Urothelial carcinoma with villoglandular differentiation

Urothelial carcinoma with villoglandular differentiation

IAP 2014 ABSTRACTS Urologic Pathology: CBS25-1 THE ANTI-TUMOR MECHANISM OF TYROSINE KINASE INHIBITORS IN CLEAR CELL RENAL CELL CARCINOMAS: INSIGHTS F...

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IAP 2014 ABSTRACTS

Urologic Pathology: CBS25-1 THE ANTI-TUMOR MECHANISM OF TYROSINE KINASE INHIBITORS IN CLEAR CELL RENAL CELL CARCINOMAS: INSIGHTS FROM A PATHOLOGIC ASSESSMENT Toyonori Tsuzuki Department of Pathology, Japanese Red Cross Nagoya Daini Hospital, Japan Angiogenesis occurs during tumor development and plays a critical role in the progression of clear cell renal cell carcinoma (CCRCC). Tyrosine kinase inhibitors (TKIs) are multi-target inhibitors of TK receptors that are standard first-line drugs for the treatment of advanced or recurrent CCRCC. Although their efficacy in preventing CCRCC progression is well established, the pathologic features of tumors treated with TKIs are rarely described in the literature. We recently reported that TKIs induced two types of vasculopathy in tumor vessels: type A in large and/or mediumsized vessels, in which there is a concentric intimal thickening that results in the narrowing or occlusion of the lumen; and type B in small vessels, which consist of hyalinized fibrous vessel walls, leading to occlusion of the lumen. TKI-induced vasculopathy was observed in or adjacent to necrotic or degenerative areas in CCRCCs, with tumor vessels showing decreased endothelial cell density; the consequent reduction in the blood supply to CCRCCs had anti-tumorigenic effects. These findings indicate that vasculopathy can serve as a prognostic marker for predicting the effectiveness of TKIs as well as patients outcome, and highlight the relevance of pathologic assessments for pharmaceutical development.

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associated with this tumor including, micropapillary urothelial carcinoma, plasmacytoid urothelial carcinoma, sarcomatoid urothelial carcinoma and small cell carcinoma. Tumors that may mimic urothelial carcinoma with villoglandular differentiation include colorectal adenocarcinoma, prostatic ductal adenocarcinoma, urachal carcinoma, villous adenoma and other entities.

Urologic Pathology: CBS25-2 PROSTATE/SEMINAL VESICLE MASS: THINK AGAIN WHEN IMMUNOHISTOCHEMISTRY DOES NOT FIT Ni Chen, Jing Gong, Ling Nie, Xueqin Chen and Qiao Zhou West China Hospital, Pathology Department, Chengdu, China A 53-year-old male complained of urination discomfort and pain for three weeks. Physical examination noted swelling of legs and enlarged prostate. Imaging studies revealed irregular mass involving the prostate and seminal vesicles with obscured structural features, enlarged peri-iliac artery and peri-aortal lymph nodes, and suspicious metastatic lesions in the 4th-5th lumbar vertebrae. Serum PSA was not elevated. Ten cores of ultrasound-directed needle biopsies of the prostate were collected and submitted to the pathology department. Routine H&E histology reveals medium sized tumor cells infiltrating fibromuscular stroma in sheets or nests.Some tumor cells were distorted with indistinct morphology and hyperchromatic nuclei. Occasional perineural invasion was observed.

Urologic Pathology: SY25-1 Urologic Pathology: CBS25-1 UROTHELIAL CARCINOMA WITH VILLOGLANDULAR DIFFERENTIATION Adeboye O. Osunkoya1,2,3 1Department of Pathology, Emory University School of Medicine, Atlanta, 2Department of Urology, Emory University School of Medicine, Atlanta, and 3Emory Winship Cancer Institute, Atlanta, GA, USA The patient is a 72-year-old man who presented with hematuria. On cystoscopy, a large friable mass was identified involving the left bladder wall. A transurethral resection of the bladder tumor was performed. Histologically, the tumor was composed of superficial finger-like processes lined by epithelium with true glandular lumina with intraluminal mucin, intimately admixed with invasive high grade urothelial carcinoma. Several glands also had cribriform features and some were lined by non-mucin producing cuboidal to columnar cells. Variable amounts of intraluminal necrosis, apoptotic bodies, and eosinophilic secretions were also present. The tumor invaded the muscularis propria (Detrusor muscle). A diagnosis of urothelial carcinoma with villoglandular differentiation with made. Urothelial carcinoma with villoglandular differentiation is a relatively recently described aggressive variant of urothelial carcinoma. Mean patient age at presentation is 70 years (range: 4684 years) with a male predominance (5:1). Other aggressive variants of urothelial carcinoma have also been

HANDLING AND STAGING OF RENAL TUMORS: AN UPDATE FOR A PRACTISING PATHOLOGIST Kiril Trpkov 1Calgary Laboratory Services, and 2University of Calgary, Canada The International Society of Urologic Pathology 2012 Conference on renal cancer discussed the staging and specimen handling of renal tumors. For specimen handling, the initial cut should be made along the long axis. Renal tumors should be sampled 1 block/cm with a minimum of 3 blocks. The length of a renal vein/caval thrombus should not be part of main tumor measurement. In cases with multiple tumors, sampling should include a minimum of 5 largest tumors. Perinephric fat invasion should be determined by examining multiple perpendicular sections of the tumor/perinephric fat interface and by sampling areas suspicious for invasion. Perinephric fat invasion was defined as either the tumor touching the fat or extending as irregular tongues into the perinephric tissue, with or without desmoplasia. Renal sinus invasion is present when the tumor is in direct contact with the sinus fat or the loose connective tissue of the sinus, clearly beyond the renal parenchyma, or if any endothelium-lined space is involved within the renal sinus, regardless of the size. When invasion of the sinus is uncertain, at least 3 blocks of tumor-renal sinus interface should be submitted. If invasion is grossly evident, or obviously not present, only 1 block is needed.

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