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by gemini-2.5-flash-lite, 2026-06-07
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This study examined immunohistochemical markers ER, PR, p53, and Ki-67 in endometriosis-associated ovarian carcinoma, finding altered steroid receptor expression and p53 contribution to pathogenesis and progression, with low Ki-67 in EOCs.
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by claude@2026-06, 2026-06-07
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This study evaluated expression of immunohistochemical markers ER, PR, p53, and Ki-67 in 19 endometriosis-associated ovarian carcinoma (EOC) cases, using routine staining and statistical analysis alongside clinicopathologic variables including tumor size, histologic type (endometrioid, clear cell, high-grade serous, mixed), ovarian capsule invasion, and TNM/FIGO stage. The authors reported that altered steroid receptor expression (ER/PR) in ovarian endometriotic tissue and EOC is linked to malignant transformation and progression, and that p53 contributes to endometriosis pathogenesis and EOC progression. They also found EOCs associated with a low Ki-67 index compared with more aggressive tumor types, but the abstract does not specify an explicit limitation such as sample size/power or a comparative control group beyond the assessed markers. This paper is centrally about endometriosis-associated ovarian carcinoma, using immunohistochemical marker patterns to support a shared pathway between endometriosis and cancer progression.
Abstract
Objective: Endometriosis association with cancers is strongly supported by epidemiological criteria and shared protective factors, being identified as endometriosis-associated ovarian carcinoma (EOC). In this context, our study objective has been the evaluation of selected immunohistochemical markers expression (ER, PR, p53, and Ki-67) in both endometriosis and EOC as an attempt to identify common pattern of expression, in support of similar molecular pathway involved in their pathogenesis. Material and Methods: Our study comprised 19 cases of EOCs. The routine and immunohistochemical staining have been performed, followed by results statistical processing. Results: The following data have been assessed in EOCs: tumor size, histological type, ovarian capsule invasion, TNM and FIGO staging. The histological types have been: endometrioid (8 cases) and non-endometrioid (11 cases of clear cell, high-grade serous, and mixed types). FIGO stages have been: stage I (4 cases), stage II (6 cases), stage III (8 cases), and stage IV (1 case). Histological grades have been: G1 (1 case), G2 (6 cases), and G3 (12 cases). Conclusions: The comparison between immunohistochemical staining and different clinicopathological variables supported that the altered expression of steroid receptors in ovarian endometriotic tissue and EOC are involved in malignant transformation and progression. p53 is contributing to endometriosis pathogenesis and EOC progression. EOCs are associated with low Ki-67 index compared to more aggressive types of tumors. In conclusion, the immunohistochemical expression of ER, PR, and p53 corroborated with clinicopathological features support the mechanism of endometriosis transition to EOC, provide tools for prognosis evaluation, and open new perspectives of therapy
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Research and Clinical Medicine (Dec 2018)
IMMUNOHISTOCHEMICAL PROFILE OF ENDOMETRIOSIS-ASSOCIATED OVARIAN CARCINOMA
Abstract
Objective: Endometriosis association with cancers is strongly supported by epidemiological criteria and shared protective factors, being identified as endometriosis-associated ovarian carcinoma (EOC). In this context, our study objective has been the evaluation of selected immunohistochemical markers expression (ER, PR, p53, and Ki-67) in both endometriosis and EOC as an attempt to identify common pattern of expression, in support of similar molecular pathway involved in their pathogenesis. Material and Methods: Our study comprised 19 cases of EOCs. The routine and immunohistochemical staining have been performed, followed by results statistical processing. Results: The following data have been assessed in EOCs: tumor size, histological type, ovarian capsule invasion, TNM and FIGO staging. The histological types have been: endometrioid (8 cases) and non-endometrioid (11 cases of clear cell, high-grade serous, and mixed types). FIGO stages have been: stage I (4 cases), stage II (6 cases), stage III (8 cases), and stage IV (1 case). Histological grades have been: G1 (1 case), G2 (6 cases), and G3 (12 cases). Conclusions: The comparison between immunohistochemical staining and different clinicopathological variables supported that the altered expression of steroid receptors in ovarian endometriotic tissue and EOC are involved in malignant transformation and progression. p53 is contributing to endometriosis pathogenesis and EOC progression. EOCs are associated with low Ki-67 index compared to more aggressive types of tumors. In conclusion, the immunohistochemical expression of ER, PR, and p53 corroborated with clinicopathological features support the mechanism of endometriosis transition to EOC, provide tools for prognosis evaluation, and open new perspectives of therapy
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