The Progression of Chronic Myeloid Leukemia to Myeloid Sarcoma: A Systematic Review

Abstract

Chronic myeloid leukemia (CML) is a slow-growing type of cancer that originates in the blood-forming cells of the bone marrow and is caused by a chromosomal mutation that is thought to occur spontaneously. CML could potentially lead to the development of myeloid sarcoma (MS), which is a rare neoplasm composed of immature myeloid cells that could evolve into a tumor mass at any anatomical site other than the bone marrow. MS can develop spontaneously or as a result of another form of myeloid neoplasm. Most instances of CML precede blast phase (BP) within two to three years after the first diagnosis of CML chronic phase (CP) at the age of pre-tyrosine kinase inhibitor (TKI) treatment. MS developing in CML patients during the era of TKI treatment is infrequently mentioned in the literature, primarily in single-case studies. As a result, the prognostic influence of MS in CML patients has not been well investigated. In the age of TKI treatment, it is uncertain whether MS and medullary BP have comparable clinical and prognostic relevance. The precise diagnosis of MS is critical for effective treatment, which is frequently delayed due to a high risk of misdiagnosis.This review focuses on the relationship between the development of MS from CML, and it culminates with recommendations for future hematology practice. A literature search was conducted in multiple databases, and the studies were appraised based on the inclusion and exclusion criteria.Finally, studies to date have shown that the existence of CML and its possible progression to MS in individuals map out the numerous implications this disease has in hematology practice. Though occurrences are uncommon in general, the prognosis for patients is bleak, necessitating the exploration and implementation of diagnostic and therapy advancements. Because there is limited evidence in the literature on its existence in the medullary chronic phase and outcomes in the era of TKI, it must be carefully investigated because it might be the first symptom of progressive illness prior to hematological progression.

Artificial intelligence performance in detecting lymphoma from medical imaging: a systematic review and meta-analysis

“…Most included studies in this review investigating the use of AI in lymphoma detection employed DL ( n = 18), with only six studies using ML. For leukemia diagnosis, the convolutional neural networks (CNN) of DL have been used, e.g., to distinguish between cases with favourable and poor prognosis of chronic myeloid leukemia [ 54 ], or to recognize blast cells in acute myeloid leukemia [ 55 ]. However, it requires far more data and computational power than ML methods, and is more prone to overfitting.…”

Leukostasis With Isolated Central Nervous System Involvement in Chronic Phase of Chronic Myelogenous Leukemia

“…In both AML and CML, MS presents as a distinct tumor mass with myeloid blasts, with or without maturation, occurring at any site outside of the BM and often considered equivalent to the diagnosis of AML [ 49 ]. However, in CML, MS may present with less percentage of blast cells compared to MS in AML, as MS may arise in various phases of CML including the CP [ 50 ]. MS is most often seen in AML, and histology shows increased blasts often staining positive for MPO, CD34, and CD68 [ 49 ].…”

A comprehensive analysis of cell‐autonomous and non‐cell‐autonomous regulation of myeloid leukemic cells: The prospect of developing novel niche‐targeting therapies

“…The blood cell malignancy characterized by differentiation arrest and abnormal proliferation of immature myeloid lineage cells or blasts leads to a condition known as myeloid leukemia (DiNardo & Cortes, 2016) that is further classified into acute myeloid leukemia (AML) and chronic myeloid leukemia (CML) depending upon the time required for the development of the disease. AML is a highly aggressive and progressive disease (Tazi et al, 2022), whereas CML is less aggressive and requires time to develop (Arzoun et al, 2022). In the case of AML, the abnormal proliferation of malignant precursors is driven by several acquired genetic abnormalities that result in the rapid disruption of normal hematopoiesis (Carter et al, 2020; Menter & Tzankov, 2022).…”