Occurrence of anMLL/LAF4 fusion gene caused by the insertion ins(11;2)(q23;q11.2q11.2) in an infant with acute lymphoblastic leukemia

2003 ◽  
Vol 37 (1) ◽  
pp. 106-109 ◽  
Author(s):  
Jochen Bruch ◽  
Monika Wilda ◽  
Andrea Teigler-Schlegel ◽  
Jochen Harbott ◽  
Arndt Borkhardt ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Fusion Gene ◽  
Lymphoblastic Leukemia

Targeting Kinase-activating Genetic Lesions to Improve Therapy of Pediatric Acute Lymphoblastic Leukemia

2018 ◽  
Vol 25 (24) ◽  
pp. 2811-2825 ◽  
Author(s):  
Raffaella Franca ◽  
Natasa K. Kuzelicki ◽  
Claudio Sorio ◽  
Eleonora Toffoletti ◽  
Oksana Montecchini ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Fusion Gene ◽  
Hematologic Malignancy ◽  
Lymphoblastic Leukemia ◽  
Point Of View ◽  
Lymphoid Cells ◽  
Gene Encoding ◽  
Pediatric All ◽  
Blast Cells ◽  
Tk Inhibitors

Acute lymphoblastic leukemia (ALL) is the most common hematologic malignancy in children, characterized by an abnormal proliferation of immature lymphoid cells. Thanks to risk-adapted combination chemotherapy treatments currently used, survival at 5 years has reached 90%. ALL is a heterogeneous disease from a genetic point of view: patients’ lymphoblasts may harbor in fact several chromosomal alterations, some of which have prognostic and therapeutic value. Of particular importance is the translocation t(9;22)(q34;q11.2) that leads to the formation of the BCR-ABL1 fusion gene, encoding a constitutively active chimeric tyrosine kinase (TK): BCR-ABL1 that is present in ~3% of pediatric ALL patients with B-immunophenotype and is associated with a poor outcome. This type of ALL is potentially treatable with specific TK inhibitors, such as imatinib. Recent studies have demonstrated the existence of a subset of BCR-ABL1 like leukemias (~10-15% of Bimmunophenotype ALL), whose blast cells have a gene expression profile similar to that of BCR-ABL1 despite the absence of t(9;22)(q34;q11.2). The precise pathogenesis of BCR-ABL1 like ALL is still to be defined, but they are mainly characterized by the activation of constitutive signal transduction pathways due to chimeric TKs different from BCR-ABL1. BCR-ABL1 like ALL patients represent a group with unfavorable outcome and are not identified by current risk criteria. In this review, we will discuss the design of targeted therapy for patients with BCR-ABL1 like ALL, which could consider TK inhibitors, and discuss innovative approaches suitable to identify the presence of patient’s specific chimeric TK fusion genes, such as targeted locus amplification or proteomic biosensors.

scholarly journals Dense Methylation of Types 1 and 2 Regulatory Regions of the CD10 Gene Promoter in Infant Acute Lymphoblastic Leukemia With MLL/AF4 Fusion Gene

2010 ◽  
Vol 32 (1) ◽  
pp. 4-10 ◽  
Author(s):  
Yasuhiro Ikawa ◽  
Naotoshi Sugimoto ◽  
Shoichi Koizumi ◽  
Akihiro Yachie ◽  
Yutaka Saikawa
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Fusion Gene ◽  
Lymphoblastic Leukemia ◽  
Gene Promoter ◽  
Regulatory Regions ◽  
Infant Acute Lymphoblastic Leukemia

scholarly journals Heterogeneous patterns of amplification of the NUP214-ABL1 fusion gene in T-cell acute lymphoblastic leukemia

Leukemia ◽  
2008 ◽  
Vol 23 (1) ◽  
pp. 125-133 ◽  
Author(s):  
C Graux ◽  
◽  
M Stevens-Kroef ◽  
M Lafage ◽  
N Dastugue ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Fusion Gene ◽  
Lymphoblastic Leukemia ◽  
Cell Acute Lymphoblastic Leukemia

scholarly journals NUTM1 is a recurrent fusion gene partner in B-cell precursor acute lymphoblastic leukemia associated with increased expression of genes on chromosome band 10p12.31-12.2

