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Article ; Online: T-ALL and thymocytes: a message of noncoding RNAs.

Wallaert, Annelynn / Durinck, Kaat / Taghon, Tom / Van Vlierberghe, Pieter / Speleman, Frank

2017 Volume 10, Issue 1, Page(s) 66

Abstract: In the last decade, the role for noncoding RNAs in disease was clearly established, starting with microRNAs and later expanded towards long noncoding RNAs. This was also the case for T cell acute lymphoblastic leukemia, which is a malignant blood ... ...

Abstract	In the last decade, the role for noncoding RNAs in disease was clearly established, starting with microRNAs and later expanded towards long noncoding RNAs. This was also the case for T cell acute lymphoblastic leukemia, which is a malignant blood disorder arising from oncogenic events during normal T cell development in the thymus. By studying the transcriptomic profile of protein-coding genes, several oncogenic events leading to T cell acute lymphoblastic leukemia (T-ALL) could be identified. In recent years, it became apparent that several of these oncogenes function via microRNAs and long noncoding RNAs. In this review, we give a detailed overview of the studies that describe the noncoding RNAome in T-ALL oncogenesis and normal T cell development.
MeSH term(s)	Animals ; Carcinogenesis/genetics ; Humans ; Lymphopoiesis/genetics ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/genetics ; RNA, Untranslated/analysis ; RNA, Untranslated/physiology ; Thymocytes
Chemical Substances	RNA, Untranslated
Language	English
Publishing date	2017-03-07
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2429631-4
ISSN	1756-8722 ; 1756-8722
ISSN (online)	1756-8722
ISSN	1756-8722
DOI	10.1186/s13045-017-0432-0
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Article ; Online: Comprehensive miRNA expression profiling in human T-cell acute lymphoblastic leukemia by small RNA-sequencing.

Wallaert, Annelynn / Van Loocke, Wouter / Hernandez, Lucie / Taghon, Tom / Speleman, Frank / Van Vlierberghe, Pieter

Scientific reports

2017 Volume 7, Issue 1, Page(s) 7901

Abstract: T-cell acute lymphoblastic leukemia (T-ALL) is a genetically heterogeneous disease that can be classified into different molecular genetic subtypes according to their mRNA gene expression profile. In this study, we applied RNA sequencing to investigate ... ...

Abstract	T-cell acute lymphoblastic leukemia (T-ALL) is a genetically heterogeneous disease that can be classified into different molecular genetic subtypes according to their mRNA gene expression profile. In this study, we applied RNA sequencing to investigate the full spectrum of miRNA expression in primary T-ALL patient samples, T-ALL leukemia cell lines and healthy donor thymocytes. Notably, this analysis revealed that genetic subtypes of human T-ALL also display unique miRNA expression signatures, which are largely conserved in human T-ALL cell lines with corresponding genetic background. Furthermore, small RNA-sequencing also unraveled the variety of isoforms that are expressed for each miRNA in T-ALL and showed that a significant number of miRNAs are actually represented by an alternative isomiR. Finally, comparison of CD34
MeSH term(s)	Gene Expression Profiling ; Humans ; MicroRNAs/analysis ; MicroRNAs/genetics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/pathology ; Sequence Analysis, RNA ; T-Lymphocytes/pathology
Chemical Substances	MicroRNAs
Language	English
Publishing date	2017-08-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-017-08148-x
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Article ; Online: Long non-coding RNAs in leukemia: biology and clinical impact.

Lammens, Tim / Durinck, Kaat / Wallaert, Annelynn / Speleman, Frank / Van Vlierberghe, Pieter

Current opinion in hematology

2017 Volume 24, Issue 4, Page(s) 353–358

Abstract: Purpose of review: Over the last years, long non-coding RNAs (lncRNAs) have emerged as putative regulators of malignant hematopoietic development. Here, we review recent literature on the involvement of lncRNAs in leukemia, including their role in ... ...

