Abstract

Context The immune system plays a significant role in controlling carcinogenesis, even though most cancers escape immune surveillance through a variety of mechanisms. Objective The aim of the present study was to evaluate the prognostic significance of the novel co-inhibitory B and T lymphocyte attenuator (BTLA) in acute myeloid leukemia (AML) patients as well as its correlation with immune cell populations and treatment outcomes. Design And Setting We conducted case control study on de novo AML patients recruited from Internal Medicine Department, Clinical Hematology and Stem Cell Transplantation Unit, Ain Shams University Hospitals, Cairo, Egypt. The study was held from November 2018 to February 2019 with one year follow up of enrolled cases. Patients and Participants A total of 60 newly diagnosed AML patients and 15 healthy controls were recruited. Interventions We investigated mRNA expression of (BTLA) on peripheral blood in AML patients, and age and sex matched healthy control. Results BTLA expression was significantly up-regulated in patients in comparison to controls (p = 0.024). The expression level of BTLA in CD13+, CD33+, HLA-DR+ patients was significantly higher than in CD13- (p = 0.003), CD33- (p Conclusions These findings provide a basis for the concept that BTLA up-regulation is involved in inhibition of antitumor immunity, and that high BTLA expression level could be considered an independent biomarker for poor prognosis and survival of AML patients.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.