Reducing unnecessary biopsies while detecting clinically significant prostate cancer including cribriform growth with the ERSPC Rotterdam risk calculator and 4Kscore

Introduction

The use of risk calculators predicting clinically significant prostate cancer (csCaP) on biopsy reduces unnecessary biopsies and overdiagnosis of indolent disease compared to a Prostate Specific Antigen (PSA) strategy. Updating these tools using more specific outcome measures and contemporary predictors could potentially lead to further reductions. Our objective was to assess clinical impact of the 4 kallikrein (4K) score, the Rotterdam Prostate Cancer Risk Calculator (RPCRC), and the combination of both for predicting csCaP based on the latest International Society of Urological Pathology grading system and cribriform growth pattern.

Histopathology of giant cell tumors of the bone: With special emphasis on fibrohistiocytic and aneurysmal bone cyst like components

Objective

The aim of this study was to define histopathological features of giant cell tumor of bone, especially accompanying fibrohistiocytic or aneurysmal bone cyst like components, in the light of our institutions experience.

German pathologist Walter Büngeler (1900–1987)—Nazi victim or political influencer in Brazil?

One of the most wellknown German pathologists of the twentieth century, Walter Büngeler became internationally known for his elemental research on leukemia and the pathology of tumors. In 1936, Büngeler left Nazi Germany for Brazil, but returned to Germany in 1942. After the war ended in 1945, Büngeler portrayed himself as a political victim who had been expelled first by the National Socialists and later by the Brazilian government, and in fact, he was able to successfully perpetuate this image and emerged unscathed from his de-Nazification procedure, continuing on to a successful university career with stations in Kiel and Munich as both professor and dean, as well as a term as DGP president. Up until very recently, Büngeler was portrayed in literature as a victim and critic of Nazism.Does this self-portrayal stand up to a critical examination of the facts? It is precisely this question that is the focus of this article. The analysis draws upon primary sources; namely, Büngeler’s own claims from a curriculum vitae filled out in 1943 as well as his de-Nazification file from the post-war period.This article exposes significant contradictions between these two sources. The statements Büngeler made in his de-Nazification file can be verified as false in all relevant aspects. Nevertheless, Büngeler managed to create a wide-reaching and successful version of himself; a picture which persisted until only very recently.     

胆囊肝样腺癌的临床影像病理分析

目的总结胆囊肝样腺癌临床病理学特征及影像学表现。 方法回顾性分析2010年1月至2019年10月海军军医大学第三附属医院收治的经手术病理诊断的6例胆囊肝样腺癌患者的临床资料、病理检查结果、影像学资料及术后随访资料。 结果本组6例胆囊肝样腺癌患者的发病年龄为49~69岁，男女发病率为2∶1，3例发生于肝脏或淋巴结转移。6例患者血清甲胎蛋白（AFP）水平均升高、肝细胞抗原（Hep-1）染色均呈阳性。1例患者MRI和CT表现动脉期呈中度-明显强化，门静脉期及延迟期强化减退，1例为轻度强化；1例为不均匀明显强化。6例患者中2例患者失访；2例患者术后5年未见复发，存活至今；1例患者术后2年发现肝转移，治疗后存活至今；1例患者术后1年复发，治疗6个月后死亡。 结论胆囊肝样腺癌好发于中老年男性，且容易发生肝脏或淋巴结转移，并通常伴有血清AFP水平升高，预后差，结合临床和影像学特征可提高对该病的诊断准确率。     

异位葡萄胎妊娠早期临床特点及诊疗：附二例报道

异位葡萄胎在临床上可以引起严重的并发症，其发病率极低，且易被漏诊、误诊。本文报道了2例异位葡萄胎患者的临床表现及病理诊断结果。患者1为部分性葡萄胎，患者2为完全性葡萄胎合并宫颈恶性肿瘤，两例患者临床上均表现为异位妊娠，并首先按照异位妊娠治疗，造成了误诊、误治；均采取手术治疗，术后病理检查确诊为异位葡萄胎。后续又补充治疗，得以痊愈。以上两例患者的诊断和治疗上均有欠缺，本文结合相关文献对病例资料进行分析总结，阐述异位葡萄胎典型临床表现和最新治疗研究进展，以期引起临床医师的重视，为早期诊断及治疗提供支持。     

中国病理学教学改革近况分析

病理学是基础医学与临床医学之间的桥梁学科,是医学生接触的第一门介绍疾病本质的课程。传统的病理学教学模式已经不能满足高等医学教育的要求,严重阻碍了医学教育事业的发展。病理学教学改革有益于医学教育创新,对提高病理学教学质量与培养高素质创新人才具有重要意义。近十年来,中国病理学教学的改革与创新主要体现在病理学精品课程的建设、教师观念的转变、教学模式的改革等方面。本文就目前国内病理学教学改革近况作一综述。     

Clinicopathological significance and prognostic implication of nuclear factor-κB activation in colorectal cancer

ObjectiveThe aim of the present study was to evaluate the clinicopathological significance of phosphorylated nuclear factor-κB (pNF-κB) expression, and its impact on epithelial–mesenchymal transition and angiogenesis in colorectal cancer (CRC).MethodsWe carried out immunohistochemistry of pNF-κB on 261 human CRC tissues, and evaluated nuclear expression, regardless of cytoplasmic expression. We also investigated the correlation between pNF-κB expression and clinicopathological characteristics, survival, and epithelial–mesenchymal transition and angiogenesis-related markers in CRC.ResultspNF-κB was expressed in the nuclei of 164 of the 261 CRC tissues (62.8%). Furthermore, pNF-κB was significantly correlated with frequent perineural invasion, lymph node metastasis, and higher pTNM stage. However, there was no significant correlation between pNF-κB expression and other clinicopathological parameters. Among the epithelial–mesenchymal transition markers examined, SNAIL expression was significantly correlated with pNF-κB expression (P = 0.001) but E-cadherin expression was not. CRC with pNF-κB expression had significantly higher SIRT1 expression levels and hypoxia-inducible factor-1α expression levels than CRC without pNF-κB expression (P < 0.001 and P < 0.001, respectively). However, there was no correlation between the expression levels of pNF-κB and VEGF. pNF-κB expression was significantly correlated with worse overall and recurrence-free survival rates (P < 0.001 and P < 0.001, respectively).ConclusionpNF-κB expression was significantly correlated with aggressive tumor behaviors and worse survival rates. Furthermore, pNF-κB expression may affect tumor invasion and progression through SNAIL-related epithelial–mesenchymal transition and SIRT1- and hypoxia-inducible factor-1α-induced angiogenesis.     

NTRK-Fusions – A new kid on the block

The neurotrophic tyrosine receptor kinases (NTRK) play an important role in the development and function of the nervous system. Fusions involving NTRK and a wide range of genes that act as fusion partners are oncogenic and activate well-known signal transduction pathways like the MAPK-ERK pathway. NTRK fusions occur in many very different tumor entities in children and youth as well as in adults. There are a few tumors like secretory breast cancer and congenital fibrosarcoma for which NTRK fusions are pathognomonic. At the same time there a large number of tumors in which NTRK fusions occur in very rare frequency (e.g., lung cancer). TRK inhibitors offer now the possibility to use NTRK fusion as antitumorigenic targets in a tumor agnostic fashion regardless of the basic histology. It is the task of modern pathology to identify such targetable fusions in a highly effective and efficient manner.