The severe shortage of kidneys for transplantation has led efforts to expand the kidney donor pool, and to accomplish this goal, kidneys from expanded-criteria donors are being considered today for transplantation. Despite the frequent use of pretransplant biopsies of donor kidneys, no consensus has been reached regarding the prognostic significance of the various pathologic findings. The pathologic evaluation is focused on determining the percentage of globally sclerosed glomeruli; degree of interstitial fibrosis; arteriolar and arterial damage, including degree of vessel wall thickening and the presence/absence of vascular thrombosis; and identifying “significant” glomerular, inflammatory tubulointerstitial or vascular pathology. This information is provided to the transplant surgeon who then makes a determination of whether to transplant or not the deceased- or living-donor kidney in question, if any or a combination of the previously mentioned findings is identified. The present article describes how these donor kidneys should be evaluated morphologically and the impact of the various findings that may be found in deciding whether the kidney should be transplanted and addresses prognostic issues related to transplantation of kidneys exhibiting some of the previously mentioned findings not deemed to be severe enough to prevent transplantation. A review of the different criteria and systems that have been used in the past will be provided to understand how the evaluation process has been viewed by various investigators and the relationship of the various findings to immediate function and prognosis of the grafts. This information is important for surgical pathologists who may be asked to do frozen sections in these kidneys before transplant and/or sign out these specimens in their practices.

Cutaneous melanoma is the fifth leading cause of new cancer diagnoses, accounting for almost 77,000 cases and more than 9000 deaths in 2013. Although these cutaneous neoplasms are so common, their mucosal counterparts are much less so. Mucosal melanomas account for approximately only 1.3% of all diagnosed melanomas. These lesions, although rare, present at a significantly advanced stage with more adverse prognoses. In addition, molecularly, these lesions have proven to be distinct entities, in that they possess mutations not usually seen in their cutaneous counterparts. They also lack the common mutations found in cutaneous melanomas. Such findings indicate different pathways in tumorigenesis for these subtypes. We present a case of a mucosal melanoma, specifically a urethral melanoma, in a 70-year-old woman, clinically diagnosed as a urethral caruncle. Only after biopsy and resection was the correct diagnosis of malignant melanoma made. As melanomas arising from the mucosal sites are a rare entity, very little has been published on staging guidelines and prognostic factors, causing a dilemma for both the patient and the physician. Further work is necessary to better define a staging system in all mucosal locations, so that accurate prognoses can be given to patients with these lesions. Lastly, metastases from a more common cutaneous site must be considered.

FigureThis issue focuses on select salivary gland neoplasms. The ever-expanding list of salivary gland neoplasms primarily but not exclusively reflects recent/new discoveries in the molecular biology of this group of neoplasms. Tumors previously unknown and/or “lumped” within the spectrum of other tumors have been defined and recognized as unique types. Still, the more common types of salivary gland neoplasms can present diagnostic difficulties owing to their relative rarity and to the fact that such cases are not common and infrequently encountered in day-to-day surgical pathology. The first case focuses on a common diagnostic problem in salivary gland pathology albeit with a slight clinical twist. Dr Deborah Chute from the Cleveland Clinic discusses the diagnosis and differential diagnosis of mucoepidermoid carcinoma by fine-needle aspiration biopsy arising in a periparotid lymph node. In addition to discussing the key cytologic features associated with mucoepidermoid carcinoma, Dr Chute provides an overview on mucoepidermoid carcinomas developing at ectopic sites, which can add confusion to the diagnosis as the clinical differential diagnosis usually does not initially include a salivary gland tumor. Aside from the cytomorphologic findings, awareness among pathologists that salivary gland tumors can occur at unusual sites is a key to arrive at the correct interpretation. In the next case, Dr Justin Bishop from Johns Hopkins University School of Medicine discusses a case of mammary analog secretory carcinoma (MASC) representing a recently defined low-grade carcinoma associated with ETV6 translocation. Prior to its identification as a unique salivary gland neoplasm with analogous features to secretory carcinoma of the breast, MASC was included within the spectrum of acinic cell adenocarcinoma as a “zymogen-poor” subtype. Mammary analog secretory carcinoma and acinic cell adenocarcinomas can be remarkably similar in their histologic features, and while the presence of ETV6 translocation would differentiate them, many laboratories do not perform such analyses. However, as discussed in this case, the immunohistochemical findings do allow for their distinction in lieu of performing molecular analysis. Although in part defined by the presence of multiple growth patterns as well as bland cytomorphology, polymorphous low-grade adenocarcinoma (PLGA) is not the only salivary gland neoplasm with such histologic findings. Drs Vaidehi Avadhani and Nebras Zeizafoun from the Mount Sinai Health System discuss a case of PLGA detailing the light microscopic and immunohistochemical findings that allow for diagnosis and differentiating it from other histologically similar neoplasms, including pleomorphic adenoma and adenoid cystic carcinoma. Furthermore, previous classifications of salivary gland neoplasms “lumped” the cribriform adenocarcinoma of minor salivary glands within the spectrum of PLGAs, but as detailed in this article, the presence of ARID1A-PRKD1 and DDX3X-PRKD1 fusions in cribriform adenocarcinoma of minor salivary glands and rarity of such fusions in PLGA support distinct classification but suggest a possible shared pathogenesis between these tumor types. Clear cells can be seen across a wide spectrum of salivary gland lesions including benign and malignant tumors. In the next case, Dr Andrew Turk from Columbia University reviews the pathologic features of the low-grade epithelial-myoepithelial carcinoma with a discussion on the differentiating features from other salivary gland neoplasms with clear cells. His discussion also includes the utility of molecular chromosomal rearrangements, specifically the presence of EWSR1-ATF1 fusion in clear cell carcinoma. The last 2 articles in this issue are reviews of specific topics in salivary gland neoplasia. In the first of these reviews, Dr Joaquín García from Mayo Clinic provides an overview of the fusion transcripts that characterize malignancies of salivary gland origin. Although discussed in several of the previous case reviews, this review details the unique molecular signatures that have been identified to date in salivary gland neoplasms. Finally, Frederik Petersson from the National University Health System of Singapore provides an exhaustive overview of high-grade transformation of differentiated salivary gland neoplasms heretofore considered “dedifferentiation,” a term more aptly used for soft tissue neoplasms. His review essentially covers all salivary gland neoplasms that may be associated with high-grade transformation discussing the process of malignant transformation of salivary gland neoplasms. We hope that you find the cases and reviews interesting, informative, and useful in your daily practice.

