59de799a-1eed-4bf8-9976-644a21c44c2d - samples
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ABSTRACT:
PROVIDER: EGAD00001004937 | EGA |
REPOSITORIES: EGA
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Project description:Adult T-cell leukemia/lymphoma (ATL) is a highly aggressive hematological malignancy derived from mature CD4+ T-lymphocytes. In this study, we performed RNA-sequencing (RNA-seq) analysis for ATL samples including 9 primary tumors and 1 ATL cell line to clarify gene expression profiles in this disease.
| EGAS00001003575 | EGA
Project description:Abstract: Adult T-cell leukemia/lymphoma (ATL) is an aggressive and fatal disease. We have examined 18 ATL patient samples using Affymetrix HG-U133A2.0 arrays. Using the BRB array program, we identified genes differentially expressed in leukemia cells compared to normal lymphocytes. Several unique genes were identified that were overexpressed in leukemia cells including TNFSF11, RGS13, MAFb, CSPG2, C/EBPalpha and TCF4. 200 of the most highly overexpressed ATL genes were analyzed by the PathwayStudio 4.0 program. ATL leukemia cells were characterized by an increase in genes linked to "central" genes CDC2/cyclin B1, SYK/LYN, PCNA and BIRC5. Because of its potential therapeutic importance, we focused our studies on the regulation and function of BIRC5, whose expression was increased in 13 of 14 leukemia samples. TCF4 reporter assays and transfection of DN-TCF4 demonstrated that TCF4 regulates BIRC5 gene expression. Functionally, transfection of ATL cells wi BIRC5 shRNA decreased BIRC5 exprression and cell viability 80%. Clinical treatment of ATL patients with Zenapax or bortezomib decreased BIRC5 expression and cell viability. These experiments represent the first direct experimental evidence that BIRC5 plays an important role in ATL cell viability and provides important insight into ATL genesis and potential targeted therapies. Experiment Overall Design: Gene expression profiles of 7 control and 18 ATL patient samples were analyzed using Affymetrix HG-U133A2.0 arrays.
2009-02-08 | E-GEOD-14317 | biostudies-arrayexpress
Project description:Adult T-cell leukemia/lymphoma (ATL) is a malignancy of mature CD4+ T-cells caused by human T-cell lymphotropic virus type 1 (HTLV-1). Recently, it has been noted that some epigenome abnormalities including DNA methylation and tri-methylation at histone H3Lys27 (H3K27me3) contribute to malignant transformation of ATL. Hence, we investigate the combined effect of DNA demethylating agents and enhancer of zeste homolog 2 (EZH2), which catalyze H3K27me3, inhibitors in ATL. Methylaome analyse revealed that OR21 and the combination changes DNA methylation.
2023-05-03 | GSE189602 | GEO
Project description:Abstract: Adult T-cell leukemia/lymphoma (ATL) is an aggressive and fatal disease. We have examined 18 ATL patient samples using Affymetrix HG-U133A2.0 arrays. Using the BRB array program, we identified genes differentially expressed in leukemia cells compared to normal lymphocytes. Several unique genes were identified that were overexpressed in leukemia cells including TNFSF11, RGS13, MAFb, CSPG2, C/EBPalpha and TCF4. 200 of the most highly overexpressed ATL genes were analyzed by the PathwayStudio 4.0 program. ATL leukemia cells were characterized by an increase in genes linked to "central" genes CDC2/cyclin B1, SYK/LYN, PCNA and BIRC5. Because of its potential therapeutic importance, we focused our studies on the regulation and function of BIRC5, whose expression was increased in 13 of 14 leukemia samples. TCF4 reporter assays and transfection of DN-TCF4 demonstrated that TCF4 regulates BIRC5 gene expression. Functionally, transfection of ATL cells wi BIRC5 shRNA decreased BIRC5 exprression and cell viability 80%. Clinical treatment of ATL patients with Zenapax or bortezomib decreased BIRC5 expression and cell viability. These experiments represent the first direct experimental evidence that BIRC5 plays an important role in ATL cell viability and provides important insight into ATL genesis and potential targeted therapies. Keywords: disease state analysis
2009-02-01 | GSE14317 | GEO
Project description:Adult T-cell leukemia/lymphoma (ATL) is a malignancy of mature CD4+ T-cells caused by human T-cell lymphotropic virus type 1 (HTLV-1). Recently, it has been noted that some epigenome abnormalities including DNA methylation and tri-methylation at histone H3Lys27 (H3K27me3) contribute to malignant transformation of ATL. Hence, we investigate the combined effect of DNA demethylating agents and enhancer of zeste homolog 2 (EZH2), which catalyze H3K27me3, inhibitors in ATL. Gene expression microarray analyses revealed that the combination changes gene expressions stronger than the single treatment.
