Evidence for a unifocal origin in familial ovarian cancer

H. H. Gallion, A. De Guarino, P. D. DePriest, J. R. Van Nagell, L. Vaccarello, J. S. Berek, M. Pieretti, P. E. Schwartz, S. Elias, Paul G McDonough, R. E. Buller

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Abstract

OBJECTIVE: The purpose of this investigation was to determine the pattern of loss of heterozygosity in multiple tumor sites from familial ovarian cancer cases. If ovarian cancer arises locally in one ovary and then metastasizes to other sites, a similar pattern should be seen in all tumor sites. However, if ovarian cancer arises multifocally throughout the peritoneal cavity, a different pattern of loss would be expected among the different sites. STUDY DESIGN: The presence or absence of loss of specific alleles for 9 loci on chromosomes 1, 6, 11, 13, 16, and 17 was determined in multiple tumor sites from 12 familial ovarian cancer cases. RESULTS: The frequency of loss of heterozygosity was as follows: chromosome 17 (100%), chromosome 13 (82%), chromosome 6 (80%), chromosome 16 (73%), chromosome 1 (57%), and chromosome 11 (22%). In every case an identical pattern was present for at least one locus. In four cases loss of the same allele was present in tumor from the ovary and all metastatic sites for all informative loci. In the remaining eight cases loss of the same allele for one to five (mean three) loci was detected. CONCLUSIONS: The pattern of loss of heterozygosity in the 12 familial ovarian cancers included in this investigation favors a unifocal origin of disease. A dual primary origin could not be absolutely excluded in 3 cases. High frequencies on chromosomes 17q and 13 suggest that loss of whole or part of these chromosomes is important in ovarian carcinogenesis.

Original languageEnglish (US)
Pages (from-to)1102-1108
Number of pages7
JournalAmerican Journal of Obstetrics and Gynecology
Volume174
Issue number4
DOIs
StatePublished - Jan 1 1996

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Ovarian Neoplasms
Loss of Heterozygosity
Chromosomes, Human, Pair 13
Chromosomes, Human, Pair 6
Chromosomes, Human, Pair 1
Alleles
Ovary
Neoplasms
Chromosomes, Human, Pair 16
Chromosomes, Human, Pair 22
Chromosomes, Human, Pair 11
Chromosomes, Human, Pair 17
Peritoneal Cavity
Carcinogenesis
Chromosomes

Keywords

  • Clonal
  • familial
  • hereditary
  • ovarian cancer
  • unifocal

ASJC Scopus subject areas

  • Obstetrics and Gynecology

Cite this

Gallion, H. H., De Guarino, A., DePriest, P. D., Van Nagell, J. R., Vaccarello, L., Berek, J. S., ... Buller, R. E. (1996). Evidence for a unifocal origin in familial ovarian cancer. American Journal of Obstetrics and Gynecology, 174(4), 1102-1108. https://doi.org/10.1016/S0002-9378(96)70651-8

Evidence for a unifocal origin in familial ovarian cancer. / Gallion, H. H.; De Guarino, A.; DePriest, P. D.; Van Nagell, J. R.; Vaccarello, L.; Berek, J. S.; Pieretti, M.; Schwartz, P. E.; Elias, S.; McDonough, Paul G; Buller, R. E.

In: American Journal of Obstetrics and Gynecology, Vol. 174, No. 4, 01.01.1996, p. 1102-1108.

