Statements (64)
| Predicate | Object |
|---|---|
| gptkbp:instance_of |
gptkb:fusion
|
| gptkbp:affects |
cell differentiation
immune response drug metabolism |
| gptkbp:associated_with |
gptkb:chronic_myeloid_leukemia
gptkb:Oncology targeted therapy clinical outcomes poor prognosis therapeutic resistance increased proliferation increased survival rates leukemogenesis clonal evolution myeloid malignancies secondary mutations BCR-ABL fusion |
| gptkbp:can_cause |
uncontrolled cell proliferation
|
| gptkbp:can_detect |
FISH analysis
bone marrow samples |
| gptkbp:can_lead_to |
drug resistance
|
| gptkbp:composed_of |
gptkb:ABL1_gene
partner gene |
| gptkbp:discovered_by |
1970s
|
| gptkbp:exhibits |
tyrosine kinase activity
|
| https://www.w3.org/2000/01/rdf-schema#label |
ABL1 fusion proteins
|
| gptkbp:influences |
cell cycle regulation
|
| gptkbp:initiated_by |
gptkb:ponatinib
|
| gptkbp:interacts_with |
other signaling pathways
|
| gptkbp:involved_in |
cell signaling
tumorigenesis |
| gptkbp:is_analyzed_in |
next-generation sequencing
Western blotting |
| gptkbp:is_characterized_by |
molecular profiling
|
| gptkbp:is_examined_in |
clinical trials
biopsy samples |
| gptkbp:is_found_in |
hematopoietic cells
|
| gptkbp:is_linked_to |
gptkb:Philadelphia_chromosome
disease progression treatment options treatment resistance increased apoptosis resistance |
| gptkbp:is_monitored_by |
BCR-ABL transcript levels
|
| gptkbp:is_recognized_by |
PCR
|
| gptkbp:is_studied_in |
animal models
laboratory research cell lines patient-derived xenografts |
| gptkbp:is_targeted_at |
gptkb:imatinib
gptkb:ruxolitinib gptkb:venetoclax gptkb:dasatinib gptkb:nilotinib afatinib combination therapies tyrosine kinase inhibitors selinexor bosutinib moleculartargeted agents |
| gptkbp:participated_in |
genomic instability
metastasis |
| gptkbp:result |
chromosomal translocation
|
| gptkbp:bfsParent |
gptkb:ABL1_gene
|
| gptkbp:bfsLayer |
8
|