Identification of the TCL1 gene involved in T-cell malignancies.

Virgilio, Laura; Narducci, Maria Grazia; Isobe, Masaharu; Billips, Linda G.; Cooper, Max D.; Croce, Carlo M.; Russo, Giandomenico

doi:10.1073/pnas.91.26.12530

Cited by 253 publications

(285 citation statements)

References 31 publications

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“…Here, a reciprocal translocation of TCL1 locus at 14q32 causes the juxtaposition to T-cell-receptor enhancers, leading to TCL1 ectopic overexpression (Russo et al, 1988;Virgilio et al, 1994). Thus, TCL1 contributes to T-PLL by increasing cell proliferation and/or cell survival.…”

Section: Introductionmentioning

confidence: 99%

The Tcl1 oncogene defines secondary hair germ cells differentiation at catagen–telogen transition and affects stem-cell marker CD34 expression

et al. 2009

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Overexpression of the TCL1 gene family plays a role in the onset of T-cell leukemias in mice and in humans. The Tcl1 gene is tightly regulated during early embryogenesis in which it participates in embryonic stem (ES)-cells proliferation and during lymphoid differentiation. Here, we provide evidences that Tcl1 is also important in mouse hair follicle (HF) and skin homeostasis. We found that Tcl1 À/À adult mice exhibit hair loss, leading to alopecia with extensive skin lesions. By analysing Tcl1 expression in the wild-type (wt) skin through different stages of hair differentiation, we observe high levels in the secondary hair germ (HG) cells and hair bulges, during early anagen and catagen-telogen transition phases. The loss of Tcl1 does not result in apparent skin morphological defects during embryonic development and at birth, but its absence causes a reduction of proliferation in anagen HFs. Importantly, we show the that absence of Tcl1 induces a significant loss of the stem-cell marker CD34 (but not a6-integrin) expression in the bulge cells, which is necessary to maintain stem-cell characteristics. Therefore, our findings indicate that Tcl1 gene(s) might have important roles in hair formation, by its involvement in cycling and self-renewal of transient amplifying (TA) and stem-cell (SC) populations.

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Section: Introductionmentioning

confidence: 99%

The Tcl1 oncogene defines secondary hair germ cells differentiation at catagen–telogen transition and affects stem-cell marker CD34 expression

et al. 2009

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“…We postulated that if the oncogene activated by these di erent rearrangements is the same, it must reside between the two clusters of breakpoints. Within this region, we have previously identi®ed two genes named TCL1 and TML1 that are activated and deregulated by chromosomal translocations and inversions (Sugimoto et al, 1999;Virgilio et al, 1994). The sequences of the TCL1 and TML1 genes are highly homologous to that of the MTCP1 (TypeB1) gene, which is also activated by juxtaposing with the TCRA/D region at 14q11 (Stern, 1996).…”

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confidence: 99%

Identification of the TCL6 genes within the breakpoint cluster region on chromosome 14q32 in T-cell leukemia

et al. 2000

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A region on chromosome 14q32.1 is often involved in chromosomal translocations and inversions with one of the T-cell receptor loci in T-cell lymphoproliferative diseases. The breakpoints of the di erent rearrangements segregate into two clusters; a cluster due to inversion on the centromeric side and a cluster due to simple balanced translocations on the telomeric side. If the target gene activated by these di erent types of chromosomal rearrangements is the same, the gene must be localized between the two clusters of breakpoints in a region of around 160 kb. Within this breakpoint cluster region, we isolated two genes; namely, TCL1 and TML1/TCL1b genes. In the course of characterizing the TML1 gene, we further identi®ed a third novel gene, which we named TCL6 (T-cell leukemia/lymphoma 6), from a region 7 kb upstream of the TML1 locus. The TCL6 gene expressed at least 11 isoforms through very complex alternativesplicing, including splicing with the TML1 gene. Those isoforms encode at least ®ve open reading frames (ORFs) with no homology to known sequences. The localization of the proteins corresponding to these ORF was determined by fusing green¯uorescence protein at the carboxyl terminal of each ORF. ORF141 and ORF72 were observed in the cytoplasmic region, while ORF105, ORF119, and ORF163 were predominantly localized in the nuclear region. Since the TCL6 gene was expressed in T-cell leukemia carrying a t(14;14) (q11;q32.1) chromosome translocation and was not expressed in normal T-cells (just like the TML1 and TCL1 genes), it is also a candidate gene potentially involved in leukemogenesis.

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“…Some structural rearrangements involving chromosome 14, namely inv(14)(q11q32), t(14;14)(q11;q32) and t(X;14)(q28;q11), result in illegitimate fusions of chromosomal regions now well identified such as TCR␣/␦, TCL1, and MTCP1/c6.1b. [16][17][18][19][20] In other rearrangements, loss of heterozygosity suggests mechanisms more closely related to tumor suppressor genes. In this respect, loss of the short arm of chromosome 8 resulting from isochromosome 8q, and partial deletion of 11q involving the ATM gene 21,22 are nonrandom events in T-PLL.…”

Section: Discussionmentioning

confidence: 99%

Abnormalities of the short arm of chromosome 12 in T cell prolymphocytic leukemia

et al. 1998

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Abnormalities of the short arm of chromosome 12 are nonrandom events in T cell prolymphocytic leukemia (T-PLL). Fluorescence in situ hybridization (FISH) studies were performed in three patients with T-PLL and one patient with T cell peripheral lymphoma and rearrangement of 12p. Whereas the rearrangements of 12p were different in the four patients, a breakpoint centromeric to the ETV6 gene was present in the three T-PLL patients. In addition, loss of heterozygosity for a chromosomal segment telomeric to ETV6 with loss of the RAD52 locus was also shown by FISH studies. In contrast, the breakpoint was telomeric to ETV6 in the patient with peripheral lymphoma.

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Identification of the TCL1 gene involved in T-cell malignancies.

Cited by 253 publications

References 31 publications

The Tcl1 oncogene defines secondary hair germ cells differentiation at catagen–telogen transition and affects stem-cell marker CD34 expression

The Tcl1 oncogene defines secondary hair germ cells differentiation at catagen–telogen transition and affects stem-cell marker CD34 expression

Identification of the TCL6 genes within the breakpoint cluster region on chromosome 14q32 in T-cell leukemia

Abnormalities of the short arm of chromosome 12 in T cell prolymphocytic leukemia

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