AimCHP2 (calcineurin B homologous protein 2) is identified as a tumor-associated antigen highly expressed in different malignancies. It plays a critical role in cancer cell development, proliferation, motility and survival. It is suggested that the human tumor related gene CHP2 expression in leukemia primary cells and leukemia cell lines significantly increase, which may play an important role in growth process of leukemia cells.MethodsIn this study, the expression of CHP2 gene was analyzed in 10 normal healthy controls and 40 patients with de novo acute leukemia (20 AML and 20 ALL). CHP2 expression was analyzed using a real-time quantitative reverse-transcriptase polymerase chain reaction (RTQ-PCR) to investigate a possible relation, association or correlation with the clinical features of AL (acute leukemia) at diagnosis, such as age, gender, lineage, HB, TLC, platelet count, BM blast cell infiltration and risk group.ResultsCHP2 was highly expressed in 13/40 AL studied patients (7/20 AML and 6/20 ALL) with mean expression level of 2.7 while it was not expressed in any of the controls.ConclusionsMany studies suggest that CHP2 expression is a novel prognostic marker in AL and thus needs to be incorporated into the patient stratification and treatment protocols. In addition, a quarter of AL patients fail therapy and novel treatments that are focused on undermining specifically the leukemic process are needed urgently.
Introduction: A link between thrombophilia and female infertility has been previously reported and the role of thrombophilia in multiple ART failures has been debated. Most meta-analyses of existing studies yield inconclusive and contradictory results that no antithrombotic therapy could, to-date, be indicated in thrombophilia patients with ART failure(s) without clinical thrombosis. As analysis of a large cohort is therefore warranted, we embarked on this study to identify the true prevalence of thrombophilia in a large number of women who presented for infertility and recurrent ART failures evaluation to detect the true prevalence of thrombophilia. Methods: This is an IRB-approved retrospective cohort analysis of Egyptian women with 3 or more ART attempts referred to our center NSA-Diagnostic Laboratories from 1/1/2009 to 1/1/2015. Females with known venous thromboembolism (VTE) prior to infertility evaluation were excluded. Aspirin use and results of thrombophilia testing were collected on all patients. Thrombophilia testing included Factor V Leiden mutation (FVL), prothrombin gene mutation, Plasminogen Activator Inhibitor-1 (PAI-1), Factor XIII level, b-Fib, HPA, ACE, ApoB, ApoE, anticardiolipin IgG and IgM (ACLG, ACLM respectively), Protein C deficiency, Protein S deficiency, antithrombin (AT), lupus anticoagulant (LA), CD16, CD56, methylenetetrahydrofolate reductase (MTHFR) A or C, and homocysteine level. Thrombophilia was categorized into simple and complex reflecting 1 and >1 homozygous mutations detected, respectively. Demographic characteristics and the prevalence of the different mutations were analyzed. Statistical analysis was performed using SPSS software version 20.0. Results: Inclusion criteria and all data were available in 2585 female subjects. Age range was 21-43. While all subjects had at least one or more mutation(s) of any kind, 305 subjects (11.8%) did not have any homozygous mutations. Simple thrombophilia (one homozygous mutation) was found in 894 patients (34.6%). Complex thrombophilia (more than one homozygous mutation) with 2, 3, 4, and 5 concomitant abnormalities was encountered: in 35.8%, 13.5%, 3.9% and 0.4%, respectively. Prevalence of homozygous and heterozygous mutations was as follows: FVL (2.9%; 21.9%), prothrombin gene mutation (0.1%; 4.0%), PAI (17.4%; 67.5%), factor XIII (1.2%; 23.7%), b-Fib (39.2%; 2.7%), HPA (10%; 30%), ACE (49.6%; 49.2%), ApoB (0.1%; 0%), ApoE (62.7%; 21.3%). ACLG was positive in 1.2%, ACLM in 3.6%, Protein C deficiency in 0.4%, Protein S deficiency in 0.2%, AT in 1.0%, LA in 1.8%, CD16 in 0.1%, CD56 in 1.1% and hyperhomocysteinemia in 0.7%. Heterozygous and homozygous MTHFR A (45.1%; 9.8%), MTHFR C (35.3%; 7.7%) mutations were noted. When compared to historical controls in the literature, similar prevalence was found for Protein C/S deficiencies, higher prevalence for FVL and Prothrombin gene mutation, and a lower prevalence for hyperhomocysteinemia in our cohort. No VTE was reported in subjects from the time of testing until data collection and follow up. Prophylactic anticoagulation with low molecular weight heparin and low dose aspirin in subjects were noted. All subjects with successful pregnancies post identification of thrombophilia were prescribed prophylactic anticoagulation with low molecular weight heparin through pregnancy and for 6 weeks postpartum. Low dose aspirin and first trimester steroids were also used. Analysis of full term pregnancy as an outcome is underway. Discussion: Thrombophilia prevalence in infertile Egyptian women presenting to our center with multiple failed ART attempts is higher for certain mutations than reported in the literature. Our cohort is unique in that women did not have a history of clinically evident VTE and had a higher prevalence of complex homozygous mutations. Our study has implications on the evaluation of female patients with infertility and helps set up the stage for future prospective and interventional trials using antithrombotic therapy. Disclosures No relevant conflicts of interest to declare.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.