Ponatinib

Shamroe, Caitlin L.; Comeau, Jill M.

doi:10.1177/1060028013501144

Cited by 43 publications

(16 citation statements)

References 16 publications

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“…The efficacy of ponatinib against multiple tyrosine kinases, such as ABL, PDGFRα, VEGFR2 and FGFR1 has been illustrated in several adult cancer types [28]. The FGFR signaling is a highly conserved signaling cascade and like other RTK family members, FGFR realizes its role by promoting several biologic processes which includes angiogenesis and regeneration [39].…”

Section: Discussionmentioning

confidence: 99%

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Novel multiple tyrosine kinase inhibitor ponatinib inhibits bFGF-activated signaling in neuroblastoma cells and suppresses neuroblastoma growth in vivo

Wang

Chen

et al. 2016

Oncotarget

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Neuroblastoma (NB) is one of the most common pediatric malignancies in children. Abnormal activation of receptor tyrosine kinases contributes to the pathological development of NB. Therefore, targeting tyrosine kinase receptors to cure NB is a promising strategy. Here, we report that a multi-targeted tyrosine kinase inhibitor ponatinib inhibited NB cell proliferation and induced NB cell apoptosis in a dose-dependent manner. In addition, ponatinib suppressed the colony formation ability of NB cells. Mechanistically, ponatinib effectively inhibited the FGFR1-activated signaling pathway. Ponatinib also enhanced the cytotoxic effects of doxorubicin on NB cells. Furthermore, ponatinib demonstrated anti-tumor efficacy in vivo by inhibiting tumor growth in an orthotopic xenograft NB mouse model. In summary, our results showed that ponatinib inhibited NB growth both in vitro and in vivo.

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Section: Discussionmentioning

confidence: 99%

“…Furthermore, inhibition of some RTKs leads to increased apoptosis of NB cells [24]. However, current RTKs inhibitors have limited therapeutic outcomes [27, 28]. …”

Section: Introductionmentioning

confidence: 99%

Novel multiple tyrosine kinase inhibitor ponatinib inhibits bFGF-activated signaling in neuroblastoma cells and suppresses neuroblastoma growth in vivo

Wang

Chen

et al. 2016

Oncotarget

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“…There are several advantages for ponatinib as a potential drug in clinical treatment of leukemia. First, the efficiency of ponatinib against resistant or intolerant CML and Ph+ ALL has been reported 37. Second, ponatinib can be used in CML and Ph+ ALL with a variety of known mutations and no mutations 38.…”

Section: Discussionmentioning

confidence: 99%

The effects of ponatinib, a multi-targeted tyrosine kinase inhibitor, against human U87 malignant glioblastoma cells

Zhang¹,

Zhou²,

Gao³

et al. 2014

OTT

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Glioblastoma is one of the most common malignant tumors in the nervous system in both adult and pediatric patients. Studies suggest that abnormal activation of receptor tyrosine kinases contributes to pathological development of glioblastoma. However, current therapies targeting tyrosine kinase receptors have poor therapeutic outcomes. Here, we examined anticancer effects of ponatinib, a multi-targeted tyrosine kinase inhibitor, on glioblastoma cells both in the U87MG cell line and in the mouse xenograft model. We showed that ponatinib treatment reduced cell viability and induced cell apoptosis in a dose-dependent manner in U87MG cells. In addition, ponatinib suppressed migration and invasion of U87MG cells effectively. Furthermore, ponatinib-treated tumors showed an obvious reduction of tumor volume and an increase of apoptosis as compared with vehicle-treated tumors in the mouse xenograft model. These findings support a potential application of ponatinib as a chemotherapeutic option against glioblastoma cells.

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“…When a patient has received several courses of chemotherapy, but the percentage of leukemia cells in the bone marrow does not decline significantly or returns to the pretreatment level soon after a short-term discontinuation, this condition is considered to be leukemia drug resistance. Currently, the development of leukemia cell drug resistance is one of the major causes of leukemia treatment failure ( 5 , 6 ).…”

Section: Introductionmentioning

confidence: 99%

Piperlongumine reverses doxorubicin resistance through the PI3K/Akt signaling pathway in K562/A02 human leukemia cells

Kang

2015

Experimental and Therapeutic Medicine

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Drug resistance is an important obstacle to human leukemia therapeutics. Piperlongumine has previously demonstrated the ability to suppress certain human tumor processes; however, the ability of piperlongumine to reverse the drug resistance of human leukemia and its mechanism of action have not yet been clearly elucidated. In this study, the doxorubicin resistance reversal effect of piperlongumine on K562/A02 human leukemia cells and the underlying mechanism were investigated. The results indicated that piperlongumine promoted doxorubicin sensitivity, apoptosis, the intracellular accumulation of rhodamine-123, the activities of caspase-3 and -8, and the expression of reactive oxygen species, p53, p27 and p-PTEN. Furthermore, it suppressed the expression of P-glycoprotein, MDR1, MRP1, survivin and p-Akt, and the transcriptional activities of NF-κB and twist, and arrested the cell cycle in the G2/M phase. The results indicate that piperlongumine has the potential to be used as a therapeutic agent for human leukemia.

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Ponatinib

Abstract: Ponatinib is a potent TKI that can overcome several resistance mechanisms in previously treated patients with CML and Ph+ ALL. Ponatinib should be reserved for patients who have failed first-line therapy, have the T315I mutation, or have progressed.

Cited by 43 publications

References 16 publications

Novel multiple tyrosine kinase inhibitor ponatinib inhibits bFGF-activated signaling in neuroblastoma cells and suppresses neuroblastoma growth in vivo

Novel multiple tyrosine kinase inhibitor ponatinib inhibits bFGF-activated signaling in neuroblastoma cells and suppresses neuroblastoma growth in vivo

The effects of ponatinib, a multi-targeted tyrosine kinase inhibitor, against human U87 malignant glioblastoma cells

Piperlongumine reverses doxorubicin resistance through the PI3K/Akt signaling pathway in K562/A02 human leukemia cells

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