Regular Article
p53 Overexpression and bcl-2 Persistence in Endometrial Carcinoma: Comparison of Papillary Serous and Endometrioid Subtypes

https://doi.org/10.1006/gyno.1996.0120Get rights and content

Abstract

Forty-two cases, including 21 uterine papillary serous carcinomas (UPSC) and 21 age-, nuclear-grade-, and clinical-stage-matched uterine endometrioid carcinomas (UEC), were studied immunohistochemically for p53 and bcl-2 in archival paraffin-embedded tissue. Compared to UEC (28.6% positive), UPSC (71.4% positive) had a significantly higher frequency of p53 overexpression (P= 0.005); furthermore, in a clinical-stage-matched fashion, a higher frequency of p53 overexpression was found in early-stage cases (P= 0.032), but not in late-stage cases. In a nuclear-grade-matched comparison, no statistical difference in p53 overexpression was identified between the two subtypes, although UPSC had stronger p53 immunoreactivity than UEC. Of UPSC, no difference in p53 overexpression was detected between tumors of early and late stages; additionally, in 5 cases, there was an abrupt transition from nonstaining morphologically benign glands to uniformly positive p53 nuclear staining in regions of intraepithelial carcinoma. Conversely, in UEC, there was a significant difference in p53 immunostaining between tumors of early and late stages (P= 0.01); no case had an abrupt transition for p53 immunostaining. For bcl-2 immunostaining, UEC had a significantly higher immunohistochemical staining score than did UPSC (P= 0.0002). In general, the staining intensity of bcl-2 diminished progressively from proliferative phase and hyperplastic endometrium to UEC and then to UPSC, with 3 of 21 (14.3%) UPSC being negative. These results suggest that p53 alteration may be an early event in the development of UPSC and may be related to its clinical aggressiveness, while it is a late event in UEC. Early detection of p53 nuclear accumulation may help to identify precursor lesions of UPSC. bcl-2 persistence is frequently associated with endometrial carcinoma, and failure to inactivate bcl-2 expression probably is related to the development of endometrial carcinoma.

References (0)

Cited by (118)

  • Proliferative and apoptotic changes in the healthy canine endometrium and in cystic endometrial hyperplasia

    2018, Theriogenology
    Citation Excerpt :

    Regeneration of the endometrium and preparation for the next proliferation phase are mainly linked to apoptotic processes, where imbalances in the expression of Bcl-2 and Bax may induce pathological conditions like endometrial hyperplasia [16]. The development of endometrial hyperplasia in women is supposed to be caused by changes in proliferation [16,17,20], and intensified through deregulation of apoptosis, mainly due to an overexpression of Bcl-2 [15,17,21–24]. Therefore human endometrial hyperplasia is considered to be a precancerous lesion with a potential for developing neoplastic processes [17,24,25].

  • Endometrial Cancer Genomics

    2017, Translational Advances in Gynecologic Cancers
  • Uterine papillary serous cancer: A review of the literature

    2012, Gynecologic Oncology
    Citation Excerpt :

    EEC is associated with inactivation of the PTEN tumor-suppressor gene, mutations in β-catenin and K-ras (Kirsten rat sarcoma viral oncogene), and defects in DNA mismatch repair resulting in microsatellite instability [41]. In contrast, UPSC displays frequent p53 (tumor protein 53) gene mutations, and human epidermal growth factor receptor 2 or HER-2-neu (human epidermal growth factor receptor 2) gene amplification [42,43]. Several studies have shown HER-2-neu overexpression in 16–62% of UPSC tumors, suggesting that HER-2-neu may be responsible for transformation and tumorigenesis in these cancers [44–46].

  • Endometrial Cancer

    2012, Obstetrics and Gynecology Clinics of North America
View all citing articles on Scopus
View full text