Abstract
Chronic myeloid leukemia (CML) and mantle cell lymphoma (MCL) are hematologic malignancies that originate from different oligopotent progenitor stem cells, namely, common myeloid and lymphoid progenitor cells, respectively. Although blastic transformation of CML can occur in the lymphoid lineage and CML has been related to non-Hodgkin lymphoma on transformation, to our knowledge, de novo and synchronous occurrence of CML and MCL has not been reported. Herein, we report the first case of synchronous CML and MCL in an otherwise healthy 38-year-old man. Potential etiologies and pathological relationships between the two malignancies are explored, including the possibility that the downstream effects of BCR-ABL may link it to an overexpression of cyclin D1, which is inherent to the etiology of MCL.
Highlights
Chronic myeloid leukemia (CML) and mantle cell lymphoma (MCL) are hematologic malignancies characterized by chromosomal translocations that are central to malignant transformation [1, 2]
From the first identification of the characteristic small chromosome in neoplastic cells from patients with CML by Nowell and Hungerford in 1960s [5], to the elucidation of the translocation and subsequent cytogenetic changes, we have come a long way understanding the biology of CML
Some of the multiple pathways signaled by the BCR/ABL kinase are JAK/STAT, PI3K/AKT, and Ras/MEK, and these pathways drive CML pathogenesis by increasing cell proliferation; survival; decreasing apoptosis; cell differentiation; and altered cell adhesion [7]
Summary
Chronic myeloid leukemia (CML) and mantle cell lymphoma (MCL) are hematologic malignancies characterized by chromosomal translocations that are central to malignant transformation [1, 2]. The sequential occurrence of CML and MCL has been reported. A literature search yielded a case report of MCL which developed in a patient with CML treated with imatinib for three years and another case of blastoid variant of MCL in a patient of CML after achieving complete cytogenetic and molecular response to imatinib [3, 4]. We report the synchronous development of CML and MCL
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