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24 results on '"Klöppel, G."'

1. ENETS standardized (synoptic) reporting for neuroendocrine tumour pathology

Author

van Velthuysen, M. L. F., Couvelard, A., Rindi, G., Fazio, N., Hörsch, D., Nieveen van Dijkum, E. J., Klöppel, G., Perren, A., van Velthuysen, M. L. F., Couvelard, A., Rindi, G., Fazio, N., Hörsch, D., Nieveen van Dijkum, E. J., Klöppel, G., and Perren, A.

Abstract

In recent years the WHO classification of neuroendocrine neoplasms (NEN) has evolved. Nomenclature as well as thresholds for grading have changed leading to potential confusion and lack of comparability of tumour reports. Therefore, the European Neuroendocrine Tumour Society (ENETS) has set-up an interdisciplinary working group to develop templates for a pathology data set for standardised reporting of NEN. Experts of various disciplines, members of the ENETS Advisory Board, formed a taskforce that discussed and decided on the structure, content and the number of templates needed for reporting the most common NEN. The selection of the required items was based on the WHO classification of digestive system tumours, the WHO classification of tumours of the lung and mediastinum and on “ENETS standard of care” reports. The final proposal of the working group was approved by the ENETS Advisory Board. Templates for synoptic reporting were created for the seven most common NEN primary sites, that is, stomach, duodenum, jejunum-ileum, appendix, colon-rectum, pancreas, lung and mediastinum. In addition, a general template for reporting biopsies was designed. The templates allow the recording of the essential items on differentiation, proliferation (Ki-67 and mitosis), neuroendocrine features (positivity for chromogranin A and synaptophysin) and stage as well as several optional markers especially helpful for the distinction of neuroendocrine tumours (NET) from neuroendocrine carcinomas (NEC). In summary, this paper presents the content and development of synoptic reports for most sites of NEN by a multidisciplinary team of international experts in the field, which could help to improve unambiguous reporting of NEN. © 2022 The Authors. Journal of Neuroendocrinology published by John Wiley & Sons Ltd on behalf of British Society for Neuroendocrinology.

Published
2022

2. Abstracts from the twenty-third meeting of the pancreatic society of Great Britain and Ireland at the Village Hotel, Leeds, UK

Author

Johnson, C., Ammori, BJ, Davides, D., Vezakis, A., Larvin, M., McMahon, KJ, Powell, JJ, Hill, G., Storey, S., Murchison, J., Fearon, K., Ross, J., Siriwardena, AK, Pearce, NW, Smithies, A., Sargen, K., Demaine, A., Kingsnorth, A., Becker, KL, Kite, P., Barclay, GR, Snider, RH, Nylen, ES, White, JC, Martin, IG, McMahon, MJ, Raraty, MGT, Ward, JB, Vaillant, C., Neoptolemos, JP, Sutton, R., Petersen, OH, Creighton, J., Lyall, R., Wilson, D., Curtis, A., Charnley, R., Howes, N., Rutherford, S., McRonald, F., Ellis, I., Whitcomb, D., Mountford, R., Manu, M., Bramhall, SR, Gur, U., Gunson, BK, Le Cornu, KJ, Mayer, AD, Mirza, DF, McMaster, P., Buckets, JAC, King, LJ, Bell, JRG, Healy, J., Amin, Z., Predolac, D., Wotherspoon, A., Thompson, J., Norton, SA, Alderson, D., Kawesha, A., Ghaneh, P., Evans, JD, Campbell, Dawiskiba, S., Lemoine, NR, Andrén-Sandberg, A., Humphreys, M., Greenhalf, W., Stoner, EA, Piotrowicz, AJK, Evans, DF, Ainley, CC, White, SA, Pollard, C., Burden, AC, Clayton, HA, Davies, JE, Swift, SM, Hales, CN, Dennison, AR, London, NJM, Sutton, CD, White, S., Berry, DP, Chillistone, D., Rees, Y., Ammann, R., Heitz, Ph, Klöppel, G., Bimmler, Daniel, Graf, Rolf, Frick, Thomas, Johnson, C., Ammori, BJ, Davides, D., Vezakis, A., Larvin, M., McMahon, KJ, Powell, JJ, Hill, G., Storey, S., Murchison, J., Fearon, K., Ross, J., Siriwardena, AK, Pearce, NW, Smithies, A., Sargen, K., Demaine, A., Kingsnorth, A., Becker, KL, Kite, P., Barclay, GR, Snider, RH, Nylen, ES, White, JC, Martin, IG, McMahon, MJ, Raraty, MGT, Ward, JB, Vaillant, C., Neoptolemos, JP, Sutton, R., Petersen, OH, Creighton, J., Lyall, R., Wilson, D., Curtis, A., Charnley, R., Howes, N., Rutherford, S., McRonald, F., Ellis, I., Whitcomb, D., Mountford, R., Manu, M., Bramhall, SR, Gur, U., Gunson, BK, Le Cornu, KJ, Mayer, AD, Mirza, DF, McMaster, P., Buckets, JAC, King, LJ, Bell, JRG, Healy, J., Amin, Z., Predolac, D., Wotherspoon, A., Thompson, J., Norton, SA, Alderson, D., Kawesha, A., Ghaneh, P., Evans, JD, Campbell, Dawiskiba, S., Lemoine, NR, Andrén-Sandberg, A., Humphreys, M., Greenhalf, W., Stoner, EA, Piotrowicz, AJK, Evans, DF, Ainley, CC, White, SA, Pollard, C., Burden, AC, Clayton, HA, Davies, JE, Swift, SM, Hales, CN, Dennison, AR, London, NJM, Sutton, CD, White, S., Berry, DP, Chillistone, D., Rees, Y., Ammann, R., Heitz, Ph, Klöppel, G., Bimmler, Daniel, Graf, Rolf, and Frick, Thomas

