Expression of erythropoietin and neuroendocrine markers in clear cell renal cell carcinoma

Abstract

Mjønes PG, Nordrum IS, Qvigstad G, Sørdal Ø, Rian LLM, Waldum HL. Expression of erythropoietin and neuroendocrine markers in clear cell renal cell carcinoma. APMIS 2017; 125: 213-222.The aim of the study was to investigate the expression of erythropoietin and neuroendocrine markers in clear cell renal cell carcinoma (CCRCC). We retrospectively reviewed the medical records and re-evaluated histopathological specimens of 33 patients with CCRCC and compared with those of 11 cases of non-CCRCC. All patients were treated with a partial or radical nephrectomy at St. Olavs Hospital, Trondheim University Hospital, between 2010 and 2016. Thirty-three patients who were diagnosed with CCRCC had a total of 35 tumours, where 34 of the tumours were CCRCC and one was papillary adenoma. Thirty-three (97%) of 34 CCRCCs were positive for erythropoietin, and the same 33 (97%) tumours demonstrated strong expression for neuron-specific enolase (NSE). Two (6%) of 34 CCRCCs had a positive reaction for synaptophysin, and three (9%) of 34 were positive for CD56. Erythropoietin and NSE were negative in non-CCRCCs, and chromogranin A was negative in all tumours. The above findings suggest that there is a strong association between CCRCC and the expression of erythropoietin and NSE.

Neuron-Specific Enolase as an Immunohistochemical Marker Is Better Than Its Reputation

“…In a recent study, we found almost all CCRCCs to express NSE, and the same tumors also expressed the hormone erythropoietin normally produced by the kidneys. 20 A number of tumors which in the past have been considered not to be of NE origin have, with improved antibodies and detection systems, displayed NE differentiation within the tumor tissue. 37 Interestingly, the carcinomas of the stomach with focal NSE expression also expressed one or more other NE markers in the same areas, thus supporting the finding of NE differentiation in these tumors.…”

“…Tumor tissue from 178 patients who were surgically treated for tumors of the breast, lung, stomach, or kidney at St. Olav’s Hospital—Trondheim University Hospital between 1995 and 2016 were included in the study. The patients were identified from previous studies 20 , 21 and by going through our records at the pathology and gastroenterology departments. To limit the study, only four tumor locations were evaluated, and the selection criteria were as follows: Various types of carcinomas and NENs from breast, lung, stomach, and kidney that were available in the archives at the pathology or gastroenterology departments were included in the study.…”

“…Carcinomas of the breast, lung, and stomach are known to occasionally express NE markers, and we wanted to see whether the same areas expressing other NE markers also expressed NSE. All 45 patients with kidney cancer were identified from a previous study, 20 and included cases of clear cell renal cell carcinoma (CCRCC), papillary renal cell carcinoma (PRCC) type 1 and type 2, and chromophobe renal cell carcinoma (chRCC). The renal cell carcinomas (RCCs) were already explored with markers against CgA, synaptophysin, NSE, and erythropoietin, and not repeated in this study.…”

Expression of the Cholecystokinin-B Receptor in Neoplastic Gastric Cells

“…IHC was performed as described previously with a few minor modifications [ 25 ]. For this study, the following antibodies were used: chromogranin A (M0869, Dako, Glostrup, Denmark, 1:200), Synaptophysin (M7315, Dako, 1:200) , CCKBR (PA5-33389, Thermo Fischer Scientific, Rockford, USA, 1:250), Pepsinogen II (Ab9013-1; Abcam, Cambridge, UK, 1:1000), and HKATPase (MA3-923; Affinity Bioreagents, Golden, CO, USA, 1:1500).…”

Correct Identification of Cell of Origin May Explain Many Aspects of Cancer: The Role of Neuroendocrine Cells as Exemplified from the Stomach

“…Moreover, the central role of gastrin is demonstrated by the fact that the most important cause of gastric cancer, Helicobacter pylori infection, predisposes to gastric cancer only after having induced oxyntic atrophy [39], which necessarily leads to hypergastrinemia. In fact, the pathogenetic mechanism for the carcinogenic effect of Helicobacter pylori gastritis may be hypergastrinemia [40]. Two years ago, the first report of increased occurrence of gastric carcinomas in patients using proton pump inhibitors (PPIs) compared with those stopping such treatment after Helicobacter pylori eradication, was published [41].…”