Abnormalities of chromosome 14 at band 14q11 in Japanese patients with adult T-cell leukemia

Sadamori, Naoki; Kusano, Mao; Nishino, Kimihiro; Tagawa, Masuko; Yao, Ei-ichi; Yamada, Yasuaki; Amagasaki, T; Kinoshita, K; Ichimaru, Michito

doi:10.1016/0165-4608(85)90019-6

Cited by 66 publications

(19 citation statements)

References 5 publications

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“…One recurring rearrangement in T-cell neoplasia is a paracentric inversion of chromosome 14 with a proximal breakpoint at q1l and a distal breakpoint at q32 (11)(12)(13). A closely related rearrangement, t(14;14)(qll;q32), is seen in T-cell neoplasia (14,15) and in phytohemagglutinin-stimulated lymphocytes from patients with ataxia-telangiectasia as well as in the leukemic cells of those patients in whom this disease evolved (13 patients with T-cell acute lymphoblastic leukemia. Thus, in some of these T-cell diseases, breaks occur in either 14q11 or 14q32, or in both bands in the same patient; in B-cell disorders, however, breaks occur essentially only in 14q32, and they rarely involve 14q11 (11).…”

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confidence: 99%

Gene encoding the alpha chain of the T-cell receptor is moved immediately downstream of c-myc in a chromosomal 8;14 translocation in a cell line from a human T-cell leukemia.

Shima¹,

Beau²,

McKeithan³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

119

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The SKW-3 cell line, which was established from the malignant cells of a patient with T-cell chronic lymphocytic leukemia, is characterized by a translocation involving chromosome 8 (band q24) and chromosome 14 (band q11) [t(8;14)(q24;q11)]. To determine the position of the gene encoding the alpha chain of the T-cell receptor and of the human protooncogene myc (c-myc) in relation to the breakpoint junctions and to evaluate their possible role in the pathogenesis of T-cell neoplasia, we applied the techniques of in situ chromosomal hybridization and Southern blot analysis to SKW-3 cells. Our results indicate that the breakpoint on chromosome 14 at band q11 occurs close to a joining sequence of the gene encoding the alpha chain of the T-cell receptor. Additional rearrangements within the alpha-chain locus appear to split the variable region cluster. As a result of the rearrangements, the constant region of this gene, as well as some variable region segments, are translocated to chromosome 8, to the 3' side of the c-myc-coding exons. The identification of a breakpoint to the 3' side of c-myc suggests that this translocation is analogous to the variant (2;8) and t(8;22) translocations observed in the B-cell malignancies.

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confidence: 99%

Gene encoding the alpha chain of the T-cell receptor is moved immediately downstream of c-myc in a chromosomal 8;14 translocation in a cell line from a human T-cell leukemia.

Shima¹,

Beau²,

McKeithan³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

119

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“…In human T-cell leukemias, a number of recurring abnormalities involving chromosome 14 band qll have been reported. The most frequent are inversion (inv) of chromosome 14 (qil ;q32), the analogous translocation t(14;14)(qll;q32) (1)(2)(3)(4)(5), and t(8;14)(q24;qll) (6)(7)(8)(9). Recent work on the molecular cloning of breakpoints associated with these abnormalities has shown that the 14q11 region involved contains the T-cell receptor (TCR) a-chain gene and that breakpoints specifically occur within the joining (J) region of this locus (6,(10)(11)(12).…”

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confidence: 99%

The breakpoint of an inversion of chromosome 14 in a T-cell leukemia: sequences downstream of the immunoglobulin heavy chain locus are implicated in tumorigenesis.

Baer

Heppell

Taylor

et al. 1987

Proc. Natl. Acad. Sci. U.S.A.

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T-cell tumors are characterized by inversions or translocations of chromosome 14. The breakpoints of these karyotypic abnormalities occur in chromosome bands 14q11 and 14q32--the same bands in which the T-cell receptor (TCR) alpha-chain and immunoglobulin heavy chain genes have been mapped, respectively. Patients with ataxia-telangiectasia are particularly prone to development of T-cell chronic lymphocytic leukemia with such chromosomal abnormalities. We now describe DNA rearrangements of the TCR alpha-chain gene in an ataxia-telangiectasia-associated leukemia containing both a normal and an inverted chromosome 14. The normal chromosome 14 has undergone a productive join of TCR alpha-chain variable (V alpha) and joining (J alpha) gene segments. The other allele of the TCR alpha-chain gene features a DNA rearrangement, about 50 kilobases from the TCR alpha-chain constant (C alpha) gene, that represents the breakpoint of the chromosome 14 inversion; this breakpoint is comprised of a TCR J alpha segment (from 14q11) fused to sequences derived from 14q32 but on the centromeric side of C mu. These results imply that 14q32 sequences located at an undetermined distance downstream of the immunoglobulin C mu locus can contribute to the development of T-cell tumors.

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“…Involvement of the T-cell receptor (TCR)a/d locus with a variety of chromosome abnormalities has been reported in many types of T-cell malignancies, and breakpoints in most of these abnormalities were found within the J or D region. Although 14q11 abnormalities have been found in 10% of ATL cases (Itoyama et al 2001), and it has previously been postulated that the TCRa/d locus might be involved in ATL (Sadamori et al 1985;Isobe et al 1990), no direct evidence in support of this hypothesis has been shown until now.…”

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confidence: 80%

TCR variable gene involvement in chromosome inversion between 14q11 and 14q24 in adult T-cell leukemia

et al. 2006

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Chromosomal translocations in T-cell malignancies frequently involve the T-cell receptor (TCR)a/d locus at chromosome 14q11. Although 14q11 abnormalities are found in about 10% of adult T-cell leukemia (ATL) cases, until now there has been no direct evidence showing involvement of the TCR locus in ATL-a malignancy closely associated with HTLV-1 infection. The breakpoints of T-cell malignancies most commonly occur within the Ja or Jd region of the TCR locus. In ATL, however, despite extensive searching no breakpoint has yet been found in that region. Using fluorescence in situ hybridization with a panel of cosmid and bacterial artificial chromosome probes derived from chromosome 14, including the variable region of the TCRa locus, comprehensive analysis of an ATL patient carrying inv(14)(q11q32) revealed that the TCR locus was indeed involved in this inversion. Molecular cloning of the breakpoint revealed the juxtaposition of TCR Va to the 14q24 region as a result of two consecutive inversions: inv(14)(q11q32) and inv(14)(q11q24). We also found a gene near the breakpoint at the 14q24 region that is downregulated in this ATL patient and is assigned in the database as a pseudogene of ADAM21 (a disintegrin and metalloproteinase domain 21). Our expression analysis, however, showed that this pseudogene was actually expressed and was capable of encoding a protein similar to ADAM21; thus we have named this gene ADAM21-like (ADAM21-L).

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Abnormalities of chromosome 14 at band 14q11 in Japanese patients with adult T-cell leukemia

Cited by 66 publications

References 5 publications

Gene encoding the alpha chain of the T-cell receptor is moved immediately downstream of c-myc in a chromosomal 8;14 translocation in a cell line from a human T-cell leukemia.

Gene encoding the alpha chain of the T-cell receptor is moved immediately downstream of c-myc in a chromosomal 8;14 translocation in a cell line from a human T-cell leukemia.

The breakpoint of an inversion of chromosome 14 in a T-cell leukemia: sequences downstream of the immunoglobulin heavy chain locus are implicated in tumorigenesis.

TCR variable gene involvement in chromosome inversion between 14q11 and 14q24 in adult T-cell leukemia

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