Published
2018

5. Nierentumoren im Erwachsenenalter

Author

Amann, Kerstin, Kain, Renate, Klöppel, Günter, Amann, K ( Kerstin ), Kain, R ( Renate ), Klöppel, G ( Günter ), Störkel, Stephan, Wild, Peter J, Moch, Holger, Amann, Kerstin, Kain, Renate, Klöppel, Günter, Amann, K ( Kerstin ), Kain, R ( Renate ), Klöppel, G ( Günter ), Störkel, Stephan, Wild, Peter J, and Moch, Holger

Published
2016

6. Consensus Guidelines Update for the Management of Functional p-NETs (F-p-NETs) and Non-Functional p-NETs (NF-p-NETs).

Author

Rindi, Guido, Falconi, M, Eriksson, B, Kaltsas, G, Bartsch, Dk, Capdevila, J, Caplin, M, Kos Kudla, B, Kwekkeboom, D, Klöppel, G, Reed, N, Kianmanesh, R, Jensen, Rt, Rindi, Guido (ORCID:0000-0003-2996-4404), Rindi, Guido, Falconi, M, Eriksson, B, Kaltsas, G, Bartsch, Dk, Capdevila, J, Caplin, M, Kos Kudla, B, Kwekkeboom, D, Klöppel, G, Reed, N, Kianmanesh, R, Jensen, Rt, and Rindi, Guido (ORCID:0000-0003-2996-4404)

Abstract

Consensus Guidelines Update for the Management of Functional p-NETs (F-p-NETs) and Non-Functional p-NETs (NF-p-NETs).

