Differentially regulated genes as putative targets of amplifications at 20q in ovarian cancers

Takafumi Watanabe, Issei Imoto, Tomoyuki Katahira, Akira Hirasawa, Isamu Ishiwata, Mitsuru Emi, Masaomi Takayama, Akira Sato, Johji Inazawa

研究成果: Article

50 引用 (Scopus)

抄録

Frequent amplification of DNA at 20q or part of 20q has been demonstrated by comparative genomic hybridization in ovarian cancer (OC), but the genetic target(s) of these amplification events remain unknown. We examined copy-number changes with respect to six candidate genes, E2F1 (20q11.2), TGIF2 (20q11.2), AIB1 (20q12), PTPN1 (20q13.1), ZNF217 (20q13.2), and BTAK (20q13), and then measured transcription levels of each candidate in 18 OC cell lines. Three distinct cores of amplification were identified: 20q11.2, harboring E2F1 and TGIF2 (region I; 1 of 18 cell lines, 5.6%); 20q13.1, harboring PTPN1 (region II; 5 lines, 27.8%); and 20q13.2, harboring ZNF217 and BTAK (region III; 6 lines, 33.3%). Among the six genes examined, expression levels of PTPN1 and ZNF217 were significantly correlated with absolute copy-number, and those of PTPN1 and TGIF2 were significantly correlated with copy-number relative to the centromere of chromosome 20 (20cen). Among 19 primary OCs examined, moreover, we observed amplification of TGIF2, PTPN1 and ZNF217 in five (26.3%), ten (52.6%), and twelve (63.2%) tumors, respectively. Expression levels of PTPN1 and ZNF217 were significantly correlated with their copy-numbers in those primary OCs. Our results suggest that 20q amplifications in OCs can be extensive and complex, probably due to synergistic or non-synergistic amplification of separate regions of 20q, involving multiple, independently amplified targets.

元の言語English
ページ(範囲)1114-1122
ページ数9
ジャーナルJapanese Journal of Cancer Research
93
発行部数10
出版物ステータスPublished - 2002 10 1
外部発表Yes

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Ovarian Neoplasms
Chromosomes, Human, Pair 20
Cell Line
Comparative Genomic Hybridization
Centromere
Genes
Gene Expression
DNA
Neoplasms

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

これを引用

Watanabe, T., Imoto, I., Katahira, T., Hirasawa, A., Ishiwata, I., Emi, M., ... Inazawa, J. (2002). Differentially regulated genes as putative targets of amplifications at 20q in ovarian cancers. Japanese Journal of Cancer Research, 93(10), 1114-1122.

Differentially regulated genes as putative targets of amplifications at 20q in ovarian cancers. / Watanabe, Takafumi; Imoto, Issei; Katahira, Tomoyuki; Hirasawa, Akira; Ishiwata, Isamu; Emi, Mitsuru; Takayama, Masaomi; Sato, Akira; Inazawa, Johji.

:: Japanese Journal of Cancer Research, 巻 93, 番号 10, 01.10.2002, p. 1114-1122.

研究成果: Article

Watanabe, T, Imoto, I, Katahira, T, Hirasawa, A, Ishiwata, I, Emi, M, Takayama, M, Sato, A & Inazawa, J 2002, 'Differentially regulated genes as putative targets of amplifications at 20q in ovarian cancers', Japanese Journal of Cancer Research, 巻. 93, 番号 10, pp. 1114-1122.
Watanabe T, Imoto I, Katahira T, Hirasawa A, Ishiwata I, Emi M その他. Differentially regulated genes as putative targets of amplifications at 20q in ovarian cancers. Japanese Journal of Cancer Research. 2002 10 1;93(10):1114-1122.
Watanabe, Takafumi ; Imoto, Issei ; Katahira, Tomoyuki ; Hirasawa, Akira ; Ishiwata, Isamu ; Emi, Mitsuru ; Takayama, Masaomi ; Sato, Akira ; Inazawa, Johji. / Differentially regulated genes as putative targets of amplifications at 20q in ovarian cancers. :: Japanese Journal of Cancer Research. 2002 ; 巻 93, 番号 10. pp. 1114-1122.
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title = "Differentially regulated genes as putative targets of amplifications at 20q in ovarian cancers",
abstract = "Frequent amplification of DNA at 20q or part of 20q has been demonstrated by comparative genomic hybridization in ovarian cancer (OC), but the genetic target(s) of these amplification events remain unknown. We examined copy-number changes with respect to six candidate genes, E2F1 (20q11.2), TGIF2 (20q11.2), AIB1 (20q12), PTPN1 (20q13.1), ZNF217 (20q13.2), and BTAK (20q13), and then measured transcription levels of each candidate in 18 OC cell lines. Three distinct cores of amplification were identified: 20q11.2, harboring E2F1 and TGIF2 (region I; 1 of 18 cell lines, 5.6{\%}); 20q13.1, harboring PTPN1 (region II; 5 lines, 27.8{\%}); and 20q13.2, harboring ZNF217 and BTAK (region III; 6 lines, 33.3{\%}). Among the six genes examined, expression levels of PTPN1 and ZNF217 were significantly correlated with absolute copy-number, and those of PTPN1 and TGIF2 were significantly correlated with copy-number relative to the centromere of chromosome 20 (20cen). Among 19 primary OCs examined, moreover, we observed amplification of TGIF2, PTPN1 and ZNF217 in five (26.3{\%}), ten (52.6{\%}), and twelve (63.2{\%}) tumors, respectively. Expression levels of PTPN1 and ZNF217 were significantly correlated with their copy-numbers in those primary OCs. Our results suggest that 20q amplifications in OCs can be extensive and complex, probably due to synergistic or non-synergistic amplification of separate regions of 20q, involving multiple, independently amplified targets.",
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T1 - Differentially regulated genes as putative targets of amplifications at 20q in ovarian cancers

