Correction to: A phase I–II study of plerixafor in combination with fludarabine, idarubicin, cytarabine, and G-CSF (PLERIFLAG regimen) for the treatment of patients with the first early-relapsed or refractory acute myeloid leukemia

Martínez‐Cuadrón, David; Boluda, Blanca; Martı́nez, Pilar; Bergua, Juan; Rodríguez‐Veiga, Rebeca; Esteve, Jordi; Vives, Susana; Serrano, Josefina; Vidriales, María‐Belén; Salamero, Olga; Cordón, Lourdes; Sempere, Amparo; Jiménez‐Ubieto, Ana; Prieto-Delgado, Julio; Díaz‐Beyá, Marina; Garrido, Ana; Benavente, Celina; Pérez-Simón, Josè Antonio; Moscardó, Federico; Sanz, Miguel Á.; Montesinos, Pau; Groups, Pethema Cooperative Study

doi:10.1007/s00277-018-3277-x

Cited by 23 publications

(1 citation statement)

References 22 publications

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“…For ex vivo drug sensitivity assays, fresh bone marrow samples from 74 patients were collected in heparinised tubes and were received by the processing laboratory within 24 hours from extraction. Sample incubation with the corresponding drugs was performed maintaining the native microenvironment, as previously described in detail (Bennett et al , ; Hernandez et al , ; Martinez‐Cuadron et al , ). After incubation for 48 hours, red blood cells were lysed and remaining cells were washed, labelled with fluorescent conjugated antibodies, and injected into the flow cytometer.…”

Section: Methodsmentioning

confidence: 99%

Improving the prediction of acute myeloid leukaemia outcomes by complementing mutational profiling with ex vivo chemosensitivity

et al. 2020

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Refractoriness to induction therapy and relapse after complete remission are the leading causes of death in patients with acute myeloid leukaemia (AML). This study focussed on the prediction of response to standard induction therapy and outcome of patients with AML using a combined strategy of mutational profiling by next-generation sequencing (NGS, n = 190) and ex vivo PharmaFlow testing (n = 74) for the 10 most widely used drugs for AML induction therapy, in a cohort of adult patients uniformly treated according to Spanish PETHEMA guidelines. We identified an adverse mutational profile (EZH2, KMT2A, U2AF1 and/or TP53 mutations) that carries a greater risk of death [hazard ratio (HR): 3Á29, P < 0Á0001]. A high correlation was found between the ex vivo PharmaFlow results and clinical induction response (69%). Clinical correlation analysis showed that the pattern of multiresistance revealed by ex vivo PharmaFlow identified patients with a high risk of death (HR: 2Á58). Patients with mutation status also ran a high risk (HR 4Á19), and the risk was increased further in patients with both adverse profiles (HR 4Á82). We have developed a new score based on NGS and ex vivo drug testing for AML patients that improves upon current prognostic risk stratification and allows clinicians to tailor treatments to minimise drug resistance.Keywords: acute myeloid leukaemia, sequencing, ex vivo sensitivity test.Refractoriness to induction therapy and relapse after achieving complete remission (CR) is a common cause of death among patients with acute myeloid leukaemia (AML). Cytogenetic and molecular alterations at diagnosis and response to therapy are the best predictors of the relative risk of AML relapse and are helpful in deciding between chemotherapy and haematopoietic stem cell transplantation (HSCT) at first CR (Onecha et al., 2018). In this respect, next-generation sequencing (NGS)-based studies have yielded important insights into the molecular pathogenesis of AML, and the mutational profile of AML is now better defined. For example, a single patient can carry up to 400 genomic variants, of

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Section: Methodsmentioning

confidence: 99%

Improving the prediction of acute myeloid leukaemia outcomes by complementing mutational profiling with ex vivo chemosensitivity

et al. 2020

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Acute Myeloid Leukemia Mutations and Future Mechanistic Target to Overcome Resistance

Uddin

Darwish

Mousa

2021

Curr. Treat. Options in Oncol.

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Redistribution, homing and organ-invasion of neoplastic stem cells in myeloid neoplasms

Valent

Sadovnik

Eisenwort

et al. 2020

Seminars in Cancer Biology

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The development of a myeloid neoplasm is a step-wise process that originates from leukemic stem cells (LSC) and includes pre-leukemic stages, overt leukemia and a drug-resistant terminal phase. Organ-invasion may occur in any stage, but is usually associated with advanced disease and a poor prognosis. Sometimes, extra-medullary organ invasion shows a metastasis-like or even sarcomalike destructive growth of neoplastic cells in local tissue sites. Examples are myeloid sarcoma, mast cell sarcoma and localized blast phase of chronic myeloid leukemia. So far, little is known about mechanisms underlying re-distribution and extramedullary dissemination of LSC in myeloid neoplasms. In this article, we discuss mechanisms through which LSC can mobilize out of the bone marrow niche, can transmigrate from the blood stream into extramedullary organs, can invade local tissue sites and can potentially create or support the formation of local stem cell niches. In addition, we discuss strategies to interfere with LSC expansion and organ invasion by targeted drug therapies.

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Correction to: A phase I–II study of plerixafor in combination with fludarabine, idarubicin, cytarabine, and G-CSF (PLERIFLAG regimen) for the treatment of patients with the first early-relapsed or refractory acute myeloid leukemia

Cited by 23 publications

References 22 publications

Improving the prediction of acute myeloid leukaemia outcomes by complementing mutational profiling with ex vivo chemosensitivity

Improving the prediction of acute myeloid leukaemia outcomes by complementing mutational profiling with ex vivo chemosensitivity

Acute Myeloid Leukemia Mutations and Future Mechanistic Target to Overcome Resistance

Redistribution, homing and organ-invasion of neoplastic stem cells in myeloid neoplasms

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