Automated quantitative analysis of DCC tumor suppressor protein in ovarian cancer tissue microarray shows association with β-catenin levels and outcome in patients with epithelial ovarian cancer

A. Bamias, Z. Yu, Paul Maurice Weinberger, S. Markakis, D. Kowalski, R. L. Camp, D. L. Rimm, M. A. Dimopoulos, A. Psyrri

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Background: The deleted in colorectal cancer (DCC) protein, the product of DCC tumor suppressor gene, is frequently altered in cancer. Preclinical data demonstrate that DCC regulates β-catenin levels. Here, we sought to determine the association of DCC with β-catenin protein levels, clinicopathological parameters and patient outcome in ovarian cancer using a method of in situ compartmentalized protein analysis. Methods: A tissue array composed of 150 advanced-stage ovarian cancers, treated with surgical debulking and platinum-paclitaxel (Taxol) combination chemotherapy, was constructed. For evaluation of protein expression, we used an immunofluorescence-based method of automated in situ quantitative measurement of protein analysis (AQUA). Results: One hundred and twelve patients (74%) had sufficient tissue for AQUA. The median follow-up time for the entire cohort was 33 months. Patients with low nuclear DCC expression had a 3-year progression-free survival (PFS) rate of 0% compared with 33% of those with high DCC expression (P = 0.0067). In multivariate analysis, low nuclear DCC expression level retained its prognostic significance for PFS. Between DCC and β-catenin, a significant relationship was found, where tumors with low DCC had low β-catenin and vice versa (P = 0.003). Conclusions: Low nuclear DCC levels predict for poor patient outcome inepithelial ovarian cancer. DCC may exert its antitumor function, in part, through regulation of β-catenin levels.

Original languageEnglish (US)
Pages (from-to)1797-1802
Number of pages6
JournalAnnals of Oncology
Volume17
Issue number12
DOIs
StatePublished - Dec 1 2006

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Tumor Suppressor Proteins
Catenins
Ovarian Neoplasms
Colorectal Neoplasms
Paclitaxel
Tumor Suppressor Genes
Disease-Free Survival
Ovarian epithelial cancer
Proteins
Combination Drug Therapy
Platinum
Fluorescent Antibody Technique
Neoplasms

Keywords

  • DCC
  • Ovarian cancer
  • Prognosis
  • β-catenin

ASJC Scopus subject areas

  • Hematology
  • Oncology

Cite this

Automated quantitative analysis of DCC tumor suppressor protein in ovarian cancer tissue microarray shows association with β-catenin levels and outcome in patients with epithelial ovarian cancer. / Bamias, A.; Yu, Z.; Weinberger, Paul Maurice; Markakis, S.; Kowalski, D.; Camp, R. L.; Rimm, D. L.; Dimopoulos, M. A.; Psyrri, A.

In: Annals of Oncology, Vol. 17, No. 12, 01.12.2006, p. 1797-1802.

Research output: Contribution to journalArticle

Bamias, A. ; Yu, Z. ; Weinberger, Paul Maurice ; Markakis, S. ; Kowalski, D. ; Camp, R. L. ; Rimm, D. L. ; Dimopoulos, M. A. ; Psyrri, A. / Automated quantitative analysis of DCC tumor suppressor protein in ovarian cancer tissue microarray shows association with β-catenin levels and outcome in patients with epithelial ovarian cancer. In: Annals of Oncology. 2006 ; Vol. 17, No. 12. pp. 1797-1802.
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abstract = "Background: The deleted in colorectal cancer (DCC) protein, the product of DCC tumor suppressor gene, is frequently altered in cancer. Preclinical data demonstrate that DCC regulates β-catenin levels. Here, we sought to determine the association of DCC with β-catenin protein levels, clinicopathological parameters and patient outcome in ovarian cancer using a method of in situ compartmentalized protein analysis. Methods: A tissue array composed of 150 advanced-stage ovarian cancers, treated with surgical debulking and platinum-paclitaxel (Taxol) combination chemotherapy, was constructed. For evaluation of protein expression, we used an immunofluorescence-based method of automated in situ quantitative measurement of protein analysis (AQUA). Results: One hundred and twelve patients (74{\%}) had sufficient tissue for AQUA. The median follow-up time for the entire cohort was 33 months. Patients with low nuclear DCC expression had a 3-year progression-free survival (PFS) rate of 0{\%} compared with 33{\%} of those with high DCC expression (P = 0.0067). In multivariate analysis, low nuclear DCC expression level retained its prognostic significance for PFS. Between DCC and β-catenin, a significant relationship was found, where tumors with low DCC had low β-catenin and vice versa (P = 0.003). Conclusions: Low nuclear DCC levels predict for poor patient outcome inepithelial ovarian cancer. DCC may exert its antitumor function, in part, through regulation of β-catenin levels.",
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AU - Bamias, A.

