From this month's Histopathology (2016)

“The extent and distribution of cardiac amyloidosis both correlate strongly with the amyloid type, suggesting fundamental, type-specific differences in the pathobiology of its deposition in the heart. Whether the patterns of deposition have prognostic or therapeutic implications remains to be determined. Although a definitive diagnosis of cardiac amyloidosis can be established on histomorphological grounds, the tendency for variable severity and mixed patterns of deposition to occur indicates that this approach is not accurate enough to replace direct typing in individual cases, although it may provide some clues regarding the ultimate type. In addition, rare forms of amyloidosis and codeposition of multiple amyloidogenic proteins occasionally occur.” Endocardial amyloid. Larsen et al. (p. 648) “This prospectively designed and retrospectively reviewed series of BRCA1 and BRCA2 protein expression in a large number of prostatectomy tissues obtained from localized PC patients showed that the protein expressions of BRCA1 and BRCA2 in the cytoplasm were significant independent prognostic factors for BCR. Hence, we believe that the results have clinical implications for the follow-up of PC patients undergoing radical prostatectomy.” BRCA1 in grade 4 prostate cancer. Kim et al. (p. 673) “The differential diagnosis of these tumours is somewhat complex and requires separation of giant cell carcinoma from other tumours currently under the designation of sarcomatoid carcinoma, mainly pleomorphic carcinoma, a tumour characterized by the presence of a mix of spindle and giant cells. In addition, as mentioned above, the syncytioptrophoblast-like type of giant cell carcinoma needs to be distinguished from metastatic disease of gonadal germ cell or gestational trophoblastic disease origin requiring detailed clinical and radiological correlation.” β HCG immunoreactivity in giant cell carcinoma of lung. Wiessferdt & Moran (p. 680) “Two reports in the literature have assessed ENT1 expression in GBC. In one study, the authors analysed different biomarkers associated with the efficacy of platinum and gemcitabine chemotherapy in BTC, including ENT1 assessment in nine GBC cases. High ENT1 expression was associated with improved OS. Murata et al., showed that low ENT1 expression was associated with poor prognosis in BTC patients treated with gemcitabine alone in a study that included 10 GBC cases and used a scoring system comparable to ours. Currently, most of the ENT1-related literature is focused on the predictive role of ENT1 for response to gemcitabine chemotherapy. Little is known about its prognostic value, owing to the lack of chemotherapy-naïve control patients in PC and BTC trials.” Survival analysis in gallbladder cancer related to ENT1 expression. Espinoza et al. (p. 722) “Our findings further support the idea that the histological growth pattern plays a role in predicting the clinical outcome of epithelioid malignant peritoneal mesothelioma, and emphasize the need to comment on predominantly solid patterns of growth. Here, we showed that the solid growth pattern was associated with aggressive clinical behaviour and a poor prognosis as compared with the tubulopapillary and micropapillary growth patterns. We validated the importance of mitotic index in epithelioid histology tumours, but other histopathological parameters, such as nuclear grade, depth of invasion, and stromal desmoplasia, were not strong predictors of outcome.” Epithelioid malignant peritoneal mesothelioma with mitotic activity. Krasinskas et al. (p. 729). “Interestingly, a considerable number of sarcomas in our series presented with a heterogeneous pattern of nuclear ATRX loss in neoplastic cells (Table 1). However, we observed the ALT phenotype in only two of eight tested sarcomas with such a pattern, which raises the question of whether this immunophenotypical heterogeneity has an impact upon telomere biology in these cases. In glioblastomas with retained nuclear ATRX expression the ALT phenotype was observed in 10 of 75 cases. Accordingly, ALT might also be provoked by an ATRX-independent mechanism in the two ALT-positive sarcomas with heterogeneous ATRX expression, perhaps by somatic mutations of H3.3-ATRX-DAXX chromatin remodelling pathway members others than ATRX.” Loss of ATRX immunoreactivity in high grade sarcoma. Koelsche et al. (p. 738)