Rapid on-site evaluation (ROSE) has repeatedly been shown to improve diagnostic performance of endoscopic ultrasound–guided fine-needle aspiration of pancreatic lesions. However, the practice of providing ROSE service varies among institutions. ROSE helps to ensure adequate sampling, appropriate specimen triage, and timely patient management. In this review, we discuss the practice and clinical significance of ROSE, the factors influencing the ROSE diagnosis, the financial considerations for providing ROSE service, and pitfalls to render a ROSE diagnosis.

Metastatic tumors to the thyroid are relatively uncommon, constituting less than 1% of all thyroid malignancies. Fine-needle aspiration of thyroid nodules is a reliable technique to diagnose primary thyroid lesions with excellent sensitivity and specificity; however, cytologic diagnosis of tumors metastatic to the thyroid can be challenging, particularly if prior clinical history is not available. Clinical presentation is very much similar to that of primary thyroid tumors. Although renal cell carcinoma appears to be the most common secondary tumor of the thyroid, any tumor can metastasize to the thyroid, particularly breast, lung, colon, stomach, and head and neck primary tumors. Carcinomas are most common, including adenocarcinoma and squamous cell carcinoma, but melanoma and sarcoma, although less frequent, are also encountered. Metastatic tumors may show low-grade cytologic features similar to well differentiated primary thyroid tumors or high-grade morphologic features as seen in anaplastic thyroid carcinoma in fine-needle aspirations. Cytologic diagnosis of a secondary thyroid tumor depends on the pathologist’s knowledge of the patient’s prior clinical history, morphologic features, and use of ancillary techniques for confirmation. Management and prognosis of these tumors depend on the stage of the primary tumor. Patients with isolated metastasis to the thyroid generally do well, whereas the prognosis of patients with widespread malignant disease is grim.

Barrett esophagus is the known precursor lesion of esophageal adenocarcinoma; however, the natural history of Barrett esophagus and its associated dysplasia is a matter of considerable debate and difficult to establish on a patient-by-patient basis. Clinical management and surveillance are currently limited by a lack of efficient and accurate predictive biomarkers of progression, and the incidence of esophageal adenocarcinoma has increased at an alarming rate. This phenomenon has attracted considerable interest in the molecular pathogenesis of Barrett esophagus and esophageal adenocarcinoma. Neoplastic transformation of Barrett esophagus appears to be a complex disease process in which multiple defective clones accumulate mutations producing a lesion with significant heterogeneity and clonal diversity. P16 inactivation, p53 loss of heterozygosity, and DNA ploidy abnormalities are all significant events in the progression of Barrett esophagus. It is clear that many molecular alterations take place during the neoplastic transformation of Barrett esophagus, and our improved understanding of the molecular pathogenesis has contributed to the progress of predictive biomarker development in preclinical studies. Although many genetic and epigenetic abnormalities have been identified, no molecular tests are available in routine clinical practice. Ideally, a panel of predictive biomarkers would allow for risk stratification into low- and high-risk subgroups, which could help decide which patients receive appropriate follow-up or therapeutic intervention. This review discusses current issues with the diagnosis and surveillance of Barrett esophagus and highlights the most promising predictive biomarkers that may supplement histology for optimal patient management.

