DNA copy number changes in schistosoma-associated and non-schistosoma-associated bladder cancer

Wael El-Rifai, Dia Kamel, Marcelo L. Larramendy, Soheir Shoman, Yehia Gad, Suhail Baithun, Mostafa El-Awady, Saad Eissa, Hussein Khaled, Sonia Soloneski, Michael Sheaff, Sakari Knuutila

Research output: Contribution to journalArticle

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Abstract

DNA copy number changes were investigated in 69 samples of schistosoma-associated (SA) and non-schistosoma-associated (NSA) squamous cell carcinoma (SCC) and transitional cell carcinoma (TCC) of the bladder by comparative genomic hybridization (CGH). DNA copy number changes were detected in 47 tumors. SA tumors had more changes than NSA tumors (mean, 7 vs. 4), whereas the number of changes in SCC and TCC tumors was similar. SA tumors displayed more gains than losses (1.7:1), whereas NSA tumors showed an equal number of gains and losses. Changes that were observed at similar frequencies in SCC and TCC, irrespective of the schistosomal status, included gains and high-level amplifications at 1q, 8q, and 20q and losses in 9p and 13q. These changes may be involved in a commom pathway for bladder tumor development and progression independent of schistosomal status or histological subtype. Losses in 3p and gains at 5p were seen only in SCC (P < 0.01) and losses in 5q were more frequent in SA-SCC than in other tumors (P < 0.05). However, changes that were more frequent in TCC than those in SCC included gains at 17q (P < 0.01) and losses in 4q (P < 0.05) and 6q (P < 0.01). Gains and high-level amplifications at 5p were seen only in SA-SCC (P < 0.01), whereas gains and high-level amplifications with minimal common overlapping regions at 11q13 were more frequently seen both in SA-SCC and SA-TCC tumors (P < 0.01). In addition to the above mentioned alterations, several other changes were also seen at lower frequencies. The variations in the DNA copy number changes observed in TCC, SCC, SA, and NSA bladder carcinomas suggest that these tumors have different genetic pathways.

Original languageEnglish (US)
Pages (from-to)871-878
Number of pages8
JournalAmerican Journal of Pathology
Volume156
Issue number3
DOIs
StatePublished - Jan 1 2000
Externally publishedYes

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DNA Copy Number Variations
Schistosoma
Urinary Bladder Neoplasms
Squamous Cell Carcinoma
Transitional Cell Carcinoma
Neoplasms
Urinary Bladder
Comparative Genomic Hybridization

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

DNA copy number changes in schistosoma-associated and non-schistosoma-associated bladder cancer. / El-Rifai, Wael; Kamel, Dia; Larramendy, Marcelo L.; Shoman, Soheir; Gad, Yehia; Baithun, Suhail; El-Awady, Mostafa; Eissa, Saad; Khaled, Hussein; Soloneski, Sonia; Sheaff, Michael; Knuutila, Sakari.

In: American Journal of Pathology, Vol. 156, No. 3, 01.01.2000, p. 871-878.

Research output: Contribution to journalArticle

El-Rifai, W, Kamel, D, Larramendy, ML, Shoman, S, Gad, Y, Baithun, S, El-Awady, M, Eissa, S, Khaled, H, Soloneski, S, Sheaff, M & Knuutila, S 2000, 'DNA copy number changes in schistosoma-associated and non-schistosoma-associated bladder cancer', American Journal of Pathology, vol. 156, no. 3, pp. 871-878. https://doi.org/10.1016/S0002-9440(10)64956-5
El-Rifai, Wael ; Kamel, Dia ; Larramendy, Marcelo L. ; Shoman, Soheir ; Gad, Yehia ; Baithun, Suhail ; El-Awady, Mostafa ; Eissa, Saad ; Khaled, Hussein ; Soloneski, Sonia ; Sheaff, Michael ; Knuutila, Sakari. / DNA copy number changes in schistosoma-associated and non-schistosoma-associated bladder cancer. In: American Journal of Pathology. 2000 ; Vol. 156, No. 3. pp. 871-878.
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abstract = "DNA copy number changes were investigated in 69 samples of schistosoma-associated (SA) and non-schistosoma-associated (NSA) squamous cell carcinoma (SCC) and transitional cell carcinoma (TCC) of the bladder by comparative genomic hybridization (CGH). DNA copy number changes were detected in 47 tumors. SA tumors had more changes than NSA tumors (mean, 7 vs. 4), whereas the number of changes in SCC and TCC tumors was similar. SA tumors displayed more gains than losses (1.7:1), whereas NSA tumors showed an equal number of gains and losses. Changes that were observed at similar frequencies in SCC and TCC, irrespective of the schistosomal status, included gains and high-level amplifications at 1q, 8q, and 20q and losses in 9p and 13q. These changes may be involved in a commom pathway for bladder tumor development and progression independent of schistosomal status or histological subtype. Losses in 3p and gains at 5p were seen only in SCC (P < 0.01) and losses in 5q were more frequent in SA-SCC than in other tumors (P < 0.05). However, changes that were more frequent in TCC than those in SCC included gains at 17q (P < 0.01) and losses in 4q (P < 0.05) and 6q (P < 0.01). Gains and high-level amplifications at 5p were seen only in SA-SCC (P < 0.01), whereas gains and high-level amplifications with minimal common overlapping regions at 11q13 were more frequently seen both in SA-SCC and SA-TCC tumors (P < 0.01). In addition to the above mentioned alterations, several other changes were also seen at lower frequencies. The variations in the DNA copy number changes observed in TCC, SCC, SA, and NSA bladder carcinomas suggest that these tumors have different genetic pathways.",
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AU - El-Rifai, Wael

