Abstract
Chronic myeloid leukemia (CML) is a clonal myeloproliferative disorder. CML cells contain a BCR-ABL gene, not typically found in normal cells that produce a protein (BCR-ABL) causing CML cells to proliferate. CML occurs in three phases: chronic, accelerated and blast crisis. Disease staging is primarily based on percent of blasts in the blood and bone marrow. Most cases of CML are diagnosed in chronic phase (CP). The major objective in CML clinical management is to prevent progression from chronic to accelerated and blast crisis phases. While earlier treatments, such as cytoreductive chemo- and interferon therapies increased overall survival rates among patients, the advent of tyrosine-kinase inhibitors (TKIs) have changed the CML treatment landscape. Despite the widespread use of these therapies, there have also been associated side effects that could potentially affect its use. Also it is necessary to avoid all deaths and complications related to the treatment, by limiting as much as possible the side-effects of the treatment while ensuring the compliance of the patients. The aim of this work was to measure the serum estrogen and its soluble receptor levels in patients with chronic myeloid leukemia in order to extrapolate their possible clinical significance. The present study included 40 (20 males and 20 females) healthy volunteers clinically free from any disease, 40 (20 males and 20 females) patients of newly diagnosed CML. Blood samples were collected from all subjects and the level of serum estrogen (E2) and serum soluble estrogen receptor (ER) were measured by enzyme linked immunosorbent assay (ELISA). The level of serum E2 (pg/ml) in both male and female patients groups with CML was significantly higher than in control group. The level of serum ER (ng/ml) in both male and female patients groups with CML was significantly lower than in control group. Estimating the serum level of E2 and soluble ER is of informative diagnostic value. Estimation serum level of E2 and soluble ER in patients with CML is of value in deciding use of antiestrogen as therapeutic target in treatment protocol. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12288-021-01451-8.