Published
2016

11. ENETS Consensus Guidelines for the Standards of Care in Neuroendocrine Tumors : Radiological Examinations

Author

Sundin, Anders, Vullierme, Marie-Pierre, Kaltsas, Gregory, Plöckinger, Ursula, Åkerström, Göran, Annibale, B., Arnold, R., Bajetta, E., Barkmanova, J., Chen, Y.J., Costa, F., Couvelard, A., Davar, J., de Herder, W., Delle, G., Eriksson, Barbro, Falconi, M., Ferone, D., Gross, D., Grossman, A., Gustafsson, B., Hyrdel, R., Ivan, D., Kianmanesh, R., Klöppel, G., Knigge, U.P., Komminoth, P., Kos-Kudla, B., Kwekkeboom, D., Lebtahi, R., Lewington, V., McNicol, A.M., Mitry, E., Nilsson, O., Öberg, Kjell, O´Connor, J., O´Toole, D., Pape, U.F., Papotti, M., Pavel, M., Perren, A., Platania, M., Rindi, G., Ruszniewski, P., Salazar, R., Scarpa, A., Scheidhauer, K., Scoazec, J.Y., Szpak, W., Taal, B., Vitek, P., Wiedenmann, B., Sundin, Anders, Vullierme, Marie-Pierre, Kaltsas, Gregory, Plöckinger, Ursula, Åkerström, Göran, Annibale, B., Arnold, R., Bajetta, E., Barkmanova, J., Chen, Y.J., Costa, F., Couvelard, A., Davar, J., de Herder, W., Delle, G., Eriksson, Barbro, Falconi, M., Ferone, D., Gross, D., Grossman, A., Gustafsson, B., Hyrdel, R., Ivan, D., Kianmanesh, R., Klöppel, G., Knigge, U.P., Komminoth, P., Kos-Kudla, B., Kwekkeboom, D., Lebtahi, R., Lewington, V., McNicol, A.M., Mitry, E., Nilsson, O., Öberg, Kjell, O´Connor, J., O´Toole, D., Pape, U.F., Papotti, M., Pavel, M., Perren, A., Platania, M., Rindi, G., Ruszniewski, P., Salazar, R., Scarpa, A., Scheidhauer, K., Scoazec, J.Y., Szpak, W., Taal, B., Vitek, P., and Wiedenmann, B.

Published
2009
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12. VHL inactivation is an important pathway for the development of malignant sporadic pancreatic endocrine tumors

Author

Schmitt, A M, Schmid, S, Rudolph, T, Anlauf, M, Prinz, C, Klöppel, G, Moch, H, Heitz, P U, Komminoth, P, Perren, A, Schmitt, A M, Schmid, S, Rudolph, T, Anlauf, M, Prinz, C, Klöppel, G, Moch, H, Heitz, P U, Komminoth, P, and Perren, A

Abstract

A small subset of familial pancreatic endocrine tumors (PET) arises in patients with von Hippel-Lindau syndrome and these tumors may have an adverse outcome compared to other familial PET. Sporadic PET rarely harbors somatic VHL mutations, but the chromosomal location of the VHL gene is frequently deleted in sporadic PET. A subset of sporadic PET shows active hypoxia signals on mRNA and protein level. To identify the frequency of functionally relevant VHL inactivation in sporadic PET and to examine a possible prognostic significance we correlated epigenetic and genetic VHL alterations with hypoxia signals. VHL mutations were absent in all 37 PETs examined. In 2 out of 35 informative PET (6%) methylation of the VHL promoter region was detected and VHL deletion by fluorescence in situ hybridization was found in 14 out of 79 PET (18%). Hypoxia inducible factor 1alpha (HIF1-alpha), carbonic anhydrase 9 (CA-9), and glucose transporter 1 (GLUT-1) protein was expressed in 19, 27, and 30% of the 152 PETs examined. Protein expression of the HIF1-alpha downstream target CA-9 correlated significantly with the expression of CA-9 RNA (P<0.001), VHL RNA (P<0.05), and VHL deletion (P<0.001) as well as with HIF1-alpha (P<0.005) and GLUT-1 immunohistochemistry (P<0.001). These PET with VHL alterations and signs of hypoxia signalling were characterized by a significantly shortened disease-free survival. We conclude that VHL gene impairment by promoter methylation and VHL deletion in nearly 25% of PET leads to the activation of the HIF-pathway. Our data suggest that VHL inactivation and consecutive hypoxia signals may be a mechanism for the development of sporadic PET with an adverse outcome.

Published
2009

15. Stoffwechselerkrankungen

Author

Böcker, W, Denk, H, Heitz, P U, Moch, H, Böcker, W ( W ), Denk, H ( H ), Heitz, P U ( P U ), Moch, H ( H ), Stallmach, T, Klöppel, G, Roth, J, Spinas, G A, Böcker, W, Denk, H, Heitz, P U, Moch, H, Böcker, W ( W ), Denk, H ( H ), Heitz, P U ( P U ), Moch, H ( H ), Stallmach, T, Klöppel, G, Roth, J, and Spinas, G A

