Prognostic factors in surgical stage I endometrial carcinoma

Lundgren, Caroline; Auer, Gert; Frankendal, B.; Nilsson, Bo; Nordström, Britta

doi:10.1080/02841860310018990

Cited by 26 publications

(30 citation statements)

References 23 publications

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“…Along with the fact of more significant spots between samples of the same histopathology but different ploidy status, we suggest that aneuploidy could be of greater impact regarding poor prognosis than the histological subtype. Interpretations from other data also highlight the importance of aneuploidy for the prognosis [21].…”

Section: Discussionmentioning

confidence: 99%

Protein profiling of genomic instability in endometrial cancer

Gemoll

Habermann

Lahmann

et al. 2011

Cell. Mol. Life Sci.

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DNA aneuploidy has been identified as a prognostic factor in the majority of epithelial malignancies. We aimed at identifying ploidy-associated protein expression in endometrial cancer of different prognostic subgroups. Comparison of gel electrophoresis-based protein expression patterns between normal endometrium (n = 5), diploid (n = 7), and aneuploid (n = 7) endometrial carcinoma detected 121 ploidy-associated protein forms, 42 differentially expressed between normal endometrium and diploid endometrioid carcinomas, 37 between diploid and aneuploid endometrioid carcinomas, and 41 between diploid endometrioid and aneuploid uterine papillary serous cancer. Proteins were identified by mass spectrometry and evaluated by Ingenuity Pathway Analysis. Targets were confirmed by liquid chromatography/mass spectrometry. Mass spectrometry identified 41 distinct polypeptides and pathway analysis resulted in high-ranked networks with vimentin and Nf-κB as central nodes. These results identify ploidy-associated protein expression differences that overrule histopathology-associated expression differences and emphasize particular protein networks in genomic stability of endometrial cancer.

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Section: Discussionmentioning

confidence: 99%

Protein profiling of genomic instability in endometrial cancer

Gemoll

Habermann

Lahmann

et al. 2011

Cell. Mol. Life Sci.

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“…12,13 However, investigators have verified the existence of p53-positive tumors with an endometrioid pattern, and in one study, p53 emerged as an important prognostic marker in this subset. 14,15 In view of the prognostic significance of p53 immunostaining with outcome, this marker has been proposed by some as a useful adjunct in the classification of selected endometrial adenocarcinomas. Based on this study, a proportion of endometrial carcinomas can be expected to pose a problem in classification for a practicing pathologist, or be classified discordantly by two or more pathologists.…”

Section: Discussionmentioning

confidence: 99%

Histologic and immunohistochemical decision-making in endometrial adenocarcinoma

et al. 2008

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Diffuse p53 immunostaining distinguishes 85% of serous (Type II) from endometrioid (Type I) carcinomas and is an independent marker for poor prognosis. Interobserver reproducibility for the diagnosis of these entities, as well as selection and prediction of p53 immunostaining results, is unknown. Reproducibility of three pathologists regarding: (1) a two (I and II) and (2) three part classification (I, II or indeterminate); (3) recommendation for p53 staining and (4) expectations of p53 staining results were computed with the kappa (k) statistic. All cases were immunostained for p53 and independently scored. A two and three tiered classification scheme achieved high (k ¼ 0.71) and moderate (k ¼ 0.49) reproducibility. Non-unanimous cases were more likely to be reclassified into an 'indeterminate' category (27 cases, 39% of passes) compared to those with unanimous (82 cases, 14% of passes) classification. Pathologists recommended p53 immunostaining with poor (k ¼ 0.28) reproducibility, but staining prediction was made with good concordance (69%, k ¼ 0.50). Moreover, p53 staining was more common in diagnostically discordant (46%) compared to concordant (16%) cases. A subset of endometrial cancers do not readily fit within a two-class system and can be culled from cases that (1) do not achieve interobserver concordance and (2) are more likely to be chosen for p53 immunostaining and (3) are more likely to stain positive for p53. Because p53 is an important marker for endometrial adenocarcinoma outcome, and cannot be predicted in advance in indeterminate cases, p53 immunostaining should be employed in cases with observer disagreement in a binary system. Keywords: p53; endometrial neoplasms; serous carcinoma; reproducibility Endometrial adenocarcinoma is a biologically diverse disease that has been divided into two subgroups based on histomorphology, biologic behavior, and underlying genetic aberrations. Type I tumors exhibit endometrioid morphology, arise in the setting of increased estrogen exposure with subsequent development of precancerous lesions (endometrial intraepithelial hyperplasia-EIN/atypical hyperplasia), are associated with frequent PTEN inactivation mutations, and have a favorable outcome. 1,2 By contrast, Type II tumors demonstrate papillary serous or clear cell morphology, are not associated with any known precursor lesions, demonstrate frequent p53 mutations, and are associated with a poor outcome. 3,4 The differences between these groups are summarized in Table 1. The observation that uterine papillary serous carcinomas have a greater tendency to metastasis and/ or recurrence in the peritoneum underscores the importance of accurate diagnosis. 5 Although the distinction between serous and endometrioid subgroups of endometrial cancer has a strong theoretical basis, subsets of endometrial adenocarcinoma have been recognized that do not fall cleanly into either of the two categories. Tumors with glandular architecture that more closely approximate endometrioid adenocarcinoma may occasionally demonstrate...

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“…Ploidy has been evaluated as prognostic factor in a number of studies and shown to be an independent prognostic factor in some of these [2,4 Á8]. Still only a limited number of aneuploid tumours relapse [2,5] which does not make it an optimal prognostic factor. Other attempts to evaluate genetic instability or its consequences have been made in order to find possible future prognostic factors.…”

Section: Discussionmentioning

confidence: 99%

2-DE protein expression in endometrial carcinoma

et al. 2006

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The objective of this study was to explore the protein expression pattern in normal endometrial mucosa (n = 5) and endometrial carcinoma (n = 15) of low (diploid) and high (aneuploid) malignancy potential by two-dimensional gel electrophoresis (2-DE). The specimens were evaluated for histopathologic subtype, stage and grade in relation to DNA ploidy. A match-set consisting of five samples from normal endometrium, eight diploid and seven aneuploid tumours was created. All the diploid and three of the aneuploid tumours were of endometrioid subtype, while the remaining four were of uterine seropapillary type. There were 192 protein spots differentiating diploid tumours from normal endometrium and 238 protein spots were separating aneuploid tumours from normal endometrium (p < 0.01). A cluster analysis based on 52 significantly deviating protein spots within the groups showed clustering and separation of the normal endometrium, diploid and aneuploid tumours. In conclusion this study showed significant differences in protein expression between normal endometrium and endometrial carcinoma as well as between endometrial carcinoma of low and high malignancy potential. In future studies these results may provide useful in finding new sensitive prognostic markers for endometrial cancer.

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Prognostic factors in surgical stage I endometrial carcinoma

Cited by 26 publications

References 23 publications

Protein profiling of genomic instability in endometrial cancer

Protein profiling of genomic instability in endometrial cancer

Histologic and immunohistochemical decision-making in endometrial adenocarcinoma

2-DE protein expression in endometrial carcinoma

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