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Keyword [BCR/ABL1]
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1. Biological Functions And Clinical Applications Of BCR-ABL1-positive Microvesicles
2. Clonal Evolution Studies Of Chronic Myeloid Leukemia And Astrocytoma
3. Leukemia Cell-derived Microvesicles Induce Malignant Transformation Of Mesenchymal Stem Cells By Horizontal Transferring BCR-ABL1mRNA And Protein
4. Molecular Cloning And Leukemogenesis Studies Of A Novel Fusion Gene Involving The PAX5Gene, PAX5-UBE2D4
5. The Research Of The Association Between BCR-ABL1 Fusion Gene Mutation And TKIs Resistance Based On Next-generation Sequencing
6. Research On Relationship And Mechanism Of Histone Methyltransferase KMT2C And BCR-ABL1-independent Resistance In Chronic Myeloid Leukemia
7. Applied Research Of Armored RNA Technology In Detection Of Dengue Virus And BCR-ABL1p210/p190Fusion Genes Of Leukemia
8. The Study Of Role And Mechanism Of MiR-96 And MiR-34a In Chronic Myeloid Leukemia
9. Lymph Node Enlargement As The Initial Presentation Of Rare BCR/ABL1 Chronic Myeloid Leukemia A Case Report And Literature Review
10. Detection Of Mutations In The Tyrosine Kinase Domain Of Chimerical BCR-ABL1 By Multicolor Melting Curve Analysis
11. The Novel Method For Ultrasensitive Detection Of Leukemia Fusion Gene Based On DNA Machine And Nucleic Acid Isothermal Amplification Technology
12. SOS1 Regulates Imatinib-Sensitivity And –Resistance With BCR-ABL1-Independent And Its Molecular Mechanismin Chronic Myelogenous Leukemia(CLM)
13. Pre-B cell receptor signaling in acute lymphoblastic leukemia
14. Pax5 haploinsufficiency cooperates with BCR-ABL1 to induce acute lymphoblastic leukemia
15. Induction of hypersignaling as a therapeutic approach for treatment of BCR-ABL1 positive Acute Lymphoblastic Leukemia (ALL) cells
16. RAS Signal Transduction: Insights from RIN1 Effector Pathway Studies
17. Normal ABL1 is a tumor suppressor and therapeutic target in BCR-ABL1-positive leukemias
18. Study On The Clinical And Pathogenic Mechanisms Of Childhood Malignant Tumors
19. Highly Sensitive Fluorescence Biosensing Of BCR/ABL1 Fusion Gene Based On Exponential Transcription-triggered Hemin Catalysis
20. IFIT2 Repress The Proliferation Of Chronic Myeloid Leukemia Cells K562 By Down-regulating BCR/ABL1
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