Detection of the der (21)t(12;21) chromosome forming the TEL-AML1 fusion gene in childhood acute lymphoblastic leukemia

Hirofumi Kobayashi, Noriko Satake, Yasuhiko Kaneko

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

The t(12;21) (p13;q22) is observed in approximately 20-25% of childhood B-lineage acute lymphoblastic leukemia (ALL) cases in both Asian and Caucasian populations. This translocation results in the fusion of TEL, a recently described ETS-like gene on 12p13, and AML1, which was shown to be involved in the formation of fusion genes with ETO and EV11 in myeloid leukemias. Fluorescence in situ hybridization (FISH) and reverse transcriptase-polymerase chain reaction (RT-PCR) analysis are useful in detecting this translocation which is not readily identified with routine cytogenetic techniques. The t(12;21) is associated with a distinct subgroup of patients characterized by an age between 1 and 10 years, an early B immunophenotype, and a good prognosis. A high incidence of the deletion of non-translocated TEL is another characteristic of leukemic cells with this translocation. TEL-AML1 hybrid protein thought to be critical in leukemogenesis possesses the HLH domain of TEL fused to almost the entire AML1 protein, although the detailed mechanisms of leukemogenesis remain obscure. RT-PCR combined with FISH analysis of posttreatment samples appears to be useful in detecting early relapse or minimal residual disease and thus, is expected to optimize the treatment strategy for patients with t(12;21).

Original languageEnglish (US)
Pages (from-to)43-50
Number of pages8
JournalLeukemia and Lymphoma
Volume28
Issue number1-2
StatePublished - 1997
Externally publishedYes

Fingerprint

Chromosomes, Human, Pair 12
Chromosomes, Human, Pair 21
Gene Fusion
Reverse Transcriptase Polymerase Chain Reaction
Fluorescence In Situ Hybridization
Precursor Cell Lymphoblastic Leukemia-Lymphoma
Myeloid Leukemia
Cytogenetic Analysis
Residual Neoplasm
Recurrence
Incidence
Population
Genes
Proteins
Therapeutics
TEL-AML1 fusion protein

Keywords

  • ALL
  • AML1
  • Chromosomal aberration
  • TEL

ASJC Scopus subject areas

  • Hematology
  • Oncology
  • Cancer Research

Cite this

Detection of the der (21)t(12;21) chromosome forming the TEL-AML1 fusion gene in childhood acute lymphoblastic leukemia. / Kobayashi, Hirofumi; Satake, Noriko; Kaneko, Yasuhiko.

In: Leukemia and Lymphoma, Vol. 28, No. 1-2, 1997, p. 43-50.

Research output: Contribution to journalArticle

@article{fe2147b73b2c4ad3ba7683d442c797f1,
title = "Detection of the der (21)t(12;21) chromosome forming the TEL-AML1 fusion gene in childhood acute lymphoblastic leukemia",
abstract = "The t(12;21) (p13;q22) is observed in approximately 20-25{\%} of childhood B-lineage acute lymphoblastic leukemia (ALL) cases in both Asian and Caucasian populations. This translocation results in the fusion of TEL, a recently described ETS-like gene on 12p13, and AML1, which was shown to be involved in the formation of fusion genes with ETO and EV11 in myeloid leukemias. Fluorescence in situ hybridization (FISH) and reverse transcriptase-polymerase chain reaction (RT-PCR) analysis are useful in detecting this translocation which is not readily identified with routine cytogenetic techniques. The t(12;21) is associated with a distinct subgroup of patients characterized by an age between 1 and 10 years, an early B immunophenotype, and a good prognosis. A high incidence of the deletion of non-translocated TEL is another characteristic of leukemic cells with this translocation. TEL-AML1 hybrid protein thought to be critical in leukemogenesis possesses the HLH domain of TEL fused to almost the entire AML1 protein, although the detailed mechanisms of leukemogenesis remain obscure. RT-PCR combined with FISH analysis of posttreatment samples appears to be useful in detecting early relapse or minimal residual disease and thus, is expected to optimize the treatment strategy for patients with t(12;21).",
keywords = "ALL, AML1, Chromosomal aberration, TEL",
author = "Hirofumi Kobayashi and Noriko Satake and Yasuhiko Kaneko",
year = "1997",
language = "English (US)",
volume = "28",
pages = "43--50",
journal = "Leukemia and Lymphoma",
issn = "1042-8194",
publisher = "Informa Healthcare",
number = "1-2",

}

TY - JOUR

T1 - Detection of the der (21)t(12;21) chromosome forming the TEL-AML1 fusion gene in childhood acute lymphoblastic leukemia

AU - Kobayashi, Hirofumi

AU - Satake, Noriko

AU - Kaneko, Yasuhiko

PY - 1997

Y1 - 1997

N2 - The t(12;21) (p13;q22) is observed in approximately 20-25% of childhood B-lineage acute lymphoblastic leukemia (ALL) cases in both Asian and Caucasian populations. This translocation results in the fusion of TEL, a recently described ETS-like gene on 12p13, and AML1, which was shown to be involved in the formation of fusion genes with ETO and EV11 in myeloid leukemias. Fluorescence in situ hybridization (FISH) and reverse transcriptase-polymerase chain reaction (RT-PCR) analysis are useful in detecting this translocation which is not readily identified with routine cytogenetic techniques. The t(12;21) is associated with a distinct subgroup of patients characterized by an age between 1 and 10 years, an early B immunophenotype, and a good prognosis. A high incidence of the deletion of non-translocated TEL is another characteristic of leukemic cells with this translocation. TEL-AML1 hybrid protein thought to be critical in leukemogenesis possesses the HLH domain of TEL fused to almost the entire AML1 protein, although the detailed mechanisms of leukemogenesis remain obscure. RT-PCR combined with FISH analysis of posttreatment samples appears to be useful in detecting early relapse or minimal residual disease and thus, is expected to optimize the treatment strategy for patients with t(12;21).

AB - The t(12;21) (p13;q22) is observed in approximately 20-25% of childhood B-lineage acute lymphoblastic leukemia (ALL) cases in both Asian and Caucasian populations. This translocation results in the fusion of TEL, a recently described ETS-like gene on 12p13, and AML1, which was shown to be involved in the formation of fusion genes with ETO and EV11 in myeloid leukemias. Fluorescence in situ hybridization (FISH) and reverse transcriptase-polymerase chain reaction (RT-PCR) analysis are useful in detecting this translocation which is not readily identified with routine cytogenetic techniques. The t(12;21) is associated with a distinct subgroup of patients characterized by an age between 1 and 10 years, an early B immunophenotype, and a good prognosis. A high incidence of the deletion of non-translocated TEL is another characteristic of leukemic cells with this translocation. TEL-AML1 hybrid protein thought to be critical in leukemogenesis possesses the HLH domain of TEL fused to almost the entire AML1 protein, although the detailed mechanisms of leukemogenesis remain obscure. RT-PCR combined with FISH analysis of posttreatment samples appears to be useful in detecting early relapse or minimal residual disease and thus, is expected to optimize the treatment strategy for patients with t(12;21).

KW - ALL

KW - AML1

KW - Chromosomal aberration

KW - TEL

UR - http://www.scopus.com/inward/record.url?scp=0031426612&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031426612&partnerID=8YFLogxK

M3 - Article

C2 - 9498702

AN - SCOPUS:0031426612

VL - 28

SP - 43

EP - 50

JO - Leukemia and Lymphoma

JF - Leukemia and Lymphoma

SN - 1042-8194

IS - 1-2

ER -