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BCR-ABL1 Tyrosine Kinase Complex Signaling Transduction: Challenges to Overcome Resistance in Chronic Myeloid Leukemia
| Content Provider | MDPI |
|---|---|
| Author | Amarante-Mendes, Gustavo P. Rana, Aamir Datoguia, Tarcila Santos Hamerschlak, Nelson Brumatti, Gabriela |
| Copyright Year | 2022 |
| Description | The constitutively active BCR-ABL1 tyrosine kinase, found in t(9;22)(q34;q11) chromosomal translocation-derived leukemia, initiates an extremely complex signaling transduction cascade that induces a strong state of resistance to chemotherapy. Targeted therapies based on tyrosine kinase inhibitors (TKIs), such as imatinib, dasatinib, nilotinib, bosutinib, and ponatinib, have revolutionized the treatment of BCR-ABL1-driven leukemia, particularly chronic myeloid leukemia (CML). However, TKIs do not cure CML patients, as some develop TKI resistance and the majority relapse upon withdrawal from treatment. Importantly, although BCR-ABL1 tyrosine kinase is necessary to initiate and establish the malignant phenotype of Ph-related leukemia, in the later advanced phase of the disease, BCR-ABL1-independent mechanisms are also in place. Here, we present an overview of the signaling pathways initiated by BCR-ABL1 and discuss the major challenges regarding immunologic/pharmacologic combined therapies. |
| Starting Page | 215 |
| e-ISSN | 19994923 |
| DOI | 10.3390/pharmaceutics14010215 |
| Journal | Pharmaceutics |
| Issue Number | 1 |
| Volume Number | 14 |
| Language | English |
| Publisher | MDPI |
| Publisher Date | 2022-01-17 |
| Access Restriction | Open |
| Subject Keyword | Pharmaceutics Oncology Bcr-abl1 Chronic Myeloid Leukemia Tyrosine Kinase Inhibitors |
| Content Type | Text |
| Resource Type | Article |