Research output: Contribution to journalArticle

Gallion, HH, De Guarino, A, DePriest, PD, Van Nagell, JR, Vaccarello, L, Berek, JS, Pieretti, M, Schwartz, PE, Elias, S, McDonough, PG & Buller, RE 1996, 'Evidence for a unifocal origin in familial ovarian cancer', American Journal of Obstetrics and Gynecology, vol. 174, no. 4, pp. 1102-1108. https://doi.org/10.1016/S0002-9378(96)70651-8
Gallion HH, De Guarino A, DePriest PD, Van Nagell JR, Vaccarello L, Berek JS et al. Evidence for a unifocal origin in familial ovarian cancer. American Journal of Obstetrics and Gynecology. 1996 Jan 1;174(4):1102-1108. https://doi.org/10.1016/S0002-9378(96)70651-8
Gallion, H. H. ; De Guarino, A. ; DePriest, P. D. ; Van Nagell, J. R. ; Vaccarello, L. ; Berek, J. S. ; Pieretti, M. ; Schwartz, P. E. ; Elias, S. ; McDonough, Paul G ; Buller, R. E. / Evidence for a unifocal origin in familial ovarian cancer. In: American Journal of Obstetrics and Gynecology. 1996 ; Vol. 174, No. 4. pp. 1102-1108.
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title = "Evidence for a unifocal origin in familial ovarian cancer",
abstract = "OBJECTIVE: The purpose of this investigation was to determine the pattern of loss of heterozygosity in multiple tumor sites from familial ovarian cancer cases. If ovarian cancer arises locally in one ovary and then metastasizes to other sites, a similar pattern should be seen in all tumor sites. However, if ovarian cancer arises multifocally throughout the peritoneal cavity, a different pattern of loss would be expected among the different sites. STUDY DESIGN: The presence or absence of loss of specific alleles for 9 loci on chromosomes 1, 6, 11, 13, 16, and 17 was determined in multiple tumor sites from 12 familial ovarian cancer cases. RESULTS: The frequency of loss of heterozygosity was as follows: chromosome 17 (100{\%}), chromosome 13 (82{\%}), chromosome 6 (80{\%}), chromosome 16 (73{\%}), chromosome 1 (57{\%}), and chromosome 11 (22{\%}). In every case an identical pattern was present for at least one locus. In four cases loss of the same allele was present in tumor from the ovary and all metastatic sites for all informative loci. In the remaining eight cases loss of the same allele for one to five (mean three) loci was detected. CONCLUSIONS: The pattern of loss of heterozygosity in the 12 familial ovarian cancers included in this investigation favors a unifocal origin of disease. A dual primary origin could not be absolutely excluded in 3 cases. High frequencies on chromosomes 17q and 13 suggest that loss of whole or part of these chromosomes is important in ovarian carcinogenesis.",
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AU - De Guarino, A.

AU - DePriest, P. D.

AU - Van Nagell, J. R.

AU - Vaccarello, L.

AU - Berek, J. S.

AU - Pieretti, M.

AU - Schwartz, P. E.

AU - Elias, S.

AU - McDonough, Paul G

AU - Buller, R. E.

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N2 - OBJECTIVE: The purpose of this investigation was to determine the pattern of loss of heterozygosity in multiple tumor sites from familial ovarian cancer cases. If ovarian cancer arises locally in one ovary and then metastasizes to other sites, a similar pattern should be seen in all tumor sites. However, if ovarian cancer arises multifocally throughout the peritoneal cavity, a different pattern of loss would be expected among the different sites. STUDY DESIGN: The presence or absence of loss of specific alleles for 9 loci on chromosomes 1, 6, 11, 13, 16, and 17 was determined in multiple tumor sites from 12 familial ovarian cancer cases. RESULTS: The frequency of loss of heterozygosity was as follows: chromosome 17 (100%), chromosome 13 (82%), chromosome 6 (80%), chromosome 16 (73%), chromosome 1 (57%), and chromosome 11 (22%). In every case an identical pattern was present for at least one locus. In four cases loss of the same allele was present in tumor from the ovary and all metastatic sites for all informative loci. In the remaining eight cases loss of the same allele for one to five (mean three) loci was detected. CONCLUSIONS: The pattern of loss of heterozygosity in the 12 familial ovarian cancers included in this investigation favors a unifocal origin of disease. A dual primary origin could not be absolutely excluded in 3 cases. High frequencies on chromosomes 17q and 13 suggest that loss of whole or part of these chromosomes is important in ovarian carcinogenesis.

AB - OBJECTIVE: The purpose of this investigation was to determine the pattern of loss of heterozygosity in multiple tumor sites from familial ovarian cancer cases. If ovarian cancer arises locally in one ovary and then metastasizes to other sites, a similar pattern should be seen in all tumor sites. However, if ovarian cancer arises multifocally throughout the peritoneal cavity, a different pattern of loss would be expected among the different sites. STUDY DESIGN: The presence or absence of loss of specific alleles for 9 loci on chromosomes 1, 6, 11, 13, 16, and 17 was determined in multiple tumor sites from 12 familial ovarian cancer cases. RESULTS: The frequency of loss of heterozygosity was as follows: chromosome 17 (100%), chromosome 13 (82%), chromosome 6 (80%), chromosome 16 (73%), chromosome 1 (57%), and chromosome 11 (22%). In every case an identical pattern was present for at least one locus. In four cases loss of the same allele was present in tumor from the ovary and all metastatic sites for all informative loci. In the remaining eight cases loss of the same allele for one to five (mean three) loci was detected. CONCLUSIONS: The pattern of loss of heterozygosity in the 12 familial ovarian cancers included in this investigation favors a unifocal origin of disease. A dual primary origin could not be absolutely excluded in 3 cases. High frequencies on chromosomes 17q and 13 suggest that loss of whole or part of these chromosomes is important in ovarian carcinogenesis.

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