Human epidermal growth factor receptor 2 fluorescence in situ hybridization and P57KIP2 immunohistochemistry using tissue microarray: Improving histopathological subtyping of hydatidiform mole

López, Consuelo Lozoya; Gouvêa, Ana Luisa Figueira; Rodrigues, Fabiana Resende; Braga, Antônio; Machado, Mirna Daumas Valente; Lopes, Vânia Silami

doi:10.1016/j.placenta.2020.07.027

Cited by 3 publications

(3 citation statements)

References 26 publications

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“…Although HM is a benign trophoblastic disease, it has a high probability of malignant transformation, especially CHMs, which have a 15% probability of malignant transformation, posing a great threat to the life of patients [18]. Currently, the clinical treatment of GTD is carried out by surgery and chemotherapy.…”

Section: Discussionmentioning

confidence: 99%

Twist-1 Stimulates the Malignant Behaviors of Hydatidiform Mole via the PI3K/AKT Pathway

Zhang,

Song,

Yin

et al. 2024

Discovery Medicine

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Background: Hydatidiform mole (HM) is a common pregnancy disease among women of gestational age. Twist-related protein 1 (Twist-1) is involved in the development of various tumors, but its role in HM is poorly defined. This study aimed to explore Twist-1 expression and its biological function in HM cells. Methods: Twist-1 expression in HM was detected by immunohistochemistry and quantitative real-time polymerase chain reaction (qRT-PCR). The effects of silencing Twist-1 on choriocarcinoma (CCA) cell proliferation were detected by cell counting kit-8 (CCK-8) and clone formation assays. CCA cell migration and invasion were detected through transwell assay. Western blot was used to detect epithelial-mesenchymal transition (EMT) and the expression of phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway-related proteins. Results: Twist-1 expression was upregulated in HM tissues (p < 0.001) and CCA cells (p < 0.01). Twist-1 silencing inhibited proliferation of BeWo and JAR cells (p < 0.01, p < 0.05) as shown by CCK-8 assay (p < 0.01) and clone formation assays (p < 0.01, p < 0.05). Twist-1 silencing inhibited the migration (p < 0.01) and invasion activity (p < 0.01, p < 0.05) of BeWo and JAR cells. Western blot results showed that Twist-1 silencing promoted E-cadherin (p < 0.01) expression, and inhibited N-cadherin (p < 0.01, p < 0.05) and vimentin (p < 0.01, p < 0.05) expression in BeWo and JAR cells. Twist-1 downregulation decreased protein levels of p-PI3K (p < 0.01) and p-AKT (p < 0.01, p < 0.05) in BeWo and JAR cells. Conclusions: Silencing Twist-1 inhibits the malignant behavior of CCA cells, which may play a part by inhibiting the EMT process and the PI3K/AKT pathway.

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Section: Discussionmentioning

confidence: 99%

Twist-1 Stimulates the Malignant Behaviors of Hydatidiform Mole via the PI3K/AKT Pathway

Zhang,

Song,

Yin

et al. 2024

Discovery Medicine

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“…The use of ancillary techniques like immunohistochemistry, FISH, karyotyping, flow cytometry or genotyping had been shown to improve the diagnostic accuracy of HMs [5,19,31,32]. P57, a paternally imprinted maternally expressed gene, is currently a widely used immunohistochemistry method in the diagnosis of HMs.…”

Section: Discussionmentioning

confidence: 99%

“…On the contrary, p57 should be positive in villous cytotrophoblasts of biparental conceptus like PMs and NMAs [11,31]. Meanwhile, most CMs are diploid, and most PMs are diandric triploid with two paternal and one maternal genome [32]. Therefore, DNA ploidy study can also assist in the differentiation between CMs and PMs.…”

