Concomitant p53 and PTEN immunoexpression to predict the risk of malignancy in endometrial polyps.

The aim of this retrospective cross-sectional study was to assess the usefulness of phosphase and tensin homolog deleted on chromosome 10 (PTEN) and p53 protein immunoexpression in predicting the risk of malignancy in endometrial polyps. The study was conducted at tertiary public hospital, university teaching center, and private practice clinic.A total of 159 patients with endometrial polyps who underwent hysteroscopic polypectomy between January 2010 to December 2014 were included. p53 and PTEN immunoexpression were assessed in histologic endometrial polyp samples. Patients were allocated into 2 groups: group A, endometrial polyps without atypia (120), and group B, endometrial polyps with atypia (39), which were subdivided into A1 (80) and B1 (21) = p53-/PTEN+ immunostaining; A2 (20) and B2 (11) = p53+/PTEN+; A3 (14) and B3 (4) = p53+/PTEN-; A4 (6) and B4 (3) = p53-/PTEN-.There was no significant difference between groups regarding clinical and epidemiologic parameters, except for age. Neoplasia incidence within groups was higher when at least 1 marker was abnormally stained (in group A, P = .0089, odds ratio [OR] = 13.94 [1.62; 120.27]; in group B, P = .0255, OR 12.73 [1.38; 117.27]). Overall neoplasia incidence was higher in group B than in group A (20.5% vs 5.8%; P = .0113). Malignant neoplasia was found more frequently in patients with p53+ (P = .0006, OR = 7.67 [2.30; 25.54]) and PTEN- (P = .0043; OR = 5.43 [1.77; 16.61]).Immunohistochemical analysis using p53 and PTEN as markers, either alone or concomitantly, can be useful to predict malignant transformation in cases of endometrial polyps.

Immunohistochemical expression of p63 in endometrial polyps: evidence that a basal cell immunophenotype is maintained.

OBJECTIVE: Although endometrial polyps likely originate from reserve cells in the basal layer, the underlying biology is not fully understood. One protein that plays an important role in regulating epithelial proliferation and differentiation is the 63-kd membrane protein (p63), which is also a marker of basal and reserve cells in the female genital tract. Our objective was to determine whether p63 is expressed differently in postmenopausal endometrial polyps than in the adjacent endometrium. DESIGN: In this study, 36 specimens of endometrial polyps and 36 samples of the adjacent endometrium were obtained from postmenopausal women through hysteroscopic surgery performed in a tertiary-care university hospital. Immunohistochemistry was used to evaluate the expression of p63 in all samples. RESULTS: The majority of endometrial polyp samples (94.4%) presented nuclear immunostaining for p63, whereas only 5.6% of adjacent endometrium samples were positive for p63 (P < 0.0001). Distribution of p63 immunostaining in the endometrial polyp samples was homogeneous. CONCLUSIONS: Our results provide evidence that a basal cell immunophenotype is maintained in the endometrial polyps seen in postmenopausal women, suggesting that p63 plays a role in the pathogenesis of such polyps.

Serum gastrin, pepsinogens, parietal cell and Helicobacter pylori antibodies in patients with gastric polyps.

OBJECTIVES: To determine serum concentration of gastrin and pepsinogens (PGs) as markers for the gastric mucosal status and to elucidate the prevalence of serum Helicobacter pylori (H pylori) IgG antibodies and parietal cell autoantibodies (PCAs) in patients with gastric polyps. METHODS: The subjects in this study were composed of 36 patients with fundic glandular polyps (FGP), 25 patients with foveolar hyperplastic polyps (FHP), and 27 asymptomatic healthy volunteers (controls). Serum concentrations of gastrin and PGs were determined by radioinmmunoassay. H. pylori IgG antibodies were measured through an enzyme-linked immunosorbent assay. PCAs were detected by an indirect immunofluorescence technique using cryostat sections of rat gastric mucosa. RESULTS: There were no significant differences between FGP patients and controls in serum concentrations of gastrin, PG I and PG II. FHP patients showed significantly higher serum gastrin, lower PG I, higher PG II levels and, as a consequence, far lower PG I/PG II ratio compared with controls. The prevalence of H pylori infection was much higher in FHP patients (84.0%), whereas lower in FGP patients (19.44%) than that in controls (40.7%) was positive in 24.0% of FHP patients, 2.78% of FGP patients and 4% of controls. CONCLUSIONS: These results suggest that FHP often develops in a gastric mucosa associated with H pylori infection, while FGP does not appear to be related to H pylori infection.