For endometrial cancer, four molecular subgroups have undergone extensive studies in recent years: POLE ultramutated (POLEmut), mismatch repair-deficient (MMRd), p53 mutant (p53abn) and those EC lacking any of these alterations, referred to as NSMP (non-specific molecular profile).
MMRd-p53abn EC and POLEmut-p53abn EC were mostly grade 3 endometrioid EC, early stage, and frequently showed morphologic features characteristic of MMRd or POLEmut EC.18/28 (60%) MMRd-p53abn EC and 7/15 (46.7%) POLEmut-p53abn EC showed subclonal p53 overexpression, suggesting TP53 mutation was a secondary event acquired during tumour progression.
Direct sequencing of polymerase epsilon (POLE) exonuclease domain hot spots and conventional immunohistochemistry (MLH1, PMS2, MSH2, MSH6, p53) were conducted to identify TCGA classification-based molecular subgroups of EC: POLE-mutated, mismatch repair deficient, no specific molecular profile, and p53 aberrant.
Do estrogen, progesterone, P53 and Ki67 receptor ratios determined from curettage materials in endometrioid-type endometrial carcinoma predict lymph node metastasis?
The co-occurrence of high-level SCNAs and TP53 mutations in some clear cell ECs is consistent with the view that a subset of clinically diagnosed clear cell ECs have molecular similarities to serous ECs.
ProMisE was applied to a retrospective cohort of women with ECs <50 yo at diagnosis, and associations between the four ProMisE molecular subtypes (MMR deficient (MMRd), POLE mutated (POLE), p53 wild type (p53wt), and p53 abnormal (p53abn)) and clinicopathological parameters, including outcomes, were assessed.
DNA ploidy status, S-phase fraction, and p53 are not independent prognostic factors for survival in endometrioid endometrial carcinoma FIGO stage I-III.
Here we aimed to evaluate the expression patterns of different p53 isoforms and their contributions to the formation and subcellular localization of p53 amyloid aggregates in both EC and endometrial nontumor cell lines.
In the present study, abnormal p53 accumulation was analyzed using immunohistochemical techniques in endometrial carcinoma samples derived from 221 consecutive patients.
As 100% (7/7) of serous EC and 3% (2/59) of the LGECs showed mutant-pattern p53 staining, histotype may serve as a surrogate for p53 assessment, such that only HGEC or ambiguous carcinomas should be routinely subjected to p53 immunostaining.
The aim of this study was to determine the joint effect of single nucleotide polymorphisms (SNPs) of MDM2, TP53, and CDKN2A (P14ARF) genes on the onset and course of endometrial cancer (EC) in postmenopausal women.
To improve our understanding of the role of EMT in these tumors, we studied a series of 89 carcinomas including 14 undifferentiated/dedifferentiated endometrial carcinomas (UECs/DECs), 49 CSs (21 endometrial, 29 tubo-ovarian and peritoneal), 17 endometrioid carcinomas (grade 1-3), and 9 high-grade serous carcinomas of the uterus, using a panel of antibodies targeting known epithelial markers (Pan-Keratin AE1/AE3 and E-cadherin), mesenchymal markers (N-cadherin), EMT transcription factors (TFs) (ZEB1, ZEB2, TWIST1), PAX8, estrogen receptors (ER), progesterone receptors (PR), and the p53 protein.
Retrospective immunohistochemical analysis of the expression of p53 and PTEN tumor suppressor proteins was conducted in 99 women with endometrial carcinoma.
These include laboratory methods to optimize staining, a description of the different patterns of staining, advice regarding the interpretation, and reporting of p53 staining and practical uses of p53 staining in endometrial carcinoma diagnosis.
This study aimed to determine the in vitro and in vivo properties of sixteen frequently used endometrial cancer (EC) cell lines, including the cell proliferation rate, morphology, hormone receptor expression patterns, PTEN, hMLH1 expression, p53 mutation, karyotype, and tumorigenicity in mouse xenograt model.
To examine the expressions of COX-2, p53 and vascular endothelial growth factor (VEGF) in endometrial cancer and their relationships with clinicopathologic characteristics.
A total of 460 endometrial cancers were stratified by ProMisE (Proactive Molecular Risk Classifier in Endometrial cancer) into 4 molecular subtypes: mismatch repair-deficient (MMRd), <i>POLE</i> mutant (POLE), p53 abnormal (p53abn), and p53 wild-type (p53wt).
On the basis of their collective experience, the authors proffer some recommendations on the use of p53 immunohistochemistry in the histotyping of endometrial carcinomas.
We analyzed the immunoexpression of p53 and Snail in 55 cases of endometrioid endometrial carcinoma (EEC), in relation with the histopathological prognosis parameters and tumoral compartments, respectively intratumoral and advancing edge areas.