Abstract	Purpose of review: Over the last years, long non-coding RNAs (lncRNAs) have emerged as putative regulators of malignant hematopoietic development. Here, we review recent literature on the involvement of lncRNAs in leukemia, including their role in driving or sustaining disease and their potential impact on diagnosis, classification, and prognosis. Recent findings: Leukemogenesis is a complex process resulting from the accumulation of multiple genetic alterations. Over the last years, advances in high-throughput sequencing and transcriptome profiling have enabled the identification of lncRNAs involved in leukemia development. lncRNAs are able to distinguish different subtypes of human leukemia and several reports have identified specific patterns of lncRNA expression associated with clinical patient characteristics. Although functional studies on the actual role of these lncRNAs during transformation remain scarce, emerging evidence suggests that complex interactions between coding and non-coding transcript are truly involved in leukemia development. Summary: Introduction of lncRNAs as an additional layer of complexity in human leukemia might provide new molecular genetic insights in the biology of this disease and could create unique opportunities for the identification of novel drug targets and diagnostic or prognostic biomarkers.
MeSH term(s)	Biomarkers ; Cell Transformation, Neoplastic/genetics ; Chromatin Assembly and Disassembly/genetics ; Drug Resistance, Neoplasm/genetics ; Gene Expression Regulation, Leukemic ; Humans ; Leukemia/diagnosis ; Leukemia/genetics ; Leukemia/metabolism ; Leukemia/mortality ; Prognosis ; RNA, Long Noncoding/genetics ; Signal Transduction
Chemical Substances	Biomarkers ; RNA, Long Noncoding
Language	English
Publishing date	2017-07
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1153887-9
ISSN	1531-7048 ; 1065-6251
ISSN (online)	1531-7048
ISSN	1065-6251
DOI	10.1097/MOH.0000000000000354
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Article ; Online: Comprehensive miRNA expression profiling in human T-cell acute lymphoblastic leukemia by small RNA-sequencing

Annelynn Wallaert / Wouter Van Loocke / Lucie Hernandez / Tom Taghon / Frank Speleman / Pieter Van Vlierberghe

Scientific Reports, Vol 7, Iss 1, Pp 1-

2017 Volume 8

Abstract: Abstract T-cell acute lymphoblastic leukemia (T-ALL) is a genetically heterogeneous disease that can be classified into different molecular genetic subtypes according to their mRNA gene expression profile. In this study, we applied RNA sequencing to ... ...

Abstract	Abstract T-cell acute lymphoblastic leukemia (T-ALL) is a genetically heterogeneous disease that can be classified into different molecular genetic subtypes according to their mRNA gene expression profile. In this study, we applied RNA sequencing to investigate the full spectrum of miRNA expression in primary T-ALL patient samples, T-ALL leukemia cell lines and healthy donor thymocytes. Notably, this analysis revealed that genetic subtypes of human T-ALL also display unique miRNA expression signatures, which are largely conserved in human T-ALL cell lines with corresponding genetic background. Furthermore, small RNA-sequencing also unraveled the variety of isoforms that are expressed for each miRNA in T-ALL and showed that a significant number of miRNAs are actually represented by an alternative isomiR. Finally, comparison of CD34+ and CD4+CD8+ healthy donor thymocytes and T-ALL miRNA profiles allowed identifying several novel miRNAs with putative oncogenic or tumor suppressor functions in T-ALL. Altogether, this study provides a comprehensive overview of miRNA expression in normal and malignant T-cells and sets the stage for functional evaluation of novel miRNAs in T-ALL disease biology.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2017-08-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
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Article ; Online: Novel biological insights in T-cell acute lymphoblastic leukemia.

Durinck, Kaat / Goossens, Steven / Peirs, Sofie / Wallaert, Annelynn / Van Loocke, Wouter / Matthijssens, Filip / Pieters, Tim / Milani, Gloria / Lammens, Tim / Rondou, Pieter / Van Roy, Nadine / De Moerloose, Barbara / Benoit, Yves / Haigh, Jody / Speleman, Frank / Poppe, Bruce / Van Vlierberghe, Pieter

Experimental hematology

2015 Volume 43, Issue 8, Page(s) 625–639

Abstract: T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive type of blood cancer that accounts for about 15% of pediatric and 25% of adult acute lymphoblastic leukemia (ALL) cases. It is considered as a paradigm for the multistep nature of cancer ... ...