The use of molecular markers in sarcomas has been primarily for diagnosis, but increasingly they are also used for prognosis and prediction of response to specific therapies. This article presents 3 case reports of sarcomas to illustrate molecular markers for prognosis/predictive purposes. The prototypical example is gastrointestinal stromal tumor, in which the response to imatinib mesylate therapy is predicted by analysis for KIT mutation. In synovial sarcomas, the type of fusion transcript correlates with the clinical course, with SST-SSX2 having better metastasis-free survival than SYT-SSX1. p53 Mutation is an important prognostic factor in multiple tumors, including Ewing sarcoma. Many studies are ongoing, and molecular analysis will become increasingly important in the treatment of sarcomas.

For the intramucosal mass-forming preinvasive neoplasms (tumoral intraepithelial neoplasms) of the gallbladder, the term intracholecystic papillary tubular neoplasm (ICPN) has been proposed as a unifying category to embrace all the entities described in the World Health Organization 2010 classification as “adenoma,” “intracystic papillary neoplasm,” and “papillary adenocarcinoma.” In essence, this category represents the gallbladder counterpart of the tumors known as intraductal papillary and intraductal tubulopapillary neoplasms in the pancreas and bile ducts. They are distinguished from nontumoral (“flat”) dysplasia by their exophytic tumor formation. They show a spectrum of dysplastic changes (adenoma-carcinoma sequence), various growth patterns, often in a mixture (papillary, tubular, and tubulopapillary), and a variety of cell lineages including biliary (MUC1+), pyloric-mucinous (MUC6+), complex-tubular (pyloric nonmucinous; MUC6+; with morule formation and β-catenin nuclear positivity), gastric-foveolar, occasionally intestinal (MUC2/CDX2), and even more rarely oncocytic, often but not always with corresponding immunophenotypic changes. Invasive carcinoma is often encountered in association with these tumors (65% of the cases), and an estimated 6% to 8% of invasive carcinomas arise from ICPNs. Invasion is common in papillary examples and those with biliary or gastric-foveolar appearance, whereas it is very low, if at all, in complex tubular-pyloric examples (although the latter often shows striking cytoarchitectural atypia as well). Extensive sampling is warranted to rule out invasive carcinoma. Carcinomas confined to above the tunica muscularis (early gallbladder carcinomas, which correspond to Tis/T1a/T1b cases) have a fairly good prognosis, especially if the possibility of T2 carcinoma (invasion through the muscularis) is ruled out by thorough sampling. More invasive examples have an aggressive behavior but still appear to be better behaving than ordinary adenocarcinomas without ICPNs, presumably partly due to early discovery of invasive carcinomas, but also partly due to differences in biologic behavior.

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In recent years, advances in our understanding of the molecular biology of prostate cancer have spawned optimism that new biomarkers will allow greater sensitivity and specificity in diagnosis as well as more accurate prediction of outcome after treatment for the individual patient. For at-risk patients with negative biopsy, multiple new markers are available, including mitochondrial DNA deletion testing (tissue), PCA3 (urine), and sarcosine (tissue or blood). For patients with diagnostically challenging prostate biopsies, multiple stain combinations (multiplex immunohistochemistry) such as quadruple staining with racemase, high-molecular-weight cytokeratin, p63, and c-myc are commonly used to confirm the diagnosis of prostate cancer; the recent addition of c-myc to create a quadruple stain provides additional diagnostic support for cancer, recognizing that there may be heterogeneity or complete lack of staining for some of the other markers. These stain combinations must, of necessity, be used together on 1 slide owing to common loss of the focus of concern on deeper sections. TMPRSS2:ERG is a useful diagnostic adjunct for select cases, with the recent introduction of antibody staining. Prostate-specific antigen, prostatic acid phosphatase, and prostate-specific membrane antigen are useful for confirming prostatic origin of cancers, as well as for predicting outcomes for select patient group. Other biomarkers are being actively investigated as companion diagnostics to predict response to treatment. This report describes the current state of immunohistochemical stains for the diagnosis of prostatic intraepithelial neoplasia, atypical small acinar proliferation, and prostate cancer.