybridoma and their mRNA levels were unaffected during 4 h of stimulation, although c-myc expression was reduced in the later stage of stimulation. Inhibitors of T cell activation, cyclosporin A and anti-LFA-1 antibody, blocked the induction of c-fos and c-ets-1 mRNAs without reducing the levels of c-myc and c-ets-2. The results indicate that the functional activation of the CTL hybridoma is associated with induction of c-fos and c-ets-1 genes.

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