Abstract	T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive type of blood cancer that accounts for about 15% of pediatric and 25% of adult acute lymphoblastic leukemia (ALL) cases. It is considered as a paradigm for the multistep nature of cancer initiation and progression. Genetic and epigenetic reprogramming events, which transform T-cell precursors into malignant T-ALL lymphoblasts, have been extensively characterized over the past decade. Despite our comprehensive understanding of the genomic landscape of human T-ALL, leukemia patients are still treated by high-dose multiagent chemotherapy, potentially followed by hematopoietic stem cell transplantation. Even with such aggressive treatment regimens, which are often associated with considerable acute and long-term side effects, about 15% of pediatric and 40% of adult T-ALL patients still relapse, owing to acquired therapy resistance, and present with very dismal survival perspectives. Unfortunately, the molecular mechanisms by which residual T-ALL tumor cells survive chemotherapy and act as a reservoir for leukemic progression and hematologic relapse remain poorly understood. Nevertheless, it is expected that enhanced molecular understanding of T-ALL disease biology will ultimately facilitate a targeted therapy driven approach that can reduce chemotherapy-associated toxicities and improve survival of refractory T-ALL patients through personalized salvage therapy. In this review, we summarize recent biological insights into the molecular pathogenesis of T-ALL and speculate how the genetic landscape of T-ALL could trigger the development of novel therapeutic strategies for the treatment of human T-ALL.
MeSH term(s)	Adolescent ; Adult ; Animals ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Cellular Reprogramming ; Child ; Child, Preschool ; Epigenesis, Genetic ; Hematopoietic Stem Cell Transplantation ; Humans ; Infant ; Precursor Cells, T-Lymphoid/metabolism ; Precursor Cells, T-Lymphoid/pathology ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/metabolism ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/pathology ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/therapy
Language	English
Publishing date	2015-08
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	185107-x
ISSN	1873-2399 ; 0531-5573 ; 0301-472X
ISSN (online)	1873-2399
ISSN	0531-5573 ; 0301-472X
DOI	10.1016/j.exphem.2015.05.017
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Article ; Online: The Notch driven long non-coding RNA repertoire in T-cell acute lymphoblastic leukemia.

Durinck, Kaat / Wallaert, Annelynn / Van de Walle, Inge / Van Loocke, Wouter / Volders, Pieter-Jan / Vanhauwaert, Suzanne / Geerdens, Ellen / Benoit, Yves / Van Roy, Nadine / Poppe, Bruce / Soulier, Jean / Cools, Jan / Mestdagh, Pieter / Vandesompele, Jo / Rondou, Pieter / Van Vlierberghe, Pieter / Taghon, Tom / Speleman, Frank

Haematologica

2014 Volume 99, Issue 12, Page(s) 1808–1816

Abstract: Genetic studies in T-cell acute lymphoblastic leukemia have uncovered a remarkable complexity of oncogenic and loss-of-function mutations. Amongst this plethora of genetic changes, NOTCH1 activating mutations stand out as the most frequently occurring ... ...