Section: Discussionmentioning

confidence: 99%

Diagnostic Utility of TSSC3 and RB1 Immunohistochemistry in Hydatidiform Mole

Chia

Aziz

Shuib

et al. 2023

IJMS

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The general notion of complete hydatidiform moles is that most of them consist entirely of paternal DNA; hence, they do not express p57, a paternally imprinted gene. This forms the basis for the diagnosis of hydatidiform moles. There are about 38 paternally imprinted genes. The aim of this study is to determine whether other paternally imprinted genes could also assist in the diagnostic approach of hydatidiform moles. This study comprised of 29 complete moles, 15 partial moles and 17 non-molar abortuses. Immunohistochemical study using the antibodies of paternal-imprinted (RB1, TSSC3 and DOG1) and maternal-imprinted (DNMT1 and GATA3) genes were performed. The antibodies’ immunoreactivity was evaluated on various placental cell types, namely cytotrophoblasts, syncytiotrophoblasts, villous stromal cells, extravillous intermediate trophoblasts and decidual cells. TSSC3 and RB1 expression were observed in all cases of partial moles and non-molar abortuses. In contrast, their expression in complete moles was identified in 31% (TSSC3) and 10.3% (RB1), respectively (p < 0.0001). DOG1 was consistently negative in all cell types in all cases. The expressions of maternally imprinted genes were seen in all cases, except for one case of complete mole where GATA3 was negative. Both TSSC3 and RB1 could serve as a useful adjunct to p57 for the discrimination of complete moles from partial moles and non-molar abortuses, especially in laboratories that lack comprehensive molecular service and in cases where p57 staining is equivocal.

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Immunohistochemical expression of BCL-2 in hydatidiform moles: a tissue microarray study

Al-Jabri,

Al-Badi,

Al-Kindi

et al. 2023

Pathologica

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Summary Background Hydatidiform moles (HM) are members of gestational trophoblastic diseases (GTD) and, in some cases, might progress to gestational trophoblastic neoplasia (GTN). HMs are either partial (PHM) or complete (CHM). Some HMs are challenging in arriving at a precise histopathological diagnosis. This study aims to investigate the expression of BCL-2 by immunohistochemistry (IHC) in HMs as well as in normal trophoblastic tissues “products of conception (POC) and placentas” using Tissue MicroArray (TMA) technique. Methods TMAs were constructed using the archival material of 237 HMs (95 PHM and 142 CHM) and 202 control normal trophoblastic tissues; POC and unremarkable placentas. Sections were immunohistochemically stained using antibodies against BCL-2. The staining was assessed semi-quantatively (intensity and percentage of the positive cells) in different cellular components (trophoblasts and stromal cells) Results BCL-2 showed cytoplasmic expression in more than 95% of trophoblasts of PHM, CHM and controls. The staining showed a significant reduction of the intensity from controls (73.7%), PHMs (76.3%) to CHM (26.9%). There was a statistically significant difference between PHM and CHM in the intensity (p-value 0.0005) and the overall scores (p-value 0.0005), but not the percentage score (p-value > 0.05). No significant difference was observed in the positivity of the villous stromal cells between the different groups. All cellular components were visible using the TMA model of two spots/case (3 mm diameter, each) in more than 90% of cases. Conclusions Decreased BCL-2 expression in CHM compared to PHM and normal trophoblasts indicates increased apoptosis and uncontrolled trophoblastic proliferation. Construction of TMA in duplicates using cores of 3 mm diameter can overcome tissue heterogeneity of complex lesions.

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Human epidermal growth factor receptor 2 fluorescence in situ hybridization and P57KIP2 immunohistochemistry using tissue microarray: Improving histopathological subtyping of hydatidiform mole

Cited by 3 publications

References 26 publications

Twist-1 Stimulates the Malignant Behaviors of Hydatidiform Mole via the PI3K/AKT Pathway

Twist-1 Stimulates the Malignant Behaviors of Hydatidiform Mole via the PI3K/AKT Pathway

Diagnostic Utility of TSSC3 and RB1 Immunohistochemistry in Hydatidiform Mole

Immunohistochemical expression of BCL-2 in hydatidiform moles: a tissue microarray study

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