Incidence of chronic myeloid leukemia in Calgary, Alberta, Canada

Chronic myeloid leukemia (CML) is a progressive clonal myeloproliferative disorder that accounts for roughly 15% of adult leukemias [1]. Most diagnoses occur in asymptomatic patients in the chronic stage, with a small proportion of cases having progressed to the accelerated phase or blast crisis depending on the blast count [2]. CML is more predominant in males than females and it is generally described to occur later in life, however the median age of diagnosis differs between cancer registries from the late 30’s in low and middle income countries up to 65 [3, 4]. There is no strong evidence for bias towards particular ethnicities despite lower incidence rates reported in several Asian countries and populations [5, 6]. Other associated risk factors include ionizing radiation, as most famously illustrated in Japanese atomic bomb survivors [7], and recently recognized lifestyle factors including smoking and body mass [8, 9].

The pathogenesis of CML stems from a distinct chromosomal translocation, named the Philadelphia (Ph) chromosome, which fuses the bcr and abl gene sequences from chromosomes 22 and 9, respectively [10]. The expressed Bcr–Abl chimeric product is an oncoprotein with constitutive tyrosine kinase activity, leading to the proliferation of myeloid cells in the bone marrow. There are rare cases of Ph-negative or atypical CML presenting with the same histopathological clinical features as BCR–ABL1 positive CML such as an elevated granulocyte count in a CBC and high proportion of myelocytes in a peripheral blood smear [11]. Otherwise, the Ph chromosome is detected by routine karyotyping in a cytogenetics facility, with FISH or RT-PCR as supporting techniques to show evidence of the translocation. The management of CML progressed extensively after imatinib was first described in 1996 as a tyrosine kinase inhibitor (TKI) specific to BCR–ABL1 [12, 13]. Since then, second- and third-generation TKIs have been developed as alternatives for patients who have become resistant to imatinib or had poor tolerability [14]. With these highly targeted treatment options, CML survival rates have improved drastically often to give a life expectancy approaching that of the general population [15]. Concurrently, its prevalence has increased in the last decade and the requirement of continuous TKI therapy in most cases will have an impact on future healthcare spending [6].

Here, we describe the incidence of CML in Calgary, a major Canadian city, for the recent years of 2011–2015. This will add to the global literature of epidemiological data for CML and aid clinician awareness as early diagnoses in the chronic phase with low BCR–ABL1 levels and blast counts will increase the likelihood of patients’ successful response to treatment [16].

The data presented here were limited by the geography and study period being considered, which skews the cohort towards a young, nonsmoking urban population. Furthermore, the summary statistics do not specify incident CML cases by phase. However, the low number of reported cases is less likely to provide accurate statistics for such classification. Future studies may also include cohort stratification by sociodemographic characteristics such as ethnicity or lifestyle factors, and consider other updated epidemiological measures such as survival rates and prevalence for CML in the TKI era.