Abstract	Genetic studies in T-cell acute lymphoblastic leukemia have uncovered a remarkable complexity of oncogenic and loss-of-function mutations. Amongst this plethora of genetic changes, NOTCH1 activating mutations stand out as the most frequently occurring genetic defect, identified in more than 50% of T-cell acute lymphoblastic leukemias, supporting a role as an essential driver for this gene in T-cell acute lymphoblastic leukemia oncogenesis. In this study, we aimed to establish a comprehensive compendium of the long non-coding RNA transcriptome under control of Notch signaling. For this purpose, we measured the transcriptional response of all protein coding genes and long non-coding RNAs upon pharmacological Notch inhibition in the human T-cell acute lymphoblastic leukemia cell line CUTLL1 using RNA-sequencing. Similar Notch dependent profiles were established for normal human CD34(+) thymic T-cell progenitors exposed to Notch signaling activity in vivo. In addition, we generated long non-coding RNA expression profiles (array data) from ex vivo isolated Notch active CD34(+) and Notch inactive CD4(+)CD8(+) thymocytes and from a primary cohort of 15 T-cell acute lymphoblastic leukemia patients with known NOTCH1 mutation status. Integration of these expression datasets with publicly available Notch1 ChIP-sequencing data resulted in the identification of long non-coding RNAs directly regulated by Notch activity in normal and malignant T cells. Given the central role of Notch in T-cell acute lymphoblastic leukemia oncogenesis, these data pave the way for the development of novel therapeutic strategies that target hyperactive Notch signaling in human T-cell acute lymphoblastic leukemia.
MeSH term(s)	Amyloid Precursor Protein Secretases/antagonists & inhibitors ; Amyloid Precursor Protein Secretases/metabolism ; Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; Blotting, Western ; Case-Control Studies ; Cell Transformation, Neoplastic/pathology ; Cells, Cultured ; Chromatin Immunoprecipitation ; Cohort Studies ; Enzyme Inhibitors/pharmacology ; Follow-Up Studies ; Gene Expression Profiling ; Humans ; Mutation/genetics ; Oligonucleotide Array Sequence Analysis ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/drug therapy ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/pathology ; Prognosis ; RNA, Long Noncoding/genetics ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction ; Receptor, Notch1/antagonists & inhibitors ; Receptor, Notch1/genetics ; Receptor, Notch1/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; Thymocytes/cytology ; Thymocytes/drug effects ; Thymocytes/metabolism
Chemical Substances	Biomarkers, Tumor ; Enzyme Inhibitors ; NOTCH1 protein, human ; RNA, Long Noncoding ; RNA, Messenger ; Receptor, Notch1 ; Amyloid Precursor Protein Secretases (EC 3.4.-)
Language	English
Publishing date	2014-12
Publishing country	Italy
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2014.115683
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Article ; Online: EV-TRACK: transparent reporting and centralizing knowledge in extracellular vesicle research.

Van Deun, Jan / Mestdagh, Pieter / Agostinis, Patrizia / Akay, Özden / Anand, Sushma / Anckaert, Jasper / Martinez, Zoraida Andreu / Baetens, Tine / Beghein, Els / Bertier, Laurence / Berx, Geert / Boere, Janneke / Boukouris, Stephanie / Bremer, Michel / Buschmann, Dominik / Byrd, James B / Casert, Clara / Cheng, Lesley / Cmoch, Anna /

Daveloose, Delphine / De Smedt, Eva / Demirsoy, Seyma / Depoorter, Victoria / Dhondt, Bert / Driedonks, Tom A P / Dudek, Aleksandra / Elsharawy, Abdou / Floris, Ilaria / Foers, Andrew D / Gärtner, Kathrin / Garg, Abhishek D / Geeurickx, Edward / Gettemans, Jan / Ghazavi, Farzaneh / Giebel, Bernd / Kormelink, Tom Groot / Hancock, Grace / Helsmoortel, Hetty / Hill, Andrew F / Hyenne, Vincent / Kalra, Hina / Kim, David / Kowal, Joanna / Kraemer, Sandra / Leidinger, Petra / Leonelli, Carina / Liang, Yaxuan / Lippens, Lien / Liu, Shu / Lo Cicero, Alessandra / Martin, Shaun / Mathivanan, Suresh / Mathiyalagan, Prabhu / Matusek, Támas / Milani, Gloria / Monguió-Tortajada, Marta / Mus, Liselot M / Muth, Dillon C / Németh, Andrea / Nolte-'t Hoen, Esther N M / O'Driscoll, Lorraine / Palmulli, Roberta / Pfaffl, Michael W / Primdal-Bengtson, Bjarke / Romano, Erminia / Rousseau, Quentin / Sahoo, Susmita / Sampaio, Natalia / Samuel, Monisha / Scicluna, Benjamin / Soen, Bieke / Steels, Anneleen / Swinnen, Johannes V / Takatalo, Maarit / Thaminy, Safia / Théry, Clotilde / Tulkens, Joeri / Van Audenhove, Isabel / van der Grein, Susanne / Van Goethem, Alan / van Herwijnen, Martijn J / Van Niel, Guillaume / Van Roy, Nadine / Van Vliet, Alexander R / Vandamme, Niels / Vanhauwaert, Suzanne / Vergauwen, Glenn / Verweij, Frederik / Wallaert, Annelynn / Wauben, Marca / Witwer, Kenneth W / Zonneveld, Marijke I / De Wever, Olivier / Vandesompele, Jo / Hendrix, An

