Assignment of the ets-Related Transcription Factor E1A-F Gene (ETV4) to Human Chromosome Region 17q21

Isobe, Masaharu; Yamagishi, Fuminori; Yoshida, Kôichi; Higashino, Fumihiro; Fujinaga, Kei

doi:10.1006/geno.1995.1158

Cited by 16 publications

(6 citation statements)

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“…ElAF belongs to the ETS oncogene family as FLII, ERG, or ETVI; has an ETS domain that is 96% (82/85 amino acids) identical to that of ETVl; and is located on 17q21 (Isobe et al, 1995); moreover, our tumor had t(17;22)(q12;q12) and EWS rearrangements, making ElAF a likely candidate as the counterpart gene for fusion with EWS. One band difference between the location of ElAF on 17q21 and the breakpoint of the translocation on 17q12 may have been caused by a different interpretation of the same chromosomal region.…”

Section: Discussionmentioning

confidence: 90%

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Fusion of anETS-family gene,EIAF, toEWS by t(17;22)(q12;q12) chromosome translocation in an undifferentiated sarcoma of infancy

Kaneko

Yoshida

Handa

et al. 1996

Genes Chromosom. Cancer

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217

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Section: Discussionmentioning

confidence: 90%

“…EZAF is a newly isolated ETS-family gene that is located on 17q21 (Isobe et al, 1995) and codes for the adenovirus E1A enhancer-binding protein (Higashino et al, 1993). Amino acid sequences of E l A F suggest that the gene is a human homologue of mouse Pea?…”

Section: Introductionmentioning

confidence: 99%

Fusion of anETS-family gene,EIAF, toEWS by t(17;22)(q12;q12) chromosome translocation in an undifferentiated sarcoma of infancy

Kaneko

Yoshida

Handa

et al. 1996

Genes Chromosom. Cancer

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217

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“…E1AF was shown to be located on 17q21 (9), and chromosomal translocation of E1AF was identified in Ewing sarcoma and undifferentiated sarcoma having a chimeric gene between EWS and E1AF (10,11). Thus, E1AF is proposed to have oncogenic properties.…”

Section: Discussionmentioning

confidence: 99%

E1AF Induces Both Matrix Metalloprotease Transcription and Cell Cycle Arrest that Occurs in the Stage of Cancer Cell Invasion

et al. 2004

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and to elucidate the relationship between tumor invasive ability and cell cycle modulation caused by E1AF. Materials and Methods Reconstruction of the expression vectorThe E1AF expression vector with a metallothionein promoter was reconstructed as follows.The full-length of E1AF cDNA was cut out by EcoR1, then BamH1 linker ligation into the pSVneoHMTTer metallothionein inducible expression vector was carried out. The vector (phMT II E1AF) contains a neomycin-resistant selective gene sequence, and ligated E1AF was transcribed and translated by adding ZnCl 2 to the medium using the hMT II-metallothionein promoter. Cells and cell cultureThe human oral squamous cell carcinoma-derived cell line Ca9.22 was used for transfection of the phMT II E1AF vector. Cells were maintained in Dulbecco's modified Eagle's medium (DMEM) supplemented with 10% fetal bovine serum (Filtron Pty Ltd, Brooklin, Australia) and antibiotics.

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“…[18][19][20][21][22][23] E1A-F is targeted for translocation in the certain cases of childhood sarcomas. 24,25 • The cdc6 cell cycle regulatory protein 26,27 which has a key role in DNA replication during S phase.…”

Section: Figurementioning

confidence: 99%

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1999

Leukemia

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Chromosomal translocations are frequently linked to multiple hematological malignancies. The study of the resulting abnormal gene products has led to fundamental advances in the understanding of cancer biology. This is the first report of t(2;15)(p23;q22) and t(2;17)(p23;q21) translocations in human malignancy. Patient 1, a 73-year-old male, was diagnosed with myeloblastic (FAB M1 sub-type) AML. Cytogenetic analysis showed a 47,XY,t(2;15)(p23;q22),+13 karyotype. Fluorescent in situ hybridization (FISH) showed that the PML gene was transferred intact to the short arm of chromosome 2 while the ALK gene on chromosome 2p23 was passively transferred to the long arm of chromosome 15. Patient 2 was a 60-year-old male diagnosed with monocytic (FAB M4-type) AML. Cytogenetic analysis showed 46,XY,t(2;17)(p23;q21) karyotype. FISH analysis showed that neither RAR␣ nor ALK were disrupted by the translocation. None of the coding region of the three genes studied were translocated in these patients. This raises the possibilities that other neighboring genes could be involved or that noncoding regulatory sequences of the studied genes could be put in contact and deregulate expression of other genes. Alternatively, displacement of ALK, RAR␣ and PML to novel positions could lead to loss of their normal regulation

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Assignment of the ets-Related Transcription Factor E1A-F Gene (ETV4) to Human Chromosome Region 17q21

Cited by 16 publications

References 0 publications

Fusion of anETS-family gene,EIAF, toEWS by t(17;22)(q12;q12) chromosome translocation in an undifferentiated sarcoma of infancy

Fusion of anETS-family gene,EIAF, toEWS by t(17;22)(q12;q12) chromosome translocation in an undifferentiated sarcoma of infancy

E1AF Induces Both Matrix Metalloprotease Transcription and Cell Cycle Arrest that Occurs in the Stage of Cancer Cell Invasion

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