Disease Information

General Information of the Disease (ID: DIS00562)

• Name: Acute lymphoblastic leukaemia
• ICD: ICD-11: 2A70

Type(s) of Resistant Mechanism of This Disease

  ADTT: Aberration of the Drug's Therapeutic Target

Drug Resistance Data Categorized by Drug

Approved Drug(s) 1 drug(s) in total

Idelalisib

Drug Sensitivity Data Categorized by Their Corresponding Mechanisms

Aberration of the Drug's Therapeutic Target (ADTT)

Key Molecule: Glucocorticoid receptor (NR3C1) [1]

• Sensitive Disease: b-lymphoblastic leukemia [ICD-11: 2A70]
• Sensitive Drug: Idelalisib
• Molecule Alteration: Phosphorylation; Down-regulation
• Experimental Note: Revealed Based on the Cell Line Data
• In Vitro Model: Nalm-6 cells; Peripheral blood; Homo sapiens (Human); CVCL_0092
• In Vitro Model: Sup-B15 cells; Bone marrow; Homo sapiens (Human); CVCL_0103
• In Vitro Model: RCH-ACV cells; Bone marrow; Homo sapiens (Human); CVCL_1851
• Experiment for Molecule Alteration: Gene expression assay; MS analysis; Electrophoretic mobility shift assay; Phospho-GR Western blot assay
• Experiment for Drug Resistance: Cell viability assay
• Mechanism Description: Through this comprehensive analysis, we discovered growth factor receptor-bound protein 2 (Grb2) as a central interactor bridging the pathways related to PI3Kalpha and beta1 integrin.

Key Molecule: Glucocorticoid receptor (NR3C1) [1]

• Sensitive Disease: b-lymphoblastic leukemia [ICD-11: 2A70]
• Sensitive Drug: Idelalisib
• Molecule Alteration: Phosphorylation; Down-regulation
• Experimental Note: Revealed Based on the Cell Line Data
• In Vitro Model: Nalm-6 cells; Peripheral blood; Homo sapiens (Human); CVCL_0092
• In Vitro Model: Sup-B15 cells; Bone marrow; Homo sapiens (Human); CVCL_0103
• In Vitro Model: RCH-ACV cells; Bone marrow; Homo sapiens (Human); CVCL_1851
• Experiment for Molecule Alteration: Gene expression assay; MS analysis; Electrophoretic mobility shift assay; Phospho-GR Western blot assay
• Experiment for Drug Resistance: Cell viability assay
• Mechanism Description: Through this comprehensive analysis, we discovered growth factor receptor-bound protein 2 (Grb2) as a central interactor bridging the pathways related to PI3Kalpha and beta1 integrin.

Key Molecule: Glucocorticoid receptor (NR3C1) [1]

• Sensitive Disease: b-lymphoblastic leukemia [ICD-11: 2A70]
• Sensitive Drug: Idelalisib
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Revealed Based on the Cell Line Data
• In Vitro Model: Nalm-6 cells; Peripheral blood; Homo sapiens (Human); CVCL_0092
• In Vitro Model: Sup-B15 cells; Bone marrow; Homo sapiens (Human); CVCL_0103
• In Vitro Model: RCH-ACV cells; Bone marrow; Homo sapiens (Human); CVCL_1851
• Experiment for Molecule Alteration: Gene expression assay; MS analysis; Electrophoretic mobility shift assay; Phospho-GR Western blot assay
• Experiment for Drug Resistance: Cell viability assay
• Mechanism Description: Through this comprehensive analysis, we discovered growth factor receptor-bound protein 2 (Grb2) as a central interactor bridging the pathways related to PI3Kalpha and beta1 integrin.

References

• Ref 1: PI3Kdelta Inhibition Potentiates Glucocorticoids in B-lymphoblastic Leukemia by Decreasing Receptor Phosphorylation and Enhancing Gene Regulation. Cancers (Basel). 2023 Dec 27;16(1):143.