Ki67 antigen immunostaining (MIB 1 monoclonal antibody) in serous ovarian tumors: Index of proliferative activity with prognostic significance

Garzetti, G. G.

doi:10.1016/0020-7292(96)81059-9

Cited by 19 publications

(30 citation statements)

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“…The findings we describe for Mcm-2 are similar to those obtained in previous studies using Ki67 (Garzetti et al, 1995;Blegen et al, 2000). Indeed, it has been shown previously that tumour cell proliferation, as assessed by the Ki67 LI, was significantly higher in cases of serous ovarian cystadenocarcinoma that recurred or progressed than in those that did not (Garzetti et al, 1995). In the present study, we did not observe the very high frequency of expression of MCMs that was seen in serous inclusions in four cases of normal ovary in a previous study (Freeman et al, 1999).…”

Section: Discussionsupporting

confidence: 91%

A novel immunohistochemical method for estimating cell cycle phase distribution in ovarian serous neoplasms: implications for the histopathological assessment of paraffin-embedded specimens

et al. 2004

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We have investigated whether immunohistochemical markers can identify differences in cell cycle phase distribution in ovarian serous neoplasms, including borderline tumours of different grades. Sections of normal ovary (n ¼ 18), serous cystadenoma (n ¼ 21), borderline serous tumours (n ¼ 21) and serous cystadenocarcinoma (n ¼ 15) were analysed by immunohistochemistry using markers of cell cycle entry (Mcm-2) and cell cycle phase, including cyclin D1 (mid-to-late G1), cyclin A (S phase), cyclin B1 (G2 phase) and phosphohistone H3 (mitosis). Double-labelling confocal microscopy confirmed marker phase specificity and phase estimations were corroborated by flow cytometry. On progression from normal ovary through serous cystadenoma and borderline tumours to cystadenocarcinomas, expression of Mcm-2 (Po0.0001), cyclin D1 (P ¼ 0.002), cyclin A (Po0.0001), cyclin B1 (Po0.0001) and phosphohistone H3 (Po0.0001) increased, paralleled by an increase in the S-phase fraction (cyclin A : Mcm-2 ratio; P ¼ 0.002). Borderline tumours of increasing grade also showed increased Mcm-2 and cyclin A expression, together with an increase in the Sphase fraction. Immunohistochemistry can be used to estimate cell cycle phase distribution in ovarian serous neoplasms, giving results similar to flow cytometric analysis and enabling direct assessment of tumour heterogeneity. Immunohistochemical estimates of the Sphase fraction may identify serous borderline tumours likely to exhibit malignant progression and/or select serous cystadenocarcinomas likely to respond to adjuvant therapy.

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Section: Discussionsupporting

confidence: 91%

A novel immunohistochemical method for estimating cell cycle phase distribution in ovarian serous neoplasms: implications for the histopathological assessment of paraffin-embedded specimens

et al. 2004

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“…However, contradictory results have been reported as well (Marks et al, 1991;Kohler et al, 1993a;Levesque et al, 1995). The observed prognostic significance of Ki-67 in the present study is consonant with the data of Garzetti et al (1995). To assess further the prognostic power of p53 and p21/WAF1, we combined the p21/WAF1 expression to that of p53.…”

Section: Discussionsupporting

confidence: 81%

“…For further correlation with the clinicopathological data, the p53-immunostaining was classified as (1) positive, when over 10% nuclei stained positive and (2) negative when less than 10% of the nuclei were positive (Kohler et al, 1993a). The Ki-67 positivity was classified into two groups: (1) low proliferation group when < 20% of the tumour cells were Ki-67-positive and (2) high proliferation group when ≥ 20% of the tumour cells were positive (Garzetti et al, 1995).…”

Section: Scoring Of the P53 And Ki-67 Immunostainingmentioning

confidence: 99%

p21/WAF1 expression as related to p53, cell proliferation and prognosis in epithelial ovarian cancer

