Acute Myeloblastic Leukemia as a Second Malignancy in a Patient With Hereditary Retinoblastoma

Nishimura, Shin‐Ichiro; Sato, Takashi; Ueda, Haruo; Ueda, Kazuhiro; Beck, Maja Nenadov

doi:10.1200/jco.2001.19.21.4182

Cited by 50 publications

(20 citation statements)

References 6 publications

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“…The advantage of topotecan combined with carboplatin is that it is more effective in our preclinical models compared with etoposide + carboplatin or etoposide + carboplatin + vincristine. In addition, there are no secondary malignancies associated with topotecan exposure as has been reported for etoposide (8). However, this does not mean that systemic topotecan exposure is not associated with significant side effects.…”

Section: Discussionmentioning

confidence: 65%

“…However, latestage bilateral retinoblastoma remains difficult to treat with this approach (7). In addition, one of the drugs used to treat retinoblastoma worldwide (etoposide) is believed to be responsible for an increase in acute myeloblastic leukemia as a secondary malignancy (8). Alternative chemotherapeutic combinations have not been identified because there are too few patients for large-scale clinical trials.…”

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confidence: 99%

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Topotecan Combination Chemotherapy in Two New Rodent Models of Retinoblastoma

Laurie

Gray

Zhang

et al. 2005

Clinical Cancer Research

118

131

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Chemotherapy combined with laser therapy and cryotherapy has improved the ocular salvage rate for children with bilateral retinoblastoma. However, children with late-stage disease often experience recurrence shortly after treatment. To improve the vision salvage rate in advanced bilateral retinoblastoma, we have developed and characterized two new rodent models of retinoblastoma for screening chemotherapeutic drug combinations. The first model is an orthotopic xenograft model in which green fluorescent protein^or luciferase-labeled human retinoblastoma cells are injected into the eyes of newborn rats.The second model uses a replication-incompetent retrovirus (LIA-E E1A ) encoding the E1A oncogene. Clonal, focal tumors arise from mouse retinal progenitor cells when LIA-E E1A is injected into the eyes of newborn p53 À/À mice. Using these two models combined with pharmacokinetic studies and cell culture experiments, we have tested the efficacy of topotecan combined with carboplatin and of topotecan combined with vincristine for the treatment of retinoblastoma. The combination of topotecan and carboplatin most effectively halted retinoblastoma progression in our rodent models and was superior to the current triple drug therapy using vincristine, carboplatin, and etoposide.Vincristine had the lowest LC 50 in culture but did not reduce tumor growth in our preclinical retinoblastoma models. Taken together, these data suggest that topotecan may be a suitable replacement for etoposide in combination chemotherapy for the treatment of retinoblastoma.

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Section: Discussionmentioning

confidence: 65%

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confidence: 99%

Topotecan Combination Chemotherapy in Two New Rodent Models of Retinoblastoma

Laurie

Gray

Zhang

et al. 2005

Clinical Cancer Research

118

131

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“…Etoposide therapy is associated with risk for acute myelocytic leukaemia, 12 and secondary leukaemias have so far been reported in two RB patients treated with etoposide. 13,14 Carboplatin may also act synergistically with etoposide in the induction of secondary leukaemias. 15,16 Because these agents are mutagenic, both of these drugs have potential to exacerbate second tumour risk in children with heritable disease.…”

Section: Introductionmentioning

confidence: 99%

Beta-lapachone inhibits proliferation and induces apoptosis in retinoblastoma cell lines

Shah

Conway

Quill

et al. 2007

Eye

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Aims To investigate the cytotoxicity of beta-lapachone, a potent agent that may selectively target tumour cells, in retinoblastoma (RB) cell lines. Methods Growth inhibitory effects of betalapachone were evaluated in Y79, WERI-RB1, and RBM human retinoblastoma cell lines. Pro-apoptotic effects of beta-lapachone were evaluated in Y79 cells by detection of caspase 3/7 activity, by enzyme-linked immunosorbent assay for nucleosome fragments, and by cellular morphological analysis. Results Beta-lapachone induced significant dose-dependent growth inhibitory effects in all three retinoblastoma cell lines. The 50% growth inhibitory concentration (IC 50 ) of this agent was 1.9 lM in Y79 cells, 1.3 lM in WERI-RB1 cells, and 0.9 lM in RBM cells. Beta-lapachone also induced proapoptotic effects in RB cells. Treatment of Y79 cells with 1.9 lM beta-lapachone (IC 50 ) resulted in a peak, fourfold induction of caspase 3/7 activity at 72 h post-treatment; a peak, 5.6-fold increase in nucleosome fragments at 96 h posttreatment; and a peak, 1.7-fold increase in the frequency of apoptotic cells at 48 h posttreatment, relative to vehicle-treated controls. Conclusion Beta-lapachone induced potent cytotoxic effects in RB cell lines at low micromolar concentrations, suggesting this agent could be useful in the clinical management of RB.

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“…Both platinum-based drugs and topoisomerase inhibitors have been reported to increase the risk of second tumors in other primary malignancies ( Hijiya et al, 2009;Klein et al, 2003;Travis et al, 1999). Some studies have reported the development of acute myelogenous leukemia and secondary leukemia in retinoblastoma survivors treated with epipodophyllotoxins and alkylating agents, respectively (Gallegos-Castorena et al, 2002;Gombos et al, 2007;Nishimura et al, 2001;Weintraub et al, 2007). In a study of 187 patients with hereditary retinoblastoma treated with carboplatin, vincristine +/-etoposide, 6 patients developed second malignancies (Turaka et al, 2011).…”

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confidence: 99%