Molecular characterization of AML with ins(21;8)(q22;q22q22) reveals similarity to t(8;21) AML

ChEBI2010-10-26 更新2026-07-21 收录

白血病分子分型

血液肿瘤遗传异常

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https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-24384 数据链接链接失效反馈

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Molecular characterization of AML with ins(21;8)(q22;q22q22) reveals similarity to t(8;21) AML

创建时间：

2010-10-26

Identification of epigenetic modifiers essential for growth and survival of AML1/ETO-positive leukemia

白血病分子分型

表观遗传靶点

Aberrant gene expression patterns in acute myeloid leukemia (AML) with balanced chromosomal translocations are often associated with direct or indirect dysregulation of epigenetic modifiers. Previousl

NIAID Data Ecosystem90

Gene expression profiling of CEBPA double and single mutant and CEBPA wild type AML.

白血病分子分型

CEBPA基因

Mutations in CCAAT/enhancer binding protein alpha (CEBPA) are seen in 5-14% of acute myeloid leukemia (AML) and have been associated with a favorable clinical outcome. Most AMLs with CEBPA mutations s

NIAID Data Ecosystem50

Supplementary Table S5 & 6: GSEA of SY-1425 response from Superenhancer Analysis Defines Novel Epigenomic Subtypes of Non-APL AML, Including an RARα Dependency Targetable by SY-1425, a Potent and Selective RARα Agonist

白血病分子分型

RARα激动剂转录响应

GSEA of transcriptional response to SY-1425 in RARA-high cell lines in perturbation gene sets & GSEA of transcriptional response to SY-1425 in RARA-high cell lines in hallmark/pathways and perturbatio

Figshare2017-10-01 更新00

Amplified EPOR/JAK2 genes define a unique subtype of acute erythroid leukemia

白血病分子分型

白血病靶向治疗

Acute erythroid leukemia (AEL) is a unique subtype of acute myeloid leukemia characterized by prominent erythroid proliferation, whose molecular basis is poorly understood. To elucidate the underlying

NIAID Data Ecosystem50

Chromatin accessibility maps of chronic lymphocytic leukemia identify subtype-specific epigenome signatures and transcription regulatory networks. Homo sapiens

癌症表观遗传学

白血病分子分型

Chronic lymphocytic leukemia (CLL) is characterized by substantial clinical heterogeneity, despite relatively few genetic alterations. To provide a basis for studying epigenome deregulation in CLL, we

NIAID Data Ecosystem40

Molecular characterization of AML with ins(21;8)(q22;q22q22) reveals similarity to t(8;21) AML

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