Browsing by Author "Sangoi, Ankur R."

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    Low-grade Oncocytic Tumor of Kidney (CD117 Negative, Cytokeratin 7 Positive): A Distinct Entity?
    (Wiley, 2019) Trpkov, Kiril; Williamson, Sean R.; Gao, Yuan; Martinek, Petr; Cheng, Liang; Sangoi, Ankur R.; Yilmaz, Asli; Wang, Cheng; Fraile, Pilar San Miguel; Montiel, Delia M. Perez; Bulimbasić, Stela; Rogala, Joanna; Hes, Ondrej; Pathology and Laboratory Medicine, School of Medicine
    Aim To describe a group of distinct low‐grade oncocytic renal tumors that demonstrate CD117 negative/Cytokeratin (CK) 7 positive immunoprofile. Methods and results We identified 28 such tumors from 4 large renal tumor archives. We performed immunohistochemistry for: CK7, CD117, PAX8, CD10, AMACR, e‐cadherin, CK20, CA9, AE1/AE3, vimentin, BerEP4, MOC31, CK5/6, p63, HMB45, melan A, CD15 and FH. In 14 cases we performed array CGH; in 9 cases with successful result. Median patient age was 66 years (range 49‐78 years) with a male‐to‐female ratio of 1:1.8. Median tumor size was 3 cm (range 1.1‐13.5 cm). All were single tumors, solid and tan‐brown, without a syndromic association. On microscopy, all cases showed solid and compact nested growth. There were frequent areas of edematous stroma with loosely arranged cells. The tumor cells had oncocytic cytoplasm with uniformly round to oval nuclei, but without significant irregularities, and showed only focal perinuclear halos. Negative CD117 and positive CK7 reactivity were present in all cases (in 2 cases there was focal and very weak CD117 reactivity). Uniform reactivity was found for: PAX8, AE1/AE3, e‐cadherin, BerEP4 and MOC31. Negative stains included: CA9, CK20, vimentin, CK5/6, p63, HMB45, Melan A and CD15. CD10 and AMACR were either negative or focally positive; FH was retained. On array CGH, there were frequent deletions at 19p13.3 (7/9), 1p36.33 (5/9) and 19q13.11 (4/9); disomic status was found in 2/9 cases. On follow‐up (mean 31.8 months, range 1‐118), all patients were alive with no disease progression. Conclusion Low‐grade oncocytic tumors that are CD117 negative/CK7positive demonstrate consistent and readily recognizable morphology, immunoprofile, and indolent behavior.
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    Tuberous sclerosis complex: Hamartin and tuberin expression in renal cysts and its discordant expression in renal neoplasms
    (Elsevier, 2016-11) Bonsib, Stephen M.; Boils, Christie; Gokden, Neriman; Grignon, David; Gu, Xin; Higgins, John P. T.; Leroy, Xavier; McKenney, Jesse K.; Nasr, Samih H.; Phillips, Carrie; Sangoi, Ankur R.; Wilson, Jon; Zhang, Ping L.; Department of Pathology and Laboratory Medicine, IU School of Medicine
    Tuberous sclerosis complex (TSC) results from mutation of TSC1 or TSC2 that encode for hamartin and tuberin. It affects the kidneys often in advance of extra-renal stigmata. We studied 14 TSC cases, and 4 possible TSC cases with multiple angiomyolipomas (AMLs) for hamartin and tuberin protein expression to determine if the staining profile could predict mutation status or likelihood of TSC with renal-limited disease. The 18 cases included 15 nephrectomies and 1 section of 6 TSC-associated renal cell carcinomas (RCC). Controls included the non-neoplastic kidney in 5 tumor nephrectomies, 4 sporadic cases of AML and 6 clear cell RCCs. In the 14 TSC cases, 9 had AMLs, 9 had RCCs, 5 had polycystic kidney disease and 8 had eosinophilic cysts (EC) lined by large eosinophilic cells. The controls and study cases showed luminal staining of proximal tubules (PT) and peripheral membrane staining in distal tubules/collecting ducts for hamartin and cytoplasmic staining for tuberin. Eosinophilic cysts had a luminal PT-like stain with hamartin and a cytoplasmic reaction for tuberin. Hamartin stained myoid cells in all AMLs. Tuberin was negative in all but 1AML, an epithelioid AML. All but 1 RCC were positive for tuberin; 13 RCCs (7 TSC/6 non-TSC) were negative for hamartin and 4 showed a weak reaction. We conclude that the ECs of TSC are proximal tubule-derived. The hamartin and tuberin staining profiles of AMLs and most RCCs are reciprocal precluding prediction of the mutation in TSC, and fail to predict if a patient with multifocal AML has TSC.