AU - Yu, Z.

AU - Weinberger, Paul Maurice

AU - Markakis, S.

AU - Kowalski, D.

AU - Camp, R. L.

AU - Rimm, D. L.

AU - Dimopoulos, M. A.

AU - Psyrri, A.

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N2 - Background: The deleted in colorectal cancer (DCC) protein, the product of DCC tumor suppressor gene, is frequently altered in cancer. Preclinical data demonstrate that DCC regulates β-catenin levels. Here, we sought to determine the association of DCC with β-catenin protein levels, clinicopathological parameters and patient outcome in ovarian cancer using a method of in situ compartmentalized protein analysis. Methods: A tissue array composed of 150 advanced-stage ovarian cancers, treated with surgical debulking and platinum-paclitaxel (Taxol) combination chemotherapy, was constructed. For evaluation of protein expression, we used an immunofluorescence-based method of automated in situ quantitative measurement of protein analysis (AQUA). Results: One hundred and twelve patients (74%) had sufficient tissue for AQUA. The median follow-up time for the entire cohort was 33 months. Patients with low nuclear DCC expression had a 3-year progression-free survival (PFS) rate of 0% compared with 33% of those with high DCC expression (P = 0.0067). In multivariate analysis, low nuclear DCC expression level retained its prognostic significance for PFS. Between DCC and β-catenin, a significant relationship was found, where tumors with low DCC had low β-catenin and vice versa (P = 0.003). Conclusions: Low nuclear DCC levels predict for poor patient outcome inepithelial ovarian cancer. DCC may exert its antitumor function, in part, through regulation of β-catenin levels.

AB - Background: The deleted in colorectal cancer (DCC) protein, the product of DCC tumor suppressor gene, is frequently altered in cancer. Preclinical data demonstrate that DCC regulates β-catenin levels. Here, we sought to determine the association of DCC with β-catenin protein levels, clinicopathological parameters and patient outcome in ovarian cancer using a method of in situ compartmentalized protein analysis. Methods: A tissue array composed of 150 advanced-stage ovarian cancers, treated with surgical debulking and platinum-paclitaxel (Taxol) combination chemotherapy, was constructed. For evaluation of protein expression, we used an immunofluorescence-based method of automated in situ quantitative measurement of protein analysis (AQUA). Results: One hundred and twelve patients (74%) had sufficient tissue for AQUA. The median follow-up time for the entire cohort was 33 months. Patients with low nuclear DCC expression had a 3-year progression-free survival (PFS) rate of 0% compared with 33% of those with high DCC expression (P = 0.0067). In multivariate analysis, low nuclear DCC expression level retained its prognostic significance for PFS. Between DCC and β-catenin, a significant relationship was found, where tumors with low DCC had low β-catenin and vice versa (P = 0.003). Conclusions: Low nuclear DCC levels predict for poor patient outcome inepithelial ovarian cancer. DCC may exert its antitumor function, in part, through regulation of β-catenin levels.

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