A historical perspective on the development of the cytarabine (7days) and daunorubicin (3days) treatment regimen for acute myelogenous leukemia: 2013 the 40th anniversary of 7+3

Lichtman, Marshall A.

doi:10.1016/j.bcmd.2012.10.005

Cited by 106 publications

(84 citation statements)

References 49 publications

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“…The overall survival rate for adults is only about 25% [1] and although the overall survival rate for children is around 65% [2], it lags significantly behind that of acute lymphoblastic leukemia, which is about 90% for the pediatric population [3]. A major cause of treatment failure is resistance to cytarabine (ara-C) and anthracycline [e.g., daunorubicin (DNR)]-based chemotherapy [4]. Thus, novel therapies are needed to overcome chemoresistance and improve the overall survival of AML patients.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of CHK1 enhances cell death induced by the Bcl-2-selective inhibitor ABT-199 in acute myeloid leukemia cells

Zhao

Niu

et al. 2016

Oncotarget

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Resistance to standard chemotherapy agents remains a major obstacle for improving treatment outcomes for acute myeloid leukemia (AML). The Bcl-2-selective inhibitor ABT-199 has demonstrated encouraging preclinical results, drug resistance remains a concern. Mcl-1 has been demonstrated to contribute to ABT-199 resistance, thus combining with therapies that target Mcl-1 could overcome such resistance. In this study, we utilized a CHK1 inhibitor, LY2603618, to decrease Mcl-1 and enhance ABT-199 efficacy. We found that LY2603618 treatment resulted in abolishment of the G2/M cell cycle checkpoint and increased DNA damage, which was partially dependent on CDK activity. LY2603618 treatment resulted in decrease of Mcl-1, which coincided with the initiation of apoptosis. Overexpression of Mcl-1 in AML cells significantly attenuated apoptosis induced by LY2603618, confirming the critical role of Mcl-1 in apoptosis induced by the agent. Simultaneous treatment with LY2603618 and ABT-199 resulted in synergistic induction of apoptosis in both AML cell lines and primary patient samples. Our findings provide new insights into overcoming a mechanism of intrinsic ABT-199 resistance in AML cells and support the clinical development of combined ABT-199 and CHK1 inhibition.

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Section: Introductionmentioning

confidence: 99%

Inhibition of CHK1 enhances cell death induced by the Bcl-2-selective inhibitor ABT-199 in acute myeloid leukemia cells

Zhao

Niu

et al. 2016

Oncotarget

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“…[1][2][3] Despite these advances, [1][2][3] treatment failure remains common and is driven by adverse leukemia genetics (translated into lower probability of achieving complete remission [CR]) [4][5][6] and by early treatment-related mortality (e-TRM, 7 most commonly caused by infections, particularly invasive fungal diseases [IFDs]), which serve as markers of poor host fitness for therapy. 8 We herein discuss novel risk-adapted and dynamic strategies for the prevention, diagnosis, and treatment of IFDs in patients with A-Leuk, with strong emphasis on pretreatment parameters that allow earlier interventions.…”

Section: Introductionmentioning

confidence: 99%

How we treat invasive fungal diseases in patients with acute leukemia: the importance of an individualized approach

Nucci

Anaissie

2014

Blood

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Invasive fungal diseases (IFDs) represent an important cause of treatment failure in adults with acute leukemia. Because of leukemia’s heterogeneity, the risk for IFDs is highly variable. We therefore apply a risk-adapted antifungal strategy with strong emphasis on pretreatment and day-15 posttreatment to allow earlier and more individualized interventions. We determine pretreatment risks for IFDs based on 4 factors: (1) host fitness for standard therapy (ie, fit, unfit, or frail); (2) leukemia resistance (high vs low probability of achieving complete remission [CR]); (3) anticipated treatment-related toxicity such as neutropenia, mucositis, and steroid-induced immunosuppression; and (4) patient exposure to opportunistic fungi. Accordingly, we stratify patients as high, intermediate, or low risk for IFDs and apply risk-adapted antifungal strategies, including primary or secondary prophylaxis and diagnostic-based preemptive or empiric therapy. Prevention of IFDs also relies on optimizing organ function, decreasing exposure to opportunistic fungi, and improving net state of immunosuppression with use of better-tolerated and investigational agents for unfit patients and those with adverse leukemia biology. Novel targeted and safe therapies that can achieve higher rates of sustained CR among patients with adverse genetics offer the best promise for reducing the burden of IFDs in these patients.

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“…The development of multidrug resistance during chemotherapy is a clinically relevant obstacle to successful treatment of AML [17,18]. Clinical resistance to chemotherapy in AML is often associated with the expression of P-glycoprotein (P-gp).…”

Section: Introductionmentioning

confidence: 99%

Association of ABCB1 polymorphisms with prognostic outcomes of anthracycline and cytarabine in Chinese patients with acute myeloid leukemia

Yin

et al. 2015

Eur J Clin Pharmacol

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A historical perspective on the development of the cytarabine (7days) and daunorubicin (3days) treatment regimen for acute myelogenous leukemia: 2013 the 40th anniversary of 7+3

Cited by 106 publications

References 49 publications

Inhibition of CHK1 enhances cell death induced by the Bcl-2-selective inhibitor ABT-199 in acute myeloid leukemia cells

Inhibition of CHK1 enhances cell death induced by the Bcl-2-selective inhibitor ABT-199 in acute myeloid leukemia cells

How we treat invasive fungal diseases in patients with acute leukemia: the importance of an individualized approach

Association of ABCB1 polymorphisms with prognostic outcomes of anthracycline and cytarabine in Chinese patients with acute myeloid leukemia

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