Kosma

Hongxiu

et al. 1999

Br J Cancer

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SummaryThe role and prognostic value of the tumour suppressor p21/WAF1 expression in epithelial ovarian cancer has not yet been defined. Therefore, the expression of p21/WAF1 was assessed immunohistochemically (IHC) in 316 epithelial ovarian malignancies in relation to p53, cell proliferation and patient survival. p21/WAF1 expression was inversely correlated with p53 and cell proliferation. Low p21/WAF1 expression was significantly associated with high grade of the tumour (P = 0.0005), advanced FIGO stage (P = 0.001) and primary residual tumour (P = 0.0001). Low p21/WAF1 expression was a marker of poor overall survival (P = 0.012). Similarly, p53-positivity and high cell proliferative activity were significant predictors of poor survival in univariate analyses. Moreover, the patients with p21-/p53+ tumours had a poorer overall (P < 0.00005) and recurrence-free (P = 0.0005) survival in univariate analyses, and the p21/p53 expression independently predicted tumour recurrence in Cox's multivariate analysis. Our results suggest that p21/WAF1 expression is mostly p53-dependent in epithelial ovarian cancer. High p21/WAF1 expression seems to function as a negative cell cycle regulator and as a marker of favourable disease outcome in epithelial ovarian cancer. In addition, the patients with their tumour expressing no or low p21/WAF1 protein but positive for p53 had a notably higher risk of recurrent disease, implicating that these patients might be more prone to treatment failures.

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“…It must be acknowledged, however, that the absence of morphologically established intermediate steps may be due to a higher rate of cellular proliferation resulting in rapid evolution to conventional serous carcinoma, obscuring discrete mor- phological intermediate stages. This is supported by a substantially higher Ki-67 nuclear labeling (proliferative) index in early conventional serous carcinoma as compared with SBT, noninvasive and invasive MPSC, 20 (and our unpublished data). Thus, the rapid progression of conventional serous carcinoma suggests that a profound loss of cell cycle regulation occurs very early in its development.…”

Section: Discussionsupporting

confidence: 54%

Diverse Tumorigenic Pathways in Ovarian Serous Carcinoma

Singer

Kurman

Chang

et al. 2002

The American Journal of Pathology

312

245

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This study was undertaken to analyze genetic alterations in 108 sporadic serous ovarian neoplasms to elucidate ovarian serous carcinogenesis. Our results demonstrate that K-ras mutations occur in approximately 50% of serous borderline tumors (SBTs), non-invasive micropapillary serous carcinomas (MPSCs), and invasive micropapillary serous carcinomas, which represent a morphological continuum of tumor progression. Moreover, progressive increase in the degree of allelic imbalance of chromosomes 1p, 5q, 8p, 18q, 22q, and Xp was observed comparing serous borderline tumors to noninvasive and invasive micropapillary serous carcinomas. In contrast, high-grade (conventional serous carcinoma) tumors contained wild-type K-ras in all 23 cases studied and a high frequency of allelic imbalance even in small (early) primary tumors similar to that found in advanced stage tumors. Based on these findings, we propose a dualistic model for ovarian serous carcinogenesis. One pathway involves a stepwise progression from SBT to noninvasive and then invasive MPSC. The other pathway is characterized by rapid progression from the ovarian surface epithelium or inclusion cysts to a conventional (high-grade) serous carcinoma.

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Ki67 antigen immunostaining (MIB 1 monoclonal antibody) in serous ovarian tumors: Index of proliferative activity with prognostic significance

Cited by 19 publications

References 0 publications

A novel immunohistochemical method for estimating cell cycle phase distribution in ovarian serous neoplasms: implications for the histopathological assessment of paraffin-embedded specimens

A novel immunohistochemical method for estimating cell cycle phase distribution in ovarian serous neoplasms: implications for the histopathological assessment of paraffin-embedded specimens

p21/WAF1 expression as related to p53, cell proliferation and prognosis in epithelial ovarian cancer

Diverse Tumorigenic Pathways in Ovarian Serous Carcinoma

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