AU - Kamel, Dia

AU - Larramendy, Marcelo L.

AU - Shoman, Soheir

AU - Gad, Yehia

AU - Baithun, Suhail

AU - El-Awady, Mostafa

AU - Eissa, Saad

AU - Khaled, Hussein

AU - Soloneski, Sonia

AU - Sheaff, Michael

AU - Knuutila, Sakari

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N2 - DNA copy number changes were investigated in 69 samples of schistosoma-associated (SA) and non-schistosoma-associated (NSA) squamous cell carcinoma (SCC) and transitional cell carcinoma (TCC) of the bladder by comparative genomic hybridization (CGH). DNA copy number changes were detected in 47 tumors. SA tumors had more changes than NSA tumors (mean, 7 vs. 4), whereas the number of changes in SCC and TCC tumors was similar. SA tumors displayed more gains than losses (1.7:1), whereas NSA tumors showed an equal number of gains and losses. Changes that were observed at similar frequencies in SCC and TCC, irrespective of the schistosomal status, included gains and high-level amplifications at 1q, 8q, and 20q and losses in 9p and 13q. These changes may be involved in a commom pathway for bladder tumor development and progression independent of schistosomal status or histological subtype. Losses in 3p and gains at 5p were seen only in SCC (P < 0.01) and losses in 5q were more frequent in SA-SCC than in other tumors (P < 0.05). However, changes that were more frequent in TCC than those in SCC included gains at 17q (P < 0.01) and losses in 4q (P < 0.05) and 6q (P < 0.01). Gains and high-level amplifications at 5p were seen only in SA-SCC (P < 0.01), whereas gains and high-level amplifications with minimal common overlapping regions at 11q13 were more frequently seen both in SA-SCC and SA-TCC tumors (P < 0.01). In addition to the above mentioned alterations, several other changes were also seen at lower frequencies. The variations in the DNA copy number changes observed in TCC, SCC, SA, and NSA bladder carcinomas suggest that these tumors have different genetic pathways.

AB - DNA copy number changes were investigated in 69 samples of schistosoma-associated (SA) and non-schistosoma-associated (NSA) squamous cell carcinoma (SCC) and transitional cell carcinoma (TCC) of the bladder by comparative genomic hybridization (CGH). DNA copy number changes were detected in 47 tumors. SA tumors had more changes than NSA tumors (mean, 7 vs. 4), whereas the number of changes in SCC and TCC tumors was similar. SA tumors displayed more gains than losses (1.7:1), whereas NSA tumors showed an equal number of gains and losses. Changes that were observed at similar frequencies in SCC and TCC, irrespective of the schistosomal status, included gains and high-level amplifications at 1q, 8q, and 20q and losses in 9p and 13q. These changes may be involved in a commom pathway for bladder tumor development and progression independent of schistosomal status or histological subtype. Losses in 3p and gains at 5p were seen only in SCC (P < 0.01) and losses in 5q were more frequent in SA-SCC than in other tumors (P < 0.05). However, changes that were more frequent in TCC than those in SCC included gains at 17q (P < 0.01) and losses in 4q (P < 0.05) and 6q (P < 0.01). Gains and high-level amplifications at 5p were seen only in SA-SCC (P < 0.01), whereas gains and high-level amplifications with minimal common overlapping regions at 11q13 were more frequently seen both in SA-SCC and SA-TCC tumors (P < 0.01). In addition to the above mentioned alterations, several other changes were also seen at lower frequencies. The variations in the DNA copy number changes observed in TCC, SCC, SA, and NSA bladder carcinomas suggest that these tumors have different genetic pathways.

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