Background: Imaging modalities are used to diagnose and clinical grading of clinically significant prostate cancer. In this study, 68Ga-PSMA PET/CT (PSMA) and multiparametric prostate MRI (mp-MRI) were compared in regard to locating intraprostatic tumor and locoregional staging.

AimThere are many scenarios where high-risk human papillomavirus (HPV) detection in formalin-fixed paraffin-embedded (FFPE) specimens is important. However, there is no Food and Drug Administration (FDA)-approved and clinically validated technique for detecting high-risk HPV in FFPE tissues. In this study, we evaluated two commercially available HPV assays which are FDA-approved for use on cytology specimens, the Aptima HPV assay and the Beckton Dickinson (BD) Onclarity assay, to detect high-risk HPV in FFPE tissues of cervical high-grade squamous intraepithelial lesion (HSIL) and squamous cell carcinoma (SCC).MethodsA total of 189 cases (46 SCC, 107 HSIL and 36 benign/normal) were tested for high-risk HPV with the Aptima HPV assay and a subset of cases (n=97) with the BD Onclarity assay.ResultsThe sensitivities of the Aptima and BD Onclarity HPV assays were 99.4% (95% CI 96.46% to 99.98%) and 75.9% (95% CI 65.27% to 84.62%), respectively; the specificity and positive predictive value (PPV) of the two assays were 100%. Negative predictive values of the Aptima and BD Onclarity HPV assays were 97.3% (95% CI 83.61% to 99.61%) and 67.7% (95% CI 58.91% to 75.47%), respectively. The kappa value (0.96) for comparison of the distribution of high-risk HPV types between the two assays was high. HPV 16 was the most common high-risk HPV type for HSIL and SCC cases. However, SCC cases had higher percentages of HPV 16 and HPV 18/45 and lower percentages of other high-risk HPV types compared with HSIL cases.ConclusionBoth assays are reliable methods for high-risk HPV detection and genotype determination in FFPE specimens, with high PPV and specificity. The Aptima HPV assay has the advantage of higher sensitivity. As far as we are aware, this is the first study comparing the Aptima HPV assay and the BD Onclarity assay in FFPE tissues. Our study results should be tested and confirmed in larger cohorts.

Background: Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumor originating from the gastrointestinal tract and have a broad spectrum of clinicopathological features affecting disease management regarding the treatment modalities. Methods: A retrospective study of 49 patients who underwent surgery for gastrointestinal tumors between 2008 and 2016 was conducted. Clinical, pathological, and immunohistochemical features of patients with and without recurrence were statistically analyzed.Results: Twenty-nine (59.1%) patients had gastric; 16 (32.6%) had small intestinal; 3 (6.1%) had mesenteric; and 1 (2.2%) had rectal GISTs. Microscopic tumor necrosis and tumor ulceration were also significant for disease recurrence (P = 0.005, P = 0.049). High-risk patients according to Miettinen’s risk classification were more likely to develop a recurrence (P < 0.001). Additionally, high-grade tumors were also a risk factor for recurrence (P < 0.001). Ki-67 levels were available in 40 patients and the mean Ki-67 level was 16.8 in patients with recurrence, which was a significant risk factor in regression analysis (HR: 1.24, 95%, CI: 1.08-1-43). Five-year disease-free survival rates of non-gastric and gastric GISTs were 62.3% and 90%, respectively (P = 0.044).Conclusion: Larger tumors and higher mitotic rates are more likely to develop recurrence. High Ki-67 levels were also associated with recurrence.

Surface epithelial changes involving endometrioid carcinomas of the uterine corpus mimicking papillary syncytial metaplasia or cervical microglandular hyperplasia are relatively common. There have been rare reports of surface epithelial changes in endometrioid carcinomas mimicking ovarian serous borderline tumor or low-grade serous carcinoma. We report an endometrioid carcinoma of the uterine corpus with striking morphologic mimicking of an ovarian serous borderline tumor with only a minimal amount of conventional endometrioid carcinoma. The tumor was diffusely positive for estrogen receptor, negative for WT1, and showed wild-type immunoreactivity with p53. Targeted sequencing revealed a KRAS mutation (G12V/D/A), but no BRAF mutation. This close mimicry of a serous borderline tumor by a uterine endometrioid carcinoma has not been emphasized in the literature and this case is unique because the features involved almost the entire neoplasm. In reporting this case, we review surface changes in endometrioid carcinomas of the uterine corpus.