Anaplastic lymphoma kinase (ALK) translocation renal cell carcinomas (RCCs) have been reported by several independent groups in recent times. The clinical behavior and histopathologic characteristics of these carcinomas are not fully understood because of the paucity of cases reported. Here, we describe 2 cases of RCC harboring a novel striatin (STRN)-ALK fusion. The first case was a 33-year-old woman with no sickle cell trait who underwent nephrectomy for right renal mass and had late recurrence in para-aortic lymph nodes twice 10 and 12 years after initial surgery. After the second recurrence, she was carefully observed without any treatment. Twenty-six years after the initial nephrectomy, the second para-aortic lymphadenectomy was performed, and gastrectomy was performed for newly developed primary gastric cancer. The resected para-aortic lymph nodes were largely replaced by metastatic carcinoma. The second case was a 38-year-old man with no sickle cell trait who underwent cytoreductive nephrectomy followed by sunitinib therapy for metastatic RCC. In both cases, the tumor showed solid, papillary, tubular, and mucinous cribriform structures. Psammoma bodies were occasionally seen in the stroma. Tumor cells had a large nucleus and prominent nucleoli with predominantly eosinophilic cytoplasm. Rhabdoid cells and signet-ring cells were also observed. Intracytoplasmic mucin deposition and background mucinous stroma were confirmed. In the second case, tumor necrosis was seen in some areas. Tumor cells exhibited diffuse positive staining for ALK in both cases. ALK translocation was confirmed by fluorescent in situ hybridization, and further gene analysis revealed a STRN-ALK fusion. These cases provide great insights into ALK translocation RCCs.

Insulinoma-associated protein 1 (INSM1) is an important biomarker of Achaete-scute homolog-like 1-driven pathways. For diagnosis of pancreatic neuroendocrine tumors (PanNET), chromogranin A (CGA), synaptophysin (SYP), and neural cell adhesion molecule (NCAM) were also considered as potential biomarkers. However, it is often difficult to diagnose it immunohistochemically. Hence, we examined the expression pattern of INSM1 in pancreatic solid tumors. We detected INSM1, CGA, SYP, and NCAM immunohistochemically, in 27 cases of NET [pure type: 25 cases, mixed adenoneuroendocrine carcinoma (MANEC): 2 cases]. We included 5 cases of solid-pseudopapillary neoplasm (SPN), 7 cases of acinar cell carcinoma (ACC), and 15 cases of pancreatic ductal adenocarcinoma (PDAC) as the control group. Nuclear expression of INSM1 was found in all PanNET pure type cases. However, expression of INSM1 was negative in PDAC, ACC, and SPN in all cases, whereas faint expression was seen in the cytoplasm from SPN. MANEC comprises of two components: neuroendocrine carcinoma and adenocarcinoma components. The NET component was positive for INSM1 expression, whereas the PDAC component does not express INSM1, which aids in distinguishing these components. Our results suggest that INSM1 is a useful immunohistochemical marker for diagnosing pancreatic neuroendocrine tumor.

It is well known that hepatocellular carcinoma (HCC) commonly involves the local branches of portal and/or hepatic veins and causes a tumor thrombus even at a relatively early stage. Vascular invasion is classified as macrovascular invasion, which is grossly recognizable (mostly in large to medium vessels), or microvascular invasion (MVI), which can be identified only by microscopic observation (mainly in small vessels such as portal vein branches in portal tracts, central veins in noncancerous liver tissue, and venous vessels in the tumor capsule and/or noncapsular fibrous septa).Although macroscopic vascular invasion in major vessels (and satellite nodules) is known to be a marker of poor outcomes after liver transplantation (LT) for HCC and is regarded as a contraindication for LT, the significance of MVI as a predictor of poor outcomes is still controversial. The controversy concerns the extent to which MVI (if it is identifiable before surgery) is a contraindication for LT, even though we know that only a minority of patients with MVI will experience HCC recurrence. MATERIALS AND METHODSWe searched the MEDLINE database (2002)(2003)(2004)(2005)(2006)(2007)(2008)(2009)(2010) to determine the significance of MVI to the outcomes of LT for HCC; we used the keywords hepatocellular carcinoma, HCC, microvascular invasion, liver transplantation, and liver resection. We also performed a full manual search of the bibliographies of selected publications and included 4 additional publications from earlier years. Publications were included if they contained data on MVI and its relationship with tumor characteristics and/or prognostic data. The search resulted in a total of 48 relevant publications.The publications were then ranked according to the classification proposed by the Oxford Centre for Evidenced-Based Medicine.

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Primary hepatic NET and NEC are very rare tumours. The NEC component in HNEC showed high proliferative activity and influenced patient prognoses.