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 Table of Contents    
Year : 2021  |  Volume : 14  |  Issue : 3  |  Page : 134-135  

Chronic myeloid leukemia versus acute myeloid leukemia in patients with retinoblastoma

1 Division of Pediatric Oncology, Children's Hospital of Philadelphia, Philadelphia, PA, USA
2 Ocular Oncology Service, Wills Eye Hospital, Thomas Jefferson University, Philadelphia, PA, USA

Date of Submission14-Aug-2021
Date of Acceptance04-Sep-2021
Date of Web Publication20-Oct-2021

Correspondence Address:
Ann-Marie Leahey
Division of PediatricOncology, Children'sHospital of Philadelphia, Philadelphia, PA 19104
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ojo.OJO_241_2021

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How to cite this article:
Leahey AM, Shields CL. Chronic myeloid leukemia versus acute myeloid leukemia in patients with retinoblastoma. Oman J Ophthalmol 2021;14:134-5

How to cite this URL:
Leahey AM, Shields CL. Chronic myeloid leukemia versus acute myeloid leukemia in patients with retinoblastoma. Oman J Ophthalmol [serial online] 2021 [cited 2022 Dec 3];14:134-5. Available from: https://www.ojoonline.org/text.asp?2021/14/3/134/328604

We read with interest the case report of chronic myeloid leukemia (CML) in chronic phase in a patient with heritable retinoblastoma (RB) who had received treatment with high-dose carboplatin, etoposide, and vincristine.[1] CML is divided into chronic, accelerated, and blast phases, resulting from the t (9;22) (q34; q11) translocation. In addition to their case and another referenced by the authors,[2] there is a third case in the literature described by Gombos et al.[3] In that series, case #4 of acute myeloid leukemia (AML) appears actually to describe a case of CML in myeloid blast crisis 22 years after the diagnosis of RB. Of note, this patient did not receive etoposide.

In contradistinction, secondary AML following treatment with topoisomerase inhibitors such as etoposide has an average latency of 1–2 years. This subtype of AML is defined by KMT2A gene (or chromosome) rearrangement. It has been shown to fuse to 20 other gene partners. Another type of secondary AML can occur after exposure to alkylating agents and presents 5–10 years following exposure. It is associated with monosomies or deletions of chromosomes 5 and 17.

Ionizing radiation is the only environmental factor implicated in the etiology of CML.[3] Based on data from survivors of atomic bombs, the average time from radiation exposure to clinical symptoms of CML is 8 years. Two of the three known patients with RB who developed CML, referenced in this report, had received external beam radiotherapy (EBRT) and the time interval to CML was over 20 years in both cases.

The patient in this case report did not share the environmental exposure to EBRT, but all three reports share the fact that there was bilateral disease and all share the common genetic milieu of heritable RB. Thus, therein may be the causal connection. Abnormalities in the RB gene, protein, and signaling pathway have been associated with CML cell survival as well as conversion to accelerated and blast phases.[5],[6],[7]

Fortunately, CML is a rare leukemia that is highly treatable with currently available tyrosine kinase inhibitors. We agree that long-term monitoring of patients with heritable RB is mandatory, but there is no evidence to suggest that treatment with etoposide leads to CML.

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Conflicts of interest

There are no conflicts of interest.

   References Top

Al-Mahrouqi HH, Ganesh A, Al-Rawas A, Khetan V, Al-Zuhaibi S. Chronic myelogenous leukemia in a child following treatment for bilateral retinoblastoma. Oman J Ophthalmol 2021;14:187-9.  Back to cited text no. 1
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Kamitori T, Umeda K, Tasaka K, Ogata H, Mikami T, Kato I, et al. Chronic myeloid leukemia following treatment for bilateral retinoblastoma. Pediatr Blood Cancer 2018;65:e27107.  Back to cited text no. 2
Gombos DS, Hungerford J, Abramson DH, Kingston J, Chantada G, Dunkel IJ, et al. Secondary acute myelogenous leukemia in patients with retinoblastoma: Is chemotherapy a factor? Ophthalmology 2007;114:1378-83.  Back to cited text no. 3
Rau RE, Loh ML. Myeloproliferative neoplasms of childhood. In: Blaney SM, Adamson PC, Helman LJ, editors. Pizzo and Poplack's Pediatric Oncology. 8th ed. Philadelphia: Wolters Kluwer; 2021. p. 496-516.  Back to cited text no. 4
Nagano K, Itagaki C, Izumi T, Nunomura K, Soda Y, Tani K, et al. RB plays a role in survival of Abl-dependent human tumor cells as a downstream effector of Abl tyrosine kinase. Oncogene 2006;25:493-502.  Back to cited text no. 5
Beck Z, Kiss A, Tóth FD, Szabó J, Bácsi A, Balogh E, et al. Alterations of P53 and RB genes and the evolution of the accelerated phase of chronic myeloid leukemia. Leuk Lymphoma 2000;38:587-97.  Back to cited text no. 6
Yin X, Zhou M, Fu Y, Yang L, Xu M, Sun T, et al. Histone demethylase RBP2 mediates the blast crisis of chronic myeloid leukemia through an RBP2/PTEN/BCR-ABL cascade. Cell Signal 2019;63:109360.  Back to cited text no. 7


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