Abstract

Die Pathologie ist die Basis für das Verständnis der Medizin. Der "Böcker" zeigt Ihnen die Zusammenhänge zwischen Krankheit und Klinik. Dabei sind Vollständigkeit, Aktualität und wissenschaftliche Genauigkeit oberstes Gebot.Die für das POL wichtigen klinisch-pathologischen Wechselbeziehungen sind so umfassend dargestellt, dass Sie die in der neuen AO gewünschten interdisziplinären Zusammenhänge problemlos erlernen.Während des Studiums der klinischen Fächer werden Sie hier immer wieder nachschlagen.Besonders praktisch:- Fragen zu Differentialdiagnosen- Ausführliches Glossar mit wichtigen Fachbegriffen- Ausführliche Beschreibung der Bildbefunde- Inkl. Pocketcard für die Kitteltasche (TNM-KLassifikation, Tumorpathologie, Färbungen)- Jetzt mit Internet-Zugang über StudentConsult: alle Inhalte und Abbildungen online VorwortI. Grundlagen1 Pathologie: Aufgaben und Methoden2 Zell- und Gewebsreaktion3 Immunreaktionen4 Entzündung5 Genetische Mechanismen6 Tumorerkrankungen7 KreislauferkrankungenII. Spezielle PathologieNervensystem8 Zentrales Nervensystem9 Peripheres Nervensystem10 SkelettmuskulaturSinnesorgane11 Auge12 OhrNeuroendokrines SystemZwischenkapitel Neuroendokrines System13 Hypophyse14 Schilddrüse15 Nebenschilddrüsen16 Nebennieren17 Disseminiertes neuroendokrines System18 Polyglanduläre Störungen Kardiovaskuläres System19 Herz20 GefäßeZwischenkapitel Blut, Knochenmark und lymphatisches System21 Blut und Knochenmark22 Lymphatisches SystemRespirationstrakt23 Obere Atemwege24 Lunge25 PleuraVerdauungstrakt26 Mundhöhle, Zähne und Speicheldrüsen27 Ösophagus28 Magen und Duodenum29 Jejunum und Ileum30 Appendix31 Kolon und Rektum32 Leber und intrahepatische Gallenwege33 Gallenblase und extra-hepatische Gallenwege34 Pankreas35 PeritoneumUrogenitaltrakt36 Niere37 Ableitende Harnwege38 Männliche Geschlechtsorgane39 Weibliche Geschlechtsorgane40 Schwangerschaft, Fetalperiode und KindesalterMamma und Haut41 Mamma42 HautStütz- und Bewegungsapparat43 Knochen und Knorpel44 Gelenke45

Published
2008

16. Allelic deletion of the MEN1 gene in duodenal gastrin and somatostatin cell neoplasms and their precursor lesions.

Author

Anlauf, M, Perren, A, Henopp, T, Rudolf, T, Garbrecht, N, Schmitt, A, Raffel, A, Gimm, O, Weihe, E, Knoefel, W T, Dralle, H, Heitz, Ph U, Komminoth, P, Klöppel, G, Anlauf, M, Perren, A, Henopp, T, Rudolf, T, Garbrecht, N, Schmitt, A, Raffel, A, Gimm, O, Weihe, E, Knoefel, W T, Dralle, H, Heitz, Ph U, Komminoth, P, and Klöppel, G

Abstract

BACKGROUND: Patients with a multiple endocrine neoplasia type 1 (MEN1)-associated Zollinger-Ellison syndrome (ZES) show multifocal duodenal gastrinomas and precursor lesions. AIMS: To test these lesions for loss of heterozygosity (LOH) of the MEN1 gene locus on chromosome 11q13, and to investigate whether the MEN1-related endocrine cell changes also involved somatostatin cells. MATERIAL AND METHODS: Tissue specimens from six patients with MEN1 and ZES were analysed by immunohistochemistry and immunofluorescence. LOH analysis was performed by fluorescence in situ hybridisation (FISH), using probes containing the MEN1 gene locus and the centromere 11 (C11) region. For simultaneous analysis of hormones and allelic deletions, a combined FISH/immunofluorescence protocol was established. RESULTS: 28 of a total of 33 duodenal neuroendocrine tumours (NETs) were gastrin-producing tumours; 13/28 (46.4%) revealed LOH on 11q13 and/or C11. Five of the NETs were somatostatin-expressing tumours, two revealing LOH. Allelic loss was detected in tumours as small as 300 microm (gastrin) and 400 microm (somatostatin) in diameter. The gastrin-producing tumours showed different deletion/retention patterns. Hyperplastic somatostatin cell lesions, similar to those of the gastrin cells, were present in all patients. The hyperplastic lesions of both cell lines consistently retained both 11q13 alleles. CONCLUSIONS: Allelic deletion of the MEN1 gene may reflect a pivotal event in the development of multifocal gastrin and somatostatin cell neoplasms in the duodenum of patients with MEN1. The observation of distinct deletion patterns in small synchronous tumours supports the concept that each gastrin-producing tumour in an individual MEN1 patient arises from an independent cell clone.