AU - Watanabe, Takafumi

AU - Imoto, Issei

AU - Katahira, Tomoyuki

AU - Hirasawa, Akira

AU - Ishiwata, Isamu

AU - Emi, Mitsuru

AU - Takayama, Masaomi

AU - Sato, Akira

AU - Inazawa, Johji

PY - 2002/10/1

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N2 - Frequent amplification of DNA at 20q or part of 20q has been demonstrated by comparative genomic hybridization in ovarian cancer (OC), but the genetic target(s) of these amplification events remain unknown. We examined copy-number changes with respect to six candidate genes, E2F1 (20q11.2), TGIF2 (20q11.2), AIB1 (20q12), PTPN1 (20q13.1), ZNF217 (20q13.2), and BTAK (20q13), and then measured transcription levels of each candidate in 18 OC cell lines. Three distinct cores of amplification were identified: 20q11.2, harboring E2F1 and TGIF2 (region I; 1 of 18 cell lines, 5.6%); 20q13.1, harboring PTPN1 (region II; 5 lines, 27.8%); and 20q13.2, harboring ZNF217 and BTAK (region III; 6 lines, 33.3%). Among the six genes examined, expression levels of PTPN1 and ZNF217 were significantly correlated with absolute copy-number, and those of PTPN1 and TGIF2 were significantly correlated with copy-number relative to the centromere of chromosome 20 (20cen). Among 19 primary OCs examined, moreover, we observed amplification of TGIF2, PTPN1 and ZNF217 in five (26.3%), ten (52.6%), and twelve (63.2%) tumors, respectively. Expression levels of PTPN1 and ZNF217 were significantly correlated with their copy-numbers in those primary OCs. Our results suggest that 20q amplifications in OCs can be extensive and complex, probably due to synergistic or non-synergistic amplification of separate regions of 20q, involving multiple, independently amplified targets.

AB - Frequent amplification of DNA at 20q or part of 20q has been demonstrated by comparative genomic hybridization in ovarian cancer (OC), but the genetic target(s) of these amplification events remain unknown. We examined copy-number changes with respect to six candidate genes, E2F1 (20q11.2), TGIF2 (20q11.2), AIB1 (20q12), PTPN1 (20q13.1), ZNF217 (20q13.2), and BTAK (20q13), and then measured transcription levels of each candidate in 18 OC cell lines. Three distinct cores of amplification were identified: 20q11.2, harboring E2F1 and TGIF2 (region I; 1 of 18 cell lines, 5.6%); 20q13.1, harboring PTPN1 (region II; 5 lines, 27.8%); and 20q13.2, harboring ZNF217 and BTAK (region III; 6 lines, 33.3%). Among the six genes examined, expression levels of PTPN1 and ZNF217 were significantly correlated with absolute copy-number, and those of PTPN1 and TGIF2 were significantly correlated with copy-number relative to the centromere of chromosome 20 (20cen). Among 19 primary OCs examined, moreover, we observed amplification of TGIF2, PTPN1 and ZNF217 in five (26.3%), ten (52.6%), and twelve (63.2%) tumors, respectively. Expression levels of PTPN1 and ZNF217 were significantly correlated with their copy-numbers in those primary OCs. Our results suggest that 20q amplifications in OCs can be extensive and complex, probably due to synergistic or non-synergistic amplification of separate regions of 20q, involving multiple, independently amplified targets.

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