GSE128254 Co-expression of long non-coding RNAs and protein-coding genes in pediatric B-cell acute lymphoblastic leukemia

In this study, we assessed the lncRNA expression profiles of 42 pediatric B-ALL (24 with and 18 without the t(12;21) translocation) and 4 bone marrows from healthy donors. We identified 117 lncRNAs that were differentially expressed (fold change> 1.5 and FDR> 0.05) between the B-ALL subgroups (ETV6-RUNX1-positive and ETV6-RUNX1-negative). The most upregulated lncRNAs in ETV6-RUNX1 positive B-ALL were TCL6, RP4-697K14.3, LOC100292680, RP11-345I18.1, LINC00599 and TRAF3IP2-AS1, while the most downregulated were RP11-135F9.1, RP11-561B11.1, AK095221, RP11-463H12.1, AC007283.4 and CCDC26. Coding-non-coding gene co-expression networks were constructed to identify lncRNAs with potential functions in ETV6-RUNX1 translocation. Levels of representative lncRNA-mRNA pairs were further detected by RT-qPCR in patients with pediatric B-ALL. Importantly, pediatric B-ALL patients who expressed low levels of the lncRNA TCL6 had lower disease-free survival than patients with high levels of TCL6. Thus, these findings provide the first detailed description of lncRNA expression profiles related to t(12;21) translocation in pediatric B-ALL. Such lncRNAs profiles might play important roles in driving normal cells to leukemic cells. These lncRNAs may provide novel molecular biomarkers and offer new basis for combating pediatric B-ALL.
Source: GEO: Gene Expression Omnibus - Category: Genetics & Stem Cells Tags: Expression profiling by array Non-coding RNA profiling by array Homo sapiens Source Type: research

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AbstractPediatric acute lymphoblastic leukemia (ALL) is defined by recurrent chromosomal aberrations including hyperdiploidy and chromosomal translocations. Many of these aberrations originatein utero and the cells transform in early childhood through acquired secondary mutations. In this review, we will discuss the most common prenatal lesions that can lead to childhood ALL, with a special emphasis on the most common translocation in childhood ALL, t(12;21), which results in theETV6-RUNX1 gene fusion. TheETV6-RUNX1 fusion arises prenatally and at a 500-fold higher frequency than the corresponding ALL. Even though the find...
Source: Cancer and Metastasis Reviews - Category: Cancer & Oncology Source Type: research
This study aims to understand patients' characteristics, "real-world" treatment practice and outcomes of pediatric ALL. METHODS: A cohort of 213 pediatric ALL patients, treated at (King Faisal Specialist Hospital and Research Center -Jeddah branch) KFSH and RC-J during the period of January 2002 to December 2015 were analyzed retrospectively. Statistical analyses were performed on patients' demographic, clinical and genetics characteristics and outcomes of different treatment protocols. Survival was evaluated using Kaplan-Meier method, and differences in survival were tested using Log-Rank. Significance was s...
Source: Asian Pacific Journal of Cancer Prevention - Category: Cancer & Oncology Tags: Asian Pac J Cancer Prev Source Type: research
Leukaemia is the most common childhood cancer and acute lymphoblastic leukaemia (ALL) is responsible for a third of all childhood cancer deaths. Despite the overall good prognosis, failure to eradicate the disease leads to relapse in ∼20% of patients and survival rates for infants are less than 50%. There is therefore a clear unmet need for less toxic and more effective targeted treatments. ETV6-RUNX1 translocation is the first-hit event in ∼25% of B-ALLs, initiating a clinically silent pre-leukaemia in utero.
Source: Experimental Hematology - Category: Hematology Authors: Tags: 3038 Source Type: research
Publication date: Available online 27 July 2019Source: Advances in Biological RegulationAuthor(s): Stien De Coninck, Geert Berx, Tom Taghon, Pieter Van Vlierberghe, Steven GoossensAbstractThe identification of the rare but recurrent t(2;14)(q22;q32) translocation involving the ZEB2 locus in T-cell acute lymphoblastic leukemia, suggested that ZEB2 is an oncogenic driver of this high-risk subtype of leukemia. ZEB2, a zinc finger E-box homeobox binding transcription factor, is a master regulator of cellular plasticity and its expression is correlated with poor overall survival of cancer patients. Recent loss- and gain-of-func...