Published
2007
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18. ADAM9 als prognostischer Marker beim human duktalen Pankreaskarzinom

Author

Grützmann, R, Lüttges, J, Alldinger, I, Kersting, S, Ammerpohl, O, Schackert, HK, Saeger, HD, Klöppel, G, Pilarsky, CH, Grützmann, R, Lüttges, J, Alldinger, I, Kersting, S, Ammerpohl, O, Schackert, HK, Saeger, HD, Klöppel, G, and Pilarsky, CH

Published
2004

19. ADAM9 als prognostischer Marker beim human duktalen Pankreaskarzinom

Author

Grützmann, R, Lüttges, J, Alldinger, I, Kersting, S, Ammerpohl, O, Schackert, HK, Saeger, HD, Klöppel, G, Pilarsky, CH, Grützmann, R, Lüttges, J, Alldinger, I, Kersting, S, Ammerpohl, O, Schackert, HK, Saeger, HD, Klöppel, G, and Pilarsky, CH

Published
2004

21. Insuffisance hépatocellulaire fulminante ou subfulminante secondaire à une infiltration métastatique du foie: une autre cause d'hépatite hypoxique?

Author

UCL - MD/MINT - Département de médecine interne, UCL - MD/CHIR - Département de chirurgie, UCL - MD/MNOP - Département de morphologie normale et pathologique, Henrion, J., Hautekeete, M, Brenard, R., Schapira, M., Somers, G, Geubel, André, Schmitz, Ann, Gerard, R., Rahier, Jacques, Hoorens, A, Klöppel, G, UCL - MD/MINT - Département de médecine interne, UCL - MD/CHIR - Département de chirurgie, UCL - MD/MNOP - Département de morphologie normale et pathologique, Henrion, J., Hautekeete, M, Brenard, R., Schapira, M., Somers, G, Geubel, André, Schmitz, Ann, Gerard, R., Rahier, Jacques, Hoorens, A, and Klöppel, G

Abstract

OBJECTIVES: The purpose of this retrospective study was to report a series of 9 new cases of fulminant hepatic failure due to metastatic liver disease and to identify signs to support a theory of hypoxia. METHODS: In these 9 cases and in 38 previously published cases of fulminant or subfulminant liver failure, we looked for clinical (shock, sepsis, and cutaneous signs of circulatory failure), laboratory (marked increase in serum aminotransferases levels) and histological (cell necrosis) parameters compatible with liver hypoxia. RESULTS: Cutaneous signs of circulatory failure or shock were observed in 3 of the 9 cases in this study, and were not due to cardiogenic or septic shock. A marked increase in serum aminotransferases levels, 10 times above the upper limit of normal, was observed in 8 of the 9 cases in the present study and in 23 of 37 cases of the literature. Liver cell necrosis was observed in 6 of the 7 autopsied patients in this series and in 20 of 34 cases in the literature. Generally, liver cell necrosis was more severe than tumor cell necrosis and was related to the degree of sinusoidal involvement by tumoral cells. In one case, hepatic blood flow was decreased despite a high level of cardiac blood flow suggesting impairment of circulation in the liver. CONCLUSIONS: These 9 cases and a review of the literature support the hypothesis of hypoxic liver cell necrosis leading to acute liver failure in cases of metastatic liver disease. However, liver hypoxia cannot explain all the reported cases and was never due to circulatory failure from cardiac or septic causes, but to the sinusoidal involvement by tumor cells.

