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Biomedical subjects

A Hoorens

Publications and source records attributed to A Hoorens.

23 records · Page 2Linked to original sources
PubMed1994

Pancreatoblastoma in an adult: its separation from acinar cell carcinoma.

Pancreatoblastomas are rare tumours, which usually occur in childhood. Here we describe a pancreatoblastoma in a 39-year-old woman. The tumour was located in the tail of the pancreas and consisted of cells forming well-differentiated acinar structures and scattered solid components ("squamoid corpuscles"). Immunocytochemically, the acinar components were positive for pancreatic enzymes and pancreatic stone protein, while the cells of the "squamoid corpuscles" lacked these markers. There was no p53 overexpression nor any mutation at codon 12 of the Ki-ras oncogene. The main differential diagnosis of this tumour was acinar cell carcinoma, because both tumours have a number of features in common (scattered solid components, positivity for pancreatic enzymes, lack of p53 overexpression and of Ki-ras mutation). Findings which distinguished the pancreatoblastoma and separated it from acinar cell carcinoma were the negativity of the solid components ("squamoid corpuscles") for neuroendocrine markers and their very weak keratin positivity. As the patient is alive and well 30 months after tumour resection, this pancreatoblastoma also differs in biology from the usual acinar cell carcinoma.

Adult↗
PubMed1993

Pancreatic acinar cell carcinoma. An analysis of cell lineage markers, p53 expression, and Ki-ras mutation.

In a series of 22 pancreatic acinar cell carcinomas, including two acinar cystadenocarcinomas, cellular differentiation was analyzed by immunocytochemistry and electron microscopy. In addition, overexpression of p53 protein and Ki-ras codon 12 mutation was studied. Four of the 20 noncystic acinar cell carcinomas showed a pure acinar pattern, nine an acinar-solid, and seven a solid pattern. All tumors stained for at least one of the following pancreatic acinar markers: trypsin (21 of 22), lipase (19 of 22), chymotrypsin (13 of 22), phospholipase A2 (nine of 22), and pancreatic stone protein (19 of 22). One-third of the tumors expressed neuroendocrine markers (synaptophysin, eight of 22; chromogranin A, six of 21) and duct cell markers (CA19.9, nine of 21; B72.3, six of 21). Cellular coexpression of trypsin and synaptophysin was demonstrated in one tumor. Electron microscopy revealed zymogen granules (nine of nine). In only one of 16 tumors a Ki-ras mutation at codon 12 was found, whereas in none of 19 tumors could overexpression of p53 protein be demonstrated. The results suggest that acinar cell carcinomas show obvious capacity to differentiate into several directions, but nevertheless constitute an entity different from ductal adenocarcinomas or endocrine tumors.

Adolescent↗
PubMed1992

Pseudotuberculous pyelonephritis associated with nephrolithiasis.

This report describes a 40-year-old man with an unusual form of granulomatous pyelonephritis, associated with nephrolithiasis, resulting in end-stage kidney disease and right pretransplant nephrectomy. The kidney specimen contained a staghorn calculus and showed chronic inflammation with confluent caseating granulomas and multinucleated giant cells, resembling renal tuberculosis. However, neither tubercle bacilli nor other microorganisms were demonstrated in the renal tissue or in urine cultures. Because these findings do not support a tuberculous etiology of the granulomatous pyelonephritis, we conclude that this patient had a pseudotuberculous reaction as a consequence of nephrolithiasis.

Adult↗
PubMed1991

Transplantation of purified islet cells in diabetic BB rats.

The ability to prepare purified islet Beta-cell aggregates was used to examine the survival of this cell type after allotransplantation in diabetic BB rats. The aggregates were intraportally implanted in numbers that were previously found to correct a streptozotocin-induced diabetic state in syngeneic or allogeneic Brown Norway recipients. When the grafts were prepared from RT1u/l donors, which shared the MHC-class I antigen with the BB recipients (RT1u/u), their implant sites became diffusely infiltrated by inflammatory cells and their metabolic function was completely lost within 5 weeks. MHC-class I incompatible islet Beta-cell allografts (RT1n/n) exhibited a longer survival, in particular when combined with other islet endocrine cells and/or when covered by a 5-week cyclosporin treatment. In the latter combination, 10 of 12 BB rat recipients remained normoglycaemic over the 10-week observation period, their liver implants presenting a comparable insulin reserve and similarly discrete mononuclear cell infiltration as streptozotocin-diabetic Brown Norway rats receiving this treatment. However, administration of cyclosporin to diabetic BB rats was associated with a morbidity that was not observed in drug-treated streptozotocin-diabetic Brown Norway animals or in untreated diabetic BB rats. It is concluded that MHC-incompatible islet Beta cells can induce a long-term normalization in diabetic BB rats provided that they are implanted under conditions which allow allograft acceptance. The standardized preparation of purified islet Beta-cell grafts can help assessing the conditions for successful transplantations in diabetes with an autoimmune origin.

Animals↗