Source: Advances in Biological Regulation - Category: Biology Source Type: research
In this study,TCF3 ‐HLF mRNA was detectable at a high level during induction therapy in a newly diagnosed t(17;19) ‐ALL case, whileTCF3 ‐PBX1 mRNA was undetectable at the end of induction therapy in most newly diagnosed t(1;19) ‐ALL cases. Using 4 t(17;19)‐ALL and 16 t(1;19)‐ALL cell lines, drug response profiling was analyzed. t(17;19)‐ALL cell lines were found to be significantly more resistant to vincristine (VCR), daunorubicin (DNR), and prednisolone (Pred) than t(1;19)‐ALL cell lines. Sensitivities to three (Pred, VCR, andl‐asparaginase [l‐Asp]), four (Pred, VCR,l‐Asp, and DNR) and five (Pred, VC...
Source: Cancer Medicine - Category: Cancer & Oncology Authors: Tags: ORIGINAL RESEARCH Source Type: research
Alla S. Koltsova1,2, Anna A. Pendina1, Olga A. Efimova1*, Olga G. Chiryaeva1, Tatyana V. Kuznetzova1 and Vladislav S. Baranov1,2 1D.O. Ott Research Institute of Obstetrics, Gynecology and Reproductology, Saint Petersburg, Russia 2Department of Genetics and Biotechnology, Saint Petersburg State University, Saint Petersburg, Russia In the present review, we focus on the phenomenon of chromothripsis, a new type of complex chromosomal rearrangements. We discuss the challenges of chromothripsis detection and its distinction from other chromoanagenesis events. Along with already known causes and mechanisms, we introdu...
Source: Frontiers in Genetics - Category: Genetics & Stem Cells Source Type: research
Conclusions This review describes how leukocyte-heparanase can be a double-edged sword in tumor progression; it can enhance tumor immune surveillance and tumor cell clearance, but also promote tumor survival and growth. We also discuss the potential of using heparanase in leukocyte therapies against tumors, and the effects of heparanase inhibitors on tumor progression and immunity. We are just beginning to understand the influence of heparanase on a pro/anti-tumor immune response, and there are still many questions to answer. How do the pro/anti-tumorigenic effects of heparanase differ across different cancer types? Does...
Source: Frontiers in Oncology - Category: Cancer & Oncology Source Type: research
Discussion This case demonstrates successful cure of pre-B-ALL complicating XLA by alloSCT with restoration of B-cell development and functional antibody response. We are aware of only one previous case of pre-B-ALL in an XLA patient (21), which suggests that human BTK deficiency in itself does not predispose to pre-B-ALL. However, there are data to suggest that BTK may act as a tumor suppressor, and BTK deficiency may predispose to tumor development following a “second hit.” Mice with a genetic deficiency in Slp65, a gene encoding an adaptor protein that functions together with BTK, have a block in progenito...
Source: Frontiers in Immunology - Category: Allergy & Immunology Source Type: research
Lei Liu1,2,3, Lin Zhang1,2, Shuo Zhao4, Xu-Yang Zhao1,2, Peng-Xiang Min4, Ya-Dong Ma4, Yue-Yuan Wang4, Yan Chen1,2, Si-Jie Tang4, Yu-Jie Zhang2,4, Jun Du2,4 and Luo Gu2,4* 1Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, China 2Jiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Collaborative Innovation Center for Cancer Personalized Medicine, Nanjing Medical University, Nanjing, China 3Department of Physiology, Xuzhou Medical University, Xuzhou, China 4Department of Physiology, Nanjing Medical University, Nanjing, China Tumor cell migration is a critical step...
Source: Frontiers in Pharmacology - Category: Drugs & Pharmacology Source Type: research
Acute lymphoblastic leukemia (ALL) is the most frequently occurring type of cancer in young children. Despite a better than 90% cure rate, ALL is still the leading cause of leukemia-related deaths in children [1]. 80% of pediatric ALLs are cancers of the B lymphocyte lineage (B-ALL) and two thirds of these involve mutation or chromosomal translocation of genes encoding transcription factors [2]. The most frequently occurring genetic abnormality in pediatric B-ALL is the t(12;21) chromosomal translocation that results in a ETV6-RUNX1 (also known as TEL-AML1) fusion gene [3].
Source: Experimental Hematology - Category: Hematology Authors: Source Type: research
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