The protein p57 is encoded by CDKN1C. This gene is known to be paternally imprinted and maternally expressed in cytotrophoblasts and villous stromal cells. We present a method for evaluating p57 antibodies (Abs) in hydatidiform mole (HM) and demonstrate the results for 4 p57 Abs in various cell types. Five cases of complete HM, diploid with 2 paternal genome sets (CHM;PP), 5 cases of partial HM, triploid with 2 paternal and 1 maternal genome sets (PHM;PPM), and 5 cases of non-HM, with diploid biparental genomes (non-HM;PM) were stained with p57 Abs: 57P06, EP183, KP10, and KP39. Assessment of the fraction of nuclei stained, and the intensity of staining of the nuclei and cytoplasm was performed. For evaluation of the Abs, the observations in cytotrophoblasts, villous stromal cells, maternal decidual cells, and intermediate trophoblasts were scored. The fraction of stained nuclei in cytotrophoblasts and villous stromal cells and the staining of cytoplasm showed to be important parameters in the evaluation of the Abs. 57P06 was evaluated as optimal. KP10 showed moderate cytoplasmatic staining in maternal decidual cells and intermediate trophoblasts, and was evaluated as good. EP183 was evaluated as poor, primarily due to nuclear staining in ≥10% of the villous stromal cells in CHM;PP. KP39 was evaluated as poor, primarily due to strong cytoplasmatic staining in some cytotrophoblasts and villous stromal cells. A structured testing of p57 for diagnosing HM is recommended. No nuclear staining was observed in syncytiotrophoblasts of CHM;PP, indicating that in syncytiotrophoblasts also, CDKN1C is paternally imprinted.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7664962PMC
http://dx.doi.org/10.1097/PAI.0000000000000807DOI Listing

Publication Analysis

Top Keywords

villous stromal
20
stromal cells
20
cytotrophoblasts villous
16
cell types
8
paternally imprinted
8
p57 abs
8
genome sets
8
abs 57p06
8
evaluation abs
8
maternal decidual
8

Similar Publications

To distinguish DNA methylation (DNAm) from cell proportion changes in whole placental villous tissue research, we developed a robust cell type-specific DNAm reference to estimate cell composition. We collated new and existing cell type DNAm profiles quantified via Illumina EPIC or 450k microarrays. To estimate cell composition, we deconvoluted whole placental samples ( = 36) with robust partial correlation based on the top 30 hyper- and hypomethylated sites identified per cell type.

View Article and Find Full Text PDF

Objective: We report the first documented case of concurrent ectopic complete hydatidiform mole (CHM) and high-grade serous carcinoma (HGSC) of the fallopian tube, associated with unique histologic features and mutations in the HGSC.

Case Report: The patient presented with pelvic pain and vaginal bleeding. Laboratory examination revealed a positive urine pregnancy test and high serum beta-human chorionic gonadotropin (β-hCG).

View Article and Find Full Text PDF

Gestational Trophoblastic Disease: Complete versus Partial Hydatidiform Moles.

Diseases

July 2024

The Arkadi M. Rywlin M.D. Department of Pathology and Laboratory Medicine, Mount Sinai Medical Center, Miami Beach, FL 33140, USA.

Hydatidiform moles, including both complete and partial moles, constitute a subset of gestational trophoblastic diseases characterized by abnormal fertilization resulting in villous hydrops and trophoblastic hyperplasia with or without embryonic development. This involves chromosomal abnormalities, where one or two sperms fertilize an empty oocyte (complete hydatidiform mole (CHM); mostly 46,XX) or two sperms fertilize one oocyte (partial hydatidiform mole (PHM); mostly 69,XXY). Notably, recurrent occurrences are associated with abnormal genomic imprinting of maternal effect genes such as (chromosome 19q13.

View Article and Find Full Text PDF

The placenta undergoes morphological and functional adaptations to adverse exposures during pregnancy. The effects ofsuboptimal maternal body mass index (BMI), preterm birth, and infection on placental histopathological phenotypes are not yet well understood, despite the association between these conditions and poor offspring outcomes. We hypothesized that suboptimal maternal prepregnancy BMI and preterm birth (with and without infection) would associate with altered placental maturity and morphometry, and that altered placental maturity would associate with poor birth outcomes.

View Article and Find Full Text PDF

Correct placental development and function are essential for adapting the mother to the ongoing pregnancy and the wellbeing of the growing fetus; however, underlying processes are still poorly understood. Only limited structural and cellular placental features are shared among species hence requiring reliable human in-vitro models. Recently established trophoblast stem cell and organoid models significantly improved placental research; however, the human placenta constitutes a multi-cellular organ with tightly orchestrated, cellular and molecular networks between trophoblasts (TBs) and villous core cells (VCCs) vital for correct placentation.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!