Published
1996

22. Internalization of Glimepiride and Glibenclamide in the Pancreatic B-cell

Author

UCL - AGRO/MILA - Département des sciences du milieu et de l'aménagement du territoire, Marynissen, G., Smets, G., Klöppel, G., Gerlache, Louis, Malaisse, Willy, UCL - AGRO/MILA - Département des sciences du milieu et de l'aménagement du territoire, Marynissen, G., Smets, G., Klöppel, G., Gerlache, Louis, and Malaisse, Willy

Abstract

When rat pancreatic islets were exposed for 30 min at 37-degrees-C to tritiated glibenclamide (2.5 muM) or glimepiride (1.5 muM), internalization of these hypoglycaemic sulphonylureas in B and non-B cells was observed by autoradiography. In the B cell, the autoradiographic grains were often associated with secretory granules.

Published
1992

24. Abstracts from the twenty-third meeting of the pancreatic society of Great Britain and Ireland at the Village Hotel, Leeds, UK

Author

Johnson, C., Ammori, BJ, Davides, D., Vezakis, A., Larvin, M., McMahon, KJ, Powell, JJ, Hill, G., Storey, S., Murchison, J., Fearon, K., Ross, J., Siriwardena, AK, Pearce, NW, Smithies, A., Sargen, K., Demaine, A., Kingsnorth, A., Becker, KL, Kite, P., Barclay, GR, Snider, RH, Nylen, ES, White, JC, Martin, IG, McMahon, MJ, Raraty, MGT, Ward, JB, Vaillant, C., Neoptolemos, JP, Sutton, R., Petersen, OH, Creighton, J., Lyall, R., Wilson, D., Curtis, A., Charnley, R., Howes, N., Rutherford, S., McRonald, F., Ellis, I., Whitcomb, D., Mountford, R., Manu, M., Bramhall, SR, Gur, U., Gunson, BK, Le Cornu, KJ, Mayer, AD, Mirza, DF, McMaster, P., Buckets, JAC, King, LJ, Bell, JRG, Healy, J., Amin, Z., Predolac, D., Wotherspoon, A., Thompson, J., Norton, SA, Alderson, D., Kawesha, A., Ghaneh, P., Evans, JD, Campbell, Dawiskiba, S., Lemoine, NR, Andrén-Sandberg, A., Humphreys, M., Greenhalf, W., Stoner, EA, Piotrowicz, AJK, Evans, DF, Ainley, CC, White, SA, Pollard, C., Burden, AC, Clayton, HA, Davies, JE, Swift, SM, Hales, CN, Dennison, AR, London, NJM, Sutton, CD, White, S., Berry, DP, Chillistone, D., Rees, Y., Ammann, R., Heitz, Ph, Klöppel, G., Bimmler, Daniel, Graf, Rolf, Frick, Thomas, Johnson, C., Ammori, BJ, Davides, D., Vezakis, A., Larvin, M., McMahon, KJ, Powell, JJ, Hill, G., Storey, S., Murchison, J., Fearon, K., Ross, J., Siriwardena, AK, Pearce, NW, Smithies, A., Sargen, K., Demaine, A., Kingsnorth, A., Becker, KL, Kite, P., Barclay, GR, Snider, RH, Nylen, ES, White, JC, Martin, IG, McMahon, MJ, Raraty, MGT, Ward, JB, Vaillant, C., Neoptolemos, JP, Sutton, R., Petersen, OH, Creighton, J., Lyall, R., Wilson, D., Curtis, A., Charnley, R., Howes, N., Rutherford, S., McRonald, F., Ellis, I., Whitcomb, D., Mountford, R., Manu, M., Bramhall, SR, Gur, U., Gunson, BK, Le Cornu, KJ, Mayer, AD, Mirza, DF, McMaster, P., Buckets, JAC, King, LJ, Bell, JRG, Healy, J., Amin, Z., Predolac, D., Wotherspoon, A., Thompson, J., Norton, SA, Alderson, D., Kawesha, A., Ghaneh, P., Evans, JD, Campbell, Dawiskiba, S., Lemoine, NR, Andrén-Sandberg, A., Humphreys, M., Greenhalf, W., Stoner, EA, Piotrowicz, AJK, Evans, DF, Ainley, CC, White, SA, Pollard, C., Burden, AC, Clayton, HA, Davies, JE, Swift, SM, Hales, CN, Dennison, AR, London, NJM, Sutton, CD, White, S., Berry, DP, Chillistone, D., Rees, Y., Ammann, R., Heitz, Ph, Klöppel, G., Bimmler, Daniel, Graf, Rolf, and Frick, Thomas

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