Smac mimetic primes apoptosis-resistant acute myeloid leukaemia cells for cytarabine-induced cell death by triggering necroptosis

Chromik, Jöerg; Safferthal, Charlotta; Serve, Hubert; Fulda, Simone

doi:10.1016/j.canlet.2013.10.018

Cited by 75 publications

(66 citation statements)

References 42 publications

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“…Previously, we demonstrated that Smac mimetics sensitize AML cells for cytarabine or demethylating agents [16,17]. Besides demethylating agents, also other epigenetic drugs including HDACIs are currently being explored for the treatment of AML [18].…”

Section: Introductionmentioning

confidence: 99%

Identification of a novel synergistic induction of cell death by Smac mimetic and HDAC inhibitors in acute myeloid leukemia cells

et al. 2015

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Section: Introductionmentioning

confidence: 99%

Identification of a novel synergistic induction of cell death by Smac mimetic and HDAC inhibitors in acute myeloid leukemia cells

et al. 2015

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“…Consequently, the remission and overall survival rates after chemotherapy are increasing for these patients; some patients with acute myeloid leukemia can obtain long-term disease-free survival (Penack, 2013;Cagnetta et al, 2014). In addition, the prognosis of some patients was good, but did not correspond with the clinical response to therapy; also, the treatment effect was poor, the symptoms were difficult to relieve, and symptoms recurred easily (Chromik et al, 2014). Therefore, it is important to identify effective methods to evaluate curative effects and prognosis after chemotherapy.…”

Section: Discussionmentioning

confidence: 99%

Effects of changes in serum endostatin and fibroblast growth factor 19 on the chemotherapeutic sensitivity in acute myeloid leukemia patients

Su¹,

Wang²,

Zhou³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. The present study aimed to explore the changes in serum endostatin and fibroblast growth factor 19 (FGF-19) in acute myeloid leukemia patients, and to determine their effects on chemotherapeutic sensitivity. Sixty acute myeloid leukemia patients and 30 healthy controls were included in the study. Patient serum endostatin and FGF-19 levels were measured on admission, and then, standard chemotherapy was administered. The patients were divided into 2 groups according to chemotherapeutic effects: 21 patients in the chemotherapeutic sensitivity group (complete remission + partial remission) and 39 in the chemotherapeutic resistance group (no remission + degradation). A receiver operating characteristic (ROC) curve was used to analyze the relationship of serum endostatin and FGF-19 levels with chemotherapeutic sensitivity in acute myeloid leukemia patients. The levels of serum endostatin and FGF-19 in acute myeloid leukemia patients before chemotherapy were significantly higher than those in the control group. Moreover, these levels significantly decreased after chemotherapy (P < 0.01). The levels of serum endostatin and FGF-19 in the chemotherapeutic sensitivity group were lower than those in the chemotherapeutic resistance group, both before and after chemotherapy (P < 0.05 and P < 0.01, respectively). ROC curve analysis showed that the predictive values of endostatin and FGF-19 were good, and there was no significant difference between these results. In conclusion, serum endostatin and FGF-19 can be used as predictors of chemotherapeutic sensitivity for acute myeloid leukemia patients, and may be important for determining prognosis.

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“…The study was terminated for administrative reasons before a MTD was determined (62). In support of the notion that Smac mimetics can be used to prime AML cells for chemotherapy, preclinical studies demonstrated synergistic interaction of Smac mimetics and cytarabine or doxorubicin in AML (40,63). The Smac mimetic BV6 synergistically triggered cell death in combination with cytarabine in AML cell lines as well as in primary AML samples (40).…”

Section: Smac Mimetic-based Combination Therapies: Clinical Translationmentioning

confidence: 93%

“…In support of the notion that Smac mimetics can be used to prime AML cells for chemotherapy, preclinical studies demonstrated synergistic interaction of Smac mimetics and cytarabine or doxorubicin in AML (40,63). The Smac mimetic BV6 synergistically triggered cell death in combination with cytarabine in AML cell lines as well as in primary AML samples (40). Moreover, the Smac mimetic LBW242 enhanced loss of cell viability upon treatment of AML cell lines with cytarabine or doxorubicin (63).…”

Section: Smac Mimetic-based Combination Therapies: Clinical Translationmentioning

confidence: 94%

“…Furthermore, various preclinical studies revealed synergistic drug interactions of Smac mimetics with a variety of cytotoxic therapies. For example, Smac mimetics have been reported to act in concert with chemotherapeutic drugs in solid tumors and hematologic malignancies (35)(36)(37)(38)(39)(40)(41). Smac mimetics were also shown to enhance the sensitivity toward radiotherapy both in vitro and in preclinical in vivo models of human cancers (42)(43)(44)(45)(46).…”

Section: Clinical Efficacy Of Smac Mimetics As Monotherapymentioning

confidence: 99%

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Promises and Challenges of Smac Mimetics as Cancer Therapeutics

Fulda

2015

Clinical Cancer Research

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165

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Smac mimetic primes apoptosis-resistant acute myeloid leukaemia cells for cytarabine-induced cell death by triggering necroptosis

Cited by 75 publications

References 42 publications

Identification of a novel synergistic induction of cell death by Smac mimetic and HDAC inhibitors in acute myeloid leukemia cells

Identification of a novel synergistic induction of cell death by Smac mimetic and HDAC inhibitors in acute myeloid leukemia cells

Effects of changes in serum endostatin and fibroblast growth factor 19 on the chemotherapeutic sensitivity in acute myeloid leukemia patients

Promises and Challenges of Smac Mimetics as Cancer Therapeutics

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