Abstract
<jats:p>The use of tyrosine kinase inhibitors (TKIs) dramatically improved long-term survival rates in chronic myeloid leukemia (CML) patients. Despite high specificity for BCR::ABL1 tyrosine kinase, TKIs can induce adverse events including increased risk of cardiovascular complications. One of the cardiovascular risk factors is an elevated homocysteine (HC) level. However, neither homocysteine status nor hyperhomocysteinemia effect on the disease course in CML patients on TKI therapy have been sufficiently studied. This paper aims to comprehensively analyze the current literature data on HC level changes and HC metabolism factors in CML patients. The review is based on the articles indexed in the PubMed, MEDLINE and other databases dealing with the mechanisms of HC metabolism genesis, transformation, and causes for its dysfunction in CML patients prior to and on therapy with TKIs of different generations. Despite the limited number of studies, a literature analysis suggests that HC level is a helpful marker of the folate cycle status, metabolic status, endothelial function, and tumor cell growth activity in CML patients.</jats:p>