An ets-related gene, ERG, is rearranged in human myeloid leukemia with t(16;21) chromosomal translocation.

Shimizu, Kimiko; Ichikawa, Hitoshi; Tojo, Arinobu; Kaneko, Yasuhiko; Maseki, Nobuo; Hayashi, Yasuhide; Ohira, Miki; Asano, Shigetaka; Ohki, Masafumi

doi:10.1073/pnas.90.21.10280

Cited by 135 publications

(96 citation statements)

References 23 publications

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“…3' and 5'-ets-2 probes hybridized to adjacent 640 kb and 51000 kb NruI fragments, respectively, establishing a continuous region (within the resolution of fragment measurements) of 41.5 Mbp (Table 1, see HCX, Figure 1). Orientations of erg and ets-2 were derived from published data (CreÂ teÂ et al, 1993;Shimizu et al, 1993). Physical linkage between erg and D21S55 was not established in this study; however, cosmid contig mapping places D21S55 proximal to erg, within 200 kb (Patil et al, 1994).…”

Section: Resultsmentioning

confidence: 77%

“…At least three ets genes form fusion proteins with RNA binding proteins in Ewing's sarcoma (Zucman et al, 1993;Jeon et al, 1995). One of these genes, erg, is involved in translocations producing similar fusion proteins in human myeloid leukemia (Shimizu et al, 1993) and its expression is associated with stromal cell-independent growth in some murine erythroleukemia cell lines (Nibbs et al, 1993). Other translocations resulting in fusion proteins involving other members of the ets family have also been described (Buijs et al, 1995;Golub et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

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Altered expression of Erg and Ets-2 transcription factors is associated with genetic changes at 21q22.2-22.3 in immortal and cervical carcinoma cell lines

1997

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Human Papillomavirus (HPV) type 16 is the most frequently detected HPV in cervical cancer. Although epidemiologic and experimental evidence indicates a prominent role for HPV infection in the development of this disease, other factors are also involved. Altered expression of the ets family transcription factors erg and ets-2 was found associated with the development of cervical carcinoma. Overexpression also occurred in a HPV-16-immortalized cervical cell line, CX16-2, which has HPV integrated at a translocation breakpoint t(19;21) involving 21q22.2-22.3, where these genes have been mapped. Six of 10 cervical carcinoma cell lines overexpressed ets-2 RNA suggesting an association of overexpression with cervical cell neoplasia. A clonally related pair of cervical carcinoma cell lines, C-4I and C-4II, showed di erential expression of erg and ets-2. C-4I overexpressed ets-2 RNA compared to normal cervical cells and C-4II. C-4II expressed a 5.3 kb erg transcript not seen in C-4I, ectocervical cells or other cervical carcinoma cell lines examined. Pulsed ®eld gel electrophoresis was used to analyse changes in DNA fragments related to structural changes and to construct a physical map encompassing erg and ets-2. Alterations in erg and ets-2 RNA expression in each of three di erent cell lines examined were associated with translocations. Association between altered expression of erg and ets-2 and altered regional structural suggests that these genes are important targets in cervical carcinogenesis.

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Section: Resultsmentioning

confidence: 77%

Section: Introductionmentioning

confidence: 99%

Altered expression of Erg and Ets-2 transcription factors is associated with genetic changes at 21q22.2-22.3 in immortal and cervical carcinoma cell lines

1997

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“…Numerous oncogenic versions of some ets family members have been described such as v-ets, the founder of the family which is one of the oncogene of the E26 leukemogenic virus (Leprince et al, 1983;Nunn et al, 1983). Other examples include the erg,¯i-1, FEV, ETV1 and PEA3 genes which are translocated in human myeloid leukemia and in Ewing's sarcoma (Delattre et al, 1992;Shimizu et al, 1993;Zucman et al, 1993;Jeon et al, 1995;Urano et al, 1996;Peter et al, 1997). A series of leukemias are associated with various Tel gene translocations (Golub et al, 1994;Papadopoulos et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

