Transcription profiling of human U937 expressing an inducible AML1-ETO construct - time series

ChEBI2009-05-14 更新2026-07-21 收录

白血病分子病理学

致癌融合蛋白转录调控

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https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-15647 数据链接链接失效反馈

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Transcription profiling of human U937 expressing an inducible AML1-ETO construct - time series

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2009-05-14

The molecular basis of T-PLL is an actionable perturbation of TCL1/ATM- and epigenetically instructed damage responses [murine SNP array]

白血病分子病理学

DNA损伤响应

T-cell prolymphocytic leukemia (T-PLL) is a rare and poor-prognostic mature T-cell malignancy. To address its incomplete molecular concept, we integrated large-scale profiling data of alterations in g

NIAID Data Ecosystem60

Expression profile of acute monocytic leukemia patients. Homo sapiens

白血病分子病理学

差异基因表达分析

To understand the pathogenesis of DNMT3A in acute monocytic leukemia (AML-M5), we identified genes that are expressed differently in leukemia cells from AML-M5 patients collected at diagnosis with DNM

NIAID Data Ecosystem30

Table1_MiRNA-142-3P and FUS can be Sponged by Long Noncoding RNA DUBR to Promote Cell Proliferation in Acute Myeloid Leukemia.XLSX

白血病分子病理学

非编码RNA调控

Acute myeloid leukemia (AML) represents a frequently occurring adulthood acute leukemia (AL). Great progresses have been achieved in the treatment of AML, but its pathogenic mechanism remains unclear.

NIAID Data Ecosystem20

Acute leukemias of different lineages have similar MLL gene fusions encoding related chimeric proteins resulting from chromosomal translocation.

白血病分子病理学

染色体融合

The MLL gene, on human chromosome 11q23, undergoes chromosomal translocation in acute leukemias, resulting in gene fusion with AF4 (chromosome 4) and ENL (chromosome 19). We report here translocation

PubMed Central1993-09-15 更新40

Myb overexpression synergizes with loss of Pten and is a dependency factor and therapeutic target in T-cell acute lymphoblastic leukemia

白血病分子病理学

肿瘤靶向治疗

T-lineage acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy that accounts for 10%–15% of pediatric and 25% of adult ALL cases. Although the prognosis of T-ALL has improved

NIAID Data Ecosystem20

Transcription profiling of human U937 expressing an inducible AML1-ETO construct - time series

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