Nature methods

2017 Volume 14, Issue 3, Page(s) 228–232

Abstract: We argue that the field of extracellular vesicle (EV) biology needs more transparent reporting to facilitate interpretation and replication of experiments. To achieve this, we describe EV-TRACK, a crowdsourcing knowledgebase (http://evtrack.org) that ... ...

Abstract	We argue that the field of extracellular vesicle (EV) biology needs more transparent reporting to facilitate interpretation and replication of experiments. To achieve this, we describe EV-TRACK, a crowdsourcing knowledgebase (http://evtrack.org) that centralizes EV biology and methodology with the goal of stimulating authors, reviewers, editors and funders to put experimental guidelines into practice.
MeSH term(s)	Biomedical Research ; Databases, Bibliographic ; Extracellular Vesicles/physiology ; Internationality
Language	English
Publishing date	2017-02-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	2169522-2
ISSN	1548-7105 ; 1548-7091
ISSN (online)	1548-7105
ISSN	1548-7091
DOI	10.1038/nmeth.4185
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Article ; Online: Unique long non-coding RNA expression signature in ETV6/RUNX1-driven B-cell precursor acute lymphoblastic leukemia.

Ghazavi, Farzaneh / De Moerloose, Barbara / Van Loocke, Wouter / Wallaert, Annelynn / Helsmoortel, Hetty H / Ferster, Alina / Bakkus, Marleen / Plat, Geneviève / Delabesse, Eric / Uyttebroeck, Anne / Van Nieuwerburgh, Filip / Deforce, Dieter / Van Roy, Nadine / Speleman, Frank / Benoit, Yves / Lammens, Tim / Van Vlierberghe, Pieter

Oncotarget

2016 Volume 7, Issue 45, Page(s) 73769–73780

Abstract: Overwhelming evidence indicates that long non-coding RNAs have essential roles in tumorigenesis. Nevertheless, their role in the molecular pathogenesis of pediatric B-cell precursor acute lymphoblastic leukemia has not been extensively explored. Here, we ...

Abstract	Overwhelming evidence indicates that long non-coding RNAs have essential roles in tumorigenesis. Nevertheless, their role in the molecular pathogenesis of pediatric B-cell precursor acute lymphoblastic leukemia has not been extensively explored. Here, we conducted a comprehensive analysis of the long non-coding RNA transcriptome in ETV6/RUNX1-positive BCP-ALL, one of the most frequent subtypes of pediatric leukemia. First, we used primary leukemia patient samples to identify an ETV6/RUNX1 specific expression signature consisting of 596 lncRNA transcripts. Next, integration of this lncRNA signature with RNA sequencing of BCP-ALL cell lines and lncRNA profiling of an in vitro model system of ETV6/RUNX1 knockdown, revealed that lnc-NKX2-3-1, lnc-TIMM21-5, lnc-ASTN1-1 and lnc-RTN4R-1 are truly regulated by the oncogenic fusion protein. Moreover, sustained inactivation of lnc-RTN4R-1 and lnc-NKX2-3-1 in ETV6/RUNX1 positive cells caused profound changes in gene expression. All together, our study defined a unique lncRNA expression signature associated with ETV6/RUNX1-positive BCP-ALL and identified lnc-RTN4R-1 and lnc-NKX2-3-1 as lncRNAs that might be functionally implicated in the biology of this prevalent subtype of human leukemia.
Language	English
Publishing date	2016--08
Publishing country	United States
Document type	Journal Article
ISSN	1949-2553
ISSN (online)	1949-2553
DOI	10.18632/oncotarget.12063
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