2023-05-03 | GSE189603 | GEO
Project description:Adult T-cell lymphoma/leukemia (ATL) is an aggressive subtype of leukemia/lymphoma caused by human T-cell leukemia virus type-1 (HTLV-1) and existing chemotherapy for ATL remains with extremely poor prognosis. Therefore, more effective therapeutic options are urgent needs for this disease. Since recent two clinical studies proved promising curability of Lenalidomide (LEN, a second-generation immunomodulatory drug [IMiDs]) for ATL patients, we investigated the direct growth-inhibitory machineries of LEN on ATL cells. Among 13 ATL-related cell lines, Hut102 and TL-Om1 exhibited best response to LEN treatment and LEN-induced functional modulation of E3-ubiquitin ligase cereblon (CRBN) induced degradation of hematopoietic-specific ikaros-family transcription factors IKZF1 and IKZF3 followed by suppression of their down-stream effectors IRF4 and c-Myc (both have been implied to promote ATL cell malignancy). Additionally, Hut102 and TL-Om1 displayed impaired expression of IKZF2 (deletion in HuT102 and altered translational variants in TL-Om1). LEN-induced growth inhibition to these two cell-lines seemed to be attributed to functional deprivation of all IKZF1/2/3. While CRBN-knockdown (KD) in HuT102 imposed LEN-resistance, IKZF2-KD in LEN-resistant ED40515 induced LEN sensitivity. DNA microarray analysis on LEN-treated HuT102 and OATL4 (LEN-resistant) displayed distinct LEN-responding transcriptional profiles; restoration of immune competency and oncogenic growth promotion respectively. Oral administration of LEN to HuT102-xenographted SCID mice demonstrated significant reduction of tumor mass. Finally, a novel form of IMiDs or cereblon modulator (CELMoD), iberdomide (IBE) exerted deeper and wider range of growth suppression to ATL cells including IKZF2 down regulation. Altogether, these findings strongly indicate the therapeutic advantages of IMiDs or CELMoD against ATL.
2024-02-15 | GSE221062 | GEO
Project description:Adult T-cell lymphoma/leukemia (ATL) is an aggressive subtype of leukemia/lymphoma caused by human T-cell leukemia virus type-1 (HTLV-1) and existing chemotherapy for ATL remains with extremely poor prognosis. Therefore, more effective therapeutic options are urgent needs for this disease. Since recent two clinical studies proved promising curability of Lenalidomide (LEN, a second-generation immunomodulatory drug [IMiDs]) for ATL patients, we investigated the direct growth-inhibitory machineries of LEN on ATL cells. Among 13 ATL-related cell lines, Hut102 and TL-Om1 exhibited best response to LEN treatment and LEN-induced functional modulation of E3-ubiquitin ligase cereblon (CRBN) induced degradation of hematopoietic-specific ikaros-family transcription factors IKZF1 and IKZF3 followed by suppression of their down-stream effectors IRF4 and c-Myc (both have been implied to promote ATL cell malignancy). Additionally, Hut102 and TL-Om1 displayed impaired expression of IKZF2 (deletion in HuT102 and altered translational variants in TL-Om1). LEN-induced growth inhibition to these two cell-lines seemed to be attributed to functional deprivation of all IKZF1/2/3. While CRBN-knockdown (KD) in HuT102 imposed LEN-resistance, IKZF2-KD in LEN-resistant ED40515 induced LEN sensitivity. DNA microarray analysis on LEN-treated HuT102 and OATL4 (LEN-resistant) displayed distinct LEN-responding transcriptional profiles; restoration of immune competency and oncogenic growth promotion respectively. Oral administration of LEN to HuT102-xenographted SCID mice demonstrated significant reduction of tumor mass. Finally, a novel form of IMiDs or cereblon modulator (CELMoD), iberdomide (IBE) exerted deeper and wider range of growth suppression to ATL cells including IKZF2 down regulation. Altogether, these findings strongly indicate the therapeutic advantages of IMiDs or CELMoD against ATL.
2024-02-15 | GSE221056 | GEO
Project description:Genomic aberration profiles of chronic type adult T-cell leuekemia/lymphoma (ATL) and acute type ATL(clinical samples) . The Cy3-labeled normal control DNA was obtained from peripheral blood mononuclear cells of healthy males.
2014-02-01 | E-MTAB-1808 | biostudies-arrayexpress
Project description:Transcriptomic studies of adult T cell leukemia and TLL1-transduced ATL cell line
| PRJDB18259 | ENA
Project description:RNA-seq analysis was performed in an adult T-cell leukemia/lymphoma cell line (TL-Om1) to analyze gene expression changes after BATF3 knockdown.
2020-02-02 | GSE140646 | GEO