Molecular phylogeny of the ETS gene family

et al. 1999

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We have constructed a molecular phylogeny of the ETS gene family. By distance and parsimony analysis of the ETS conserved domains we show that the family containing so far 29 di erent genes in vertebrates can be divided into 13 groups of genes namely ETS, ER71, GABP, PEA3, ERG, ERF, ELK, DETS4, ELF, ESE, TEL, YAN, SPI. Since the three dimensional structure of the ETS domain has revealed a similarity with the winged-helix ± turn ± helix proteins, we used two of them (CAP and HSF) to root the tree. This allowed us to show that the family can be divided into ®ve subfamilies: ETS, DETS4, ELF, TEL and SPI. The ETS subfamily comprises the ETS, ER71, GABP, PEA3, ERG, ERF and the ELK groups which appear more related to each other than to any other ETS family members. The fact that some members of these subfamilies were identi®ed in early metazoans such as diploblasts and sponges suggests that the diversi®cation of ETS family genes predates the diversi®cation of metazoans. By the combined analysis of both the ETS and the PNT domains, which are conserved in some members of the family, we showed that the GABP group, and not the ERG group, is the one most closely related to the ETS group. We also observed that the speed of accumulation of mutations in the various genes of the family is highly variable. Noticeably, paralogous members of the ELK group exhibit strikingly di erent evolutionary speed suggesting that the evolutionary pressure they support is very di erent.

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“…The FUS gene, which maps to 16p11 and encodes a nuclear RNA binding protein, is fused to the CHOP gene in the t(12;16) (q13;p11) that characterizes myxoid liposarcomas (MLS) and to the ERG gene in acute myeloid leukemia (AML) with t(16;21)(p11;q22) (Crozat et al, 1993;Ichikawa et al, 1994;Panagopoulos et al, 1994b;Rabbitts et al, 1993;Shimizu et al, 1993;A Ê man et al, 1992). In both translocations, the central and C-terminal part of FUS are replaced by either the full length CHOP protein (MLS; Crozat et al, 1993;Rabbitts et al, 1993) or the ETS-binding domain and the C-terminal part of ERG (Ichikawa et al, 1994;Panagopoulos et al, 1994b;Shimizu et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

Characteristic sequence motifs at the breakpoints of the hybrid genes FUS/CHOP, EWS/CHOP and FUS/ERG in myxoid liposarcoma and acute myeloid leukemia

et al. 1997

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We have sequenced the breakpoint regions in one acute myeloid leukemia (AML) with t(16;21)(p11;q22) resulting in the formation of a FUS/ERG hybrid gene and in four myxoid liposarcomas (MLS), three of which had the translocation t(12;16) (q13;p11) and a FUS/CHOP fusion gene and one with t(12;22;20)(q13;q12;q11) and an EWS/CHOP hybrid gene. The breakpoints were localized to intron 7 of FUS, intron 1 of CHOP, an intronic sequence of ERG and intron 7 of EWS. In two MLS cases with t(12;16) and in the AML, the breaks in intron 7 of FUS had occurred close to each other, a few nucleotides downstream from a TG dinucleotide repeat region. The break in the two MLS had occurred in the same ATGGTG hexamer and in the AML 40 nucleotides upstream from the hexamer. The third case of t(12;16) MLS had a break upstream and near a TCdinucleotide repeat region and a sequence similar to the chi bacterial recombination element was found tō ank the breakpoint. In the MLS with the EWS/ CHOP hybrid gene, the break in intron 7 of EWS had occurred close to an Alu sequence. Similarly, in all 4 MLS, the breaks in intron 1 of CHOP were near an Alu sequence. No Alu or other repetitive sequences were found 250 bp upstream or downstream from the break in the ERG intron involved in the AML case. In the AML, the MLS with ESW/CHOP and in one MLS with FUS/CHOP there were one, two and six, respectively, nucleotide identity between the contributing germline sequences in the breakpoint. In the other two MLS cases, two and three extra nucleotides of unknown origin were inserted between the FUS and CHOP sequences. At the junction and/or in its close vicinity, identical oligomers, frequently containing a trinucleotide TGG, were found in both partner genes. Our data thus show that all four genes-FUS, EWS, CHOP and ERG-contain characteristic motifs in the breakpoint regions which may serve as speci®c recognition sites for DNA-binding proteins and have functional importance in the recombination events taking place between the chromosomes. Di erent sequence motifs may, however, play a role in each individual case.

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An ets-related gene, ERG, is rearranged in human myeloid leukemia with t(16;21) chromosomal translocation.

Abstract: The t(16;21)(pll;q22) translocation is a nonrandom chromosomal abnormality found in several types of myeloid leukemia, which show variable cytomorphological features. We constructed rodent-human somatic cell hybrids containing the der (16)

Cited by 135 publications

References 23 publications

Altered expression of Erg and Ets-2 transcription factors is associated with genetic changes at 21q22.2-22.3 in immortal and cervical carcinoma cell lines

Altered expression of Erg and Ets-2 transcription factors is associated with genetic changes at 21q22.2-22.3 in immortal and cervical carcinoma cell lines

Molecular phylogeny of the ETS gene family

Characteristic sequence motifs at the breakpoints of the hybrid genes FUS/CHOP, EWS/CHOP and FUS/ERG in myxoid liposarcoma and acute myeloid leukemia

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