Control of Ph+ and additional chromosomal abnormalities in chronic myeloid leukemia by tyrosine kinase inhibitors

Ansari, Sana; Verma, Malkhey

doi:10.1007/s12032-023-02116-4

Cited by 4 publications

(2 citation statements)

References 111 publications

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“…In addition to T315I, there are also E255V mutations that contain second mutations that exhibit different resistance to ponatinib. Meanwhile, compound mutations are mostly located in the p-loop in patients with CML, yet more likely to contain T315I 27 . Patients with compound mutations are more likely to progress during follow-up 28 , 29 .…”

Section: Mechanisms Of Tki Resistancementioning

confidence: 99%

“…Influx transporters include organic cation transporter 1 (OCT1 or SLC22A1), organic anion-transporting polypeptide 1A2 (SCL01A2 or OATP1A2), OCTN2 and MATE1 46 , 51 . OCT1 is the main transporter responsible for TKI uptake, and its expression or activity affects the level of drug response 7 , 13 , 27 . Other transporters have been identified as intermediaries in TKI transportation.…”

Section: Mechanisms Of Tki Resistancementioning

confidence: 99%

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Mechanisms underlying therapeutic resistance of tyrosine kinase inhibitors in chronic myeloid leukemia

Sun,

Hu,

Han

et al. 2024

Int. J. Biol. Sci.

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Chronic myeloid leukemia (CML) is a malignant clonal disease involving hematopoietic stem cells that is characterized by myeloid cell proliferation in bone marrow and peripheral blood, and the presence of the Philadelphia (Ph) chromosome with BCR-ABL fusion gene. Treatment of CML has dramatically improved since the advent of tyrosine kinase inhibitors (TKI). However, there are a small subset of CML patients who develop resistance to TKI. Mutations in the ABL kinase domain (KD) are currently recognized as the leading cause of TKI resistance in CML. In this review, we discuss the concept of resistance and summarize recent advances exploring the mechanisms underlying CML resistance. Overcoming TKI resistance appears to be the most successful approach to reduce the burden of leukemia and enhance cures for CML. Advances in new strategies to combat drug resistance may rapidly change the management of TKI-resistant CML and expand the prospects for available therapies.

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Section: Mechanisms Of Tki Resistancementioning

confidence: 99%

Section: Mechanisms Of Tki Resistancementioning

confidence: 99%

Mechanisms underlying therapeutic resistance of tyrosine kinase inhibitors in chronic myeloid leukemia

Sun,

Hu,

Han

et al. 2024

Int. J. Biol. Sci.

View full text Add to dashboard Cite

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Impact of additional cytogenetic aberrations at diagnosis on prognosis of adults patients with Philadelphia chromosome positive acute lymphoblastic leukemia undergoing allogeneic hematopoietic cell transplantation: a retrospective analysis

Zheng,

Zhao,

Luo

et al. 2024

Ann Hematol

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Impact of Additional Cytogenetic Aberrations at Diagnosis on Prognosis of Adults Patients with Philadelphia Chromosome Positive Acute Lymphoblastic Leukemia Undergoing Allogeneic Hematopoietic Cell Transplantation：A Retrospective Analysis

zheng,

Zhao,

Luo

et al. 2024

Preprint

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Additional chromosomal abnormalities(ACAs) at diagnosis are associated with inferior prognosis in chronic myelogenous leukemia. However, the prognostic significance of ACAs in adult patients with Philadelphia Chromosome Positive acute lymphoblastic leukemia (Ph + ALL) receiving TKI-targeted drugs and allogeneic hematopoietic stem cell transplantation(HSCT) is unknown. One hundred eighty-eight adult patients with Ph + ALL were retrospectively analysed, evaluating the effect of ACAs on outcomes of transplantation. One hundred thirty-six patients were included in the study. ACAs are observed in 60 cases (44%). The major-route ACAs are detected in more than 5% are as follows: +der(22), +der(9), + 8, -7 and complex karyotype. The median follow-up was 26.4 months. In the subgroup analyses of major route ACAs, three-year cumulative incidence of relapse (CIR) and progression-free survival(PFS) are statistically significant in + 8[66.7% vs.23.7%, P = 0.024; 77.8% vs. 23.7%, P = 0.0087], -7[53.8% vs. 23.7%, P = 0.035%; 61.5% vs. 32.9%, P = 0.033], and complex karyotypes[42.9% vs. 23.7%, P = 0.027; 47.6% vs. 23.7%] compared with isolated t(9;22). Additionally, the 3-year CIR for Ph + ALL with + der(22) is 44% vs. 23.7% for standard Ph + ALL(P = 0.045). The 3-year overall survival (OS) in the − 7 group is 46.5%, which is statistically significant compared with the other groups(P = 0.001). In multivariate analyses, three years CIR and PFS are statistically significant in + der(22), + 8, -7 and complex karyotype compared with standard Ph + ALL(P < 0.05). More importantly, Ph + ALL with − 7 was negatively associated with the rate of 3-year OS(P = 0.012). Partial ACAs at diagnosis appear to have a significant prognostic impact on transplantation outcomes in patients with Ph + ALL.

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Control of Ph+ and additional chromosomal abnormalities in chronic myeloid leukemia by tyrosine kinase inhibitors

Cited by 4 publications

References 111 publications

Mechanisms underlying therapeutic resistance of tyrosine kinase inhibitors in chronic myeloid leukemia

Mechanisms underlying therapeutic resistance of tyrosine kinase inhibitors in chronic myeloid leukemia

Impact of additional cytogenetic aberrations at diagnosis on prognosis of adults patients with Philadelphia chromosome positive acute lymphoblastic leukemia undergoing allogeneic hematopoietic cell transplantation: a retrospective analysis

Impact of Additional Cytogenetic Aberrations at Diagnosis on Prognosis of Adults Patients with Philadelphia Chromosome Positive Acute Lymphoblastic Leukemia Undergoing Allogeneic Hematopoietic Cell Transplantation：A Retrospective Analysis

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