Haematologica ◽  
2019 ◽  
Vol 104 (10) ◽  
pp. e455-e459 ◽  
Author(s):  
Femke M. Hormann ◽  
Alex Q. Hoogkamer ◽  
H. Berna Beverloo ◽  
Aurélie Boeree ◽  
Ilse Dingjan ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
B Cell ◽  
Fusion Gene ◽  
Lymphoblastic Leukemia ◽  
Chromosome Band ◽  
Cell Precursor ◽  
Expression Of Genes

scholarly journals PDGFRB mutation and tyrosine kinase inhibitor resistance in Ph-like acute lymphoblastic leukemia

Blood ◽  
2018 ◽  
Vol 131 (20) ◽  
pp. 2256-2261 ◽  
Author(s):  
Yingchi Zhang ◽  
Yufeng Gao ◽  
Hui Zhang ◽  
Jingliao Zhang ◽  
Fuhong He ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Tyrosine Kinase Inhibitor ◽  
Kinase Inhibitor ◽  
Fusion Gene ◽  
Lymphoblastic Leukemia ◽  
Genomic Profiling ◽  
Functional Studies ◽  
Key Points ◽  
Tki Resistance ◽  
Inhibitor Resistance

Key Points AGGF1-PDGFRB is a novel oncogenic fusion gene in Ph-like ALL. Genomic profiling and functional studies identified a novel PDGFRB mutation directly related to TKI resistance.

Exploring the oncogenic and therapeutic target potential of the MYB-TYK2 fusion gene in B-cell acute lymphoblastic leukemia

2022 ◽  
Author(s):  
Paniz Tavakoli Shirazi ◽  
Laura N. Eadie ◽  
Susan L. Heatley ◽  
Elyse C. Page ◽  
Maxime François ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
B Cell ◽  
Therapeutic Target ◽  
Fusion Gene ◽  
Lymphoblastic Leukemia ◽  
Cell Acute Lymphoblastic Leukemia

Down-regulated FOXO1 in refractory/relapse childhood B-cell acute lymphoblastic leukemia

2020 ◽  
Author(s):  
HUI ZHANG ◽  
Chuang Jiang ◽  
Haiyan Liu ◽  
Wenge Hao ◽  
Pengfei Wang ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
B Cell ◽  
Fusion Gene ◽  
Lymphoblastic Leukemia ◽  
Expression Level ◽  
Luciferase Reporter ◽  
Loss Of Function ◽  
Transcription Activity ◽  
Real Time Quantitative Pcr ◽  
Induction Failure

Abstract Background Refractory/relapsed acute lymphoblastic leukemia (RR-ALL) remains to be a leading cause of treatment failure and subsequent death. Forkhead box O1 (FOXO1) belongs to the forkhead family of transcription factors, its specific role in RR-ALL has not yet been determined in B-cell ALL (B-ALL). The purpose of this study was to investigate the expression and prognostic value in ALL. Methods RNA sequencing was applied to an ALL case with induction failure to identify the causal events. The transcription activity was examined with luciferase reporter assay. FOXO1 mRNA expression level was examined using real-time quantitative PCR. Association analysis was performed to correlate FOXO1 transcription with childhood B-ALL prognosis and relapse. Results In this ALL case with induction failure, we successfully identified a novel MEIS1-FOXO1 fusion gene. The transcription activity of MEIS1-FOXO1 was significantly abolished as compared to wild-type FOXO1. Low FOXO1 expression level was strongly associate with unfavorable subtype, MRD positivity and relapse. Conclusions FOXO1 loss of function associates with ALL high-risk stratification and relapse, which might be due to drug resistance.

scholarly journals Identification of a novel fusion gene in a pre-B acute lymphoblastic leukemia with t(1;19)(q23;p13)

2004 ◽  
Vol 95 (6) ◽  
pp. 503-507 ◽  
Author(s):  
Yasuhiro Yuki ◽  
Issei Imoto ◽  
Masue Imaizumi ◽  
Shigeyoshi Hibi ◽  
Yasuhiko Kaneko ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Fusion Gene ◽  
Lymphoblastic Leukemia

Prognostic Significance of the TEL-AML1 Fusion Gene in Pediatric Acute Lymphoblastic Leukemia in Turkey

2003 ◽  
Vol 25 (3) ◽  
pp. 204-208 ◽  
Author(s):  
Ugur Ozbek ◽  
Sema Sirma ◽  
Leyla Agaoglu ◽  
Lebriz Yuksel ◽  
Sema Anak ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Fusion Gene ◽  
Lymphoblastic Leukemia ◽  
Prognostic Significance ◽  
Pediatric Acute Lymphoblastic Leukemia
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