This SuperSeries is composed of the SubSeries listed below.
Suboptimal evolutionary novel environments promote singular altered gravity responses of transcriptome during Drosophila metamorphosis.
Sex, Age
View SamplesGenome-wide transcriptional profiling showed that reducing gravity levels in the International Space Station (ISS) causes important alterations in Drosophila gene expression intimately linked to imposed spaceflight-related environmental constrains during Drosophila metamorphosis. However, simulation experiments on ground testing space-related environmental constraints, show differential responses. Curiously, although particular genes are not common in the different experiments, the same GO groups including a large multigene family related with behavior, stress response and organogenesis are over represented in them. A global and integrative analysis using the gene expression dynamics inspector (GEDI) self-organizing maps, reveals different degrees in the responses of the transcriptome when using different environmental conditions or microgravity/hypergravity simulation devices
Suboptimal evolutionary novel environments promote singular altered gravity responses of transcriptome during Drosophila metamorphosis.
No sample metadata fields
View SamplesGenome-wide transcriptional profiling shows that reducing gravity levels in the International Space Station (ISS) causes important alterations in Drosophila gene expression. However, simulation experiments on ground, without space constraints, show weaker effects than space environment. A global and integrative analysis using the gene expression dynamics inspector (GEDI) self-organizing maps, reveals a subtle response of the transcriptome using different populations and microgravity and hypergravity simulation devices. These results suggest that, in addition to behavioural responses that can be detected also at the gene expression level, the transcriptome is finely tuned to normal gravity.
No associated publication
No sample metadata fields
View SamplesChronic lymphocytic leukemia (CLL) is characterized by the accumulation of malignant CD5+ B lymphocytes (CLL cells) in the peripheral blood, and their progressive infiltration in lymphoid organs.
No associated publication
Specimen part
View SamplesChronic lymphocytic leukemia (CLL) is characterized by the accumulation of malignant CD5+ B lymphocytes (CLL cells) in the peripheral blood, and their progressive infiltration in lymphoid organs. Despite the efforts made, CLL remains an incurable disease. It is therefore crucial to continue searching for new therapeutic agents and targets. Arsenic trioxide (ATO) induces apoptosis in all CLL cases and it could constitute an efficient therapy for this disease.
No associated publication
Specimen part
View SamplesSeveral bacterial human pathogens regulate the production of virulence factors by temperature, expressing them only at 37 C. Accordingly we show that the production of all P. aeruginosa virulence factors that are dependent on the QS transcriptional regulator RhlR, but only a fraction that are activated by LasR, are induced at 37 C compared to 30 C or 25 C. The RhlR-dependent induction at 37 C is a posttranscriptional effect due to an RNA thermometer of the ROSE family that thermoregulates the expression of rhlAB operon involved in rhamnolipids production, a virulence associated trait. This RNA structure also affects the expression of the downstream rhlR gene. A second thermometer is present upstream lasI and causes a reduced expression of this gene at lower temperatures without causing a significant decrease of the autoinducer 3-oxo-dodecanoyl homoserine lactone.
Regulation of Pseudomonas aeruginosa virulence factors by two novel RNA thermometers.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
PI3K inhibition synergizes with glucocorticoids but antagonizes with methotrexate in T-cell acute lymphoblastic leukemia.
Sex, Age, Specimen part, Cell line
View SamplesThe PI3K pathway is frequently hyperactivated in primary T-cell acute lymphoblastic leukemia (T-ALL) cells. Activation of the PI3K pathway has been suggested as one mechanism of glucocorticoid resistance in T-ALL, and patients harboring mutations in the PI3K negative regulator PTEN may be at increased risk of induction failure and relapse. In this study, we identified Myc as an important downstream integrator of PI3K pathway activity in T-ALL and we provide data supportive of an association of higher PI3K activity with glucocorticoid resistance and worse clinical outcome. The PI3K inhibitor AS605240 showed anti-leukemic activity and strong synergism with glucocorticoids both in vitro and in a NOD/SCID xenograft model of T-ALL. In contrast, PI3K inhibition showed antagonism with methotrexate and daunorubicin, drugs that preferentially target dividing cells. This antagonistic interaction, however, could be circumvented by the use of correct drug scheduling schemes. Our data indicate the potential benefits and difficulties for the incorporation of PI3K inhibitors in T-ALL therapy.
PI3K inhibition synergizes with glucocorticoids but antagonizes with methotrexate in T-cell acute lymphoblastic leukemia.
Sex, Age, Specimen part
View SamplesThe PI3K pathway is frequently hyperactivated in primary T-cell acute lymphoblastic leukemia (T-ALL) cells. Activation of the PI3K pathway has been suggested as one mechanism of glucocorticoid resistance in T-ALL, and patients harboring mutations in the PI3K negative regulator PTEN may be at increased risk of induction failure and relapse. In this study, we identified Myc as an important downstream integrator of PI3K pathway activity in T-ALL and we provide data supportive of an association of higher PI3K activity with glucocorticoid resistance and worse clinical outcome. The PI3K inhibitor AS605240 showed anti-leukemic activity and strong synergism with glucocorticoids both in vitro and in a NOD/SCID xenograft model of T-ALL. In contrast, PI3K inhibition showed antagonism with methotrexate and daunorubicin, drugs that preferentially target dividing cells. This antagonistic interaction, however, could be circumvented by the use of correct drug scheduling schemes. Our data indicate the potential benefits and difficulties for the incorporation of PI3K inhibitors in T-ALL therapy.
PI3K inhibition synergizes with glucocorticoids but antagonizes with methotrexate in T-cell acute lymphoblastic leukemia.
Sex, Specimen part
View SamplesIn our efforts to evaluate the function of the IL-8 receptor CXCR2 in Acute Lymphoblastic Leukemia (ALL) cells, we made use of SB225002 (N-(2-hydroxy-4-nitrophenyl)-N-(2-bromophenyl)urea), a drug initially described as a CXCR2 antagonist. Although the CXCR2 receptor was found to be non-functional in ALL, B- and T-ALL cell lines were sensitive to SB225002.
SB225002 Induces Cell Death and Cell Cycle Arrest in Acute Lymphoblastic Leukemia Cells through the Activation of GLIPR1.
Specimen part, Cell line
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