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Immunohistochemical analysis of c-erbB-2, Bcl-2, p53, p21, p63 and Ki-67 expression in hydatidiform moles. | LitMetric

Immunohistochemical analysis of c-erbB-2, Bcl-2, p53, p21, p63 and Ki-67 expression in hydatidiform moles.

Pathol Res Pract

Pathology Department, Farhet Hached Hospital, 4000 Sousse, Tunisia; Medicine Faculty of Sousse, University of Sousse, 4000 Sousse, Tunisia.

Published: March 2019

Hydatidiform moles (HM) are characterized by an abnormal proliferating trophoblast with a potential for a malignant transformation. Similar to other human tumors, trophoblastic pathogenesis is likely a multistep process involving several molecular and genetic alterations. The study was performed to investigate the expression patterns of c-erbB-2 and Bcl-2 oncoproteins, p53, p21 and p63 tumor suppressor proteins and Ki-67 cell proliferation marker in HM. We conducted a retrospective study of 220 gestational products, including 39 hydropic abortions (HA), 41 partial HM (PHM) and 140 complete HM (CHM). The expression of c-erbB-2, Bcl-2, p53, p21, p63 and Ki-67 was investigated by immunohistochemistry on archival tissues. c-erbB-2 expression was observed in three PHM and 10 CHM. Bcl-2 immunostaining was significantly higher in PHM (61%) and CHM (70.7%) compared with HA (7.7%, p =  0.001 and p <  0.0001, respectively). p53 expression was stronger in CHM (73.6%) compared with PHM (24.4%, p < 0.0001) and HA (12.8%, p < 0.0001). p21 staining was observed as well in molar and non-molar gestations (p >  0.05). p63 immunoexpression was significantly described in CHM (85.7%) and PHM (78%) compared with HA (10.2%, p < 0.0001 and p = 0.0001, respectively). Ki-67 was significantly expressed in CHM (72.1%) compared with HA (46.2%, p = 0.005). Altered expression of Bcl-2, p53, p63 and Ki-67 reflects the HM pathological development. Immunohistochemical analysis is beneficial to recognize the HM molecular and pathogenic mechanisms. Furthermore, it could serve as a useful adjunct to conventional methods for refining HM diagnosis.

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http://dx.doi.org/10.1016/j.prp.2018.12.015DOI Listing

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