Search

Your search keyword '"Offerhaus, G.J.A"' showing total 295 results
Start Over Author "Offerhaus, G.J.A"
295 results on '"Offerhaus, G.J.A"'

2. Impact of classical and basal-like molecular subtypes on overall survival in resected pancreatic cancer in the SPACIOUS-2 multicentre study

Author

Suurmeijer, J.A., Soer, E.C., Dings, M.P.G., Kim, Y., Strijker, M., Bonsing, B.A., Brosens, L.A.A., Busch, O.R., Groen, J.V., Halfwerk, J.B.G., Slooff, R.A.E., Laarhoven, H.W.M. van, Molenaar, I.Q., Offerhaus, G.J.A., Morreau, J., Vijver, M.J. van de, Sarasqueta, A.F., Verheij, J., Besselink, M.G., Bijlsma, M.F., Dijk, F., Dutch Pancreatic Cancer Grp, Graduate School, Surgery, CCA - Cancer Treatment and Quality of Life, AGEM - Amsterdam Gastroenterology Endocrinology Metabolism, Pathology, CCA - Imaging and biomarkers, Center of Experimental and Molecular Medicine, and CCA - Cancer Treatment and quality of life

Subjects
Pancreatic Neoplasms, Humans, Regression Analysis, Surgery, Prognosis
Abstract

Background The recently identified classical and basal-like molecular subtypes of pancreatic cancer impact on overall survival (OS). However, the added value of routine subtyping in both clinical practice and randomized trials is still unclear, as most studies do not consider clinicopathological parameters. This study examined the clinical prognostic value of molecular subtyping in patients with resected pancreatic cancer. Methods Subtypes were determined on fresh-frozen resected pancreatic cancer samples from three Dutch centres using the Purity Independent Subtyping of Tumours classification. Patient, treatment, and histopathological variables were compared between subtypes. The prognostic value of subtyping in (simulated) pre- and postoperative settings was assessed using Kaplan–Meier and Cox regression analyses. Results Of 199 patients with resected pancreatic cancer, 164 (82.4 per cent) were classified as the classical and 35 (17.6 per cent) as the basal-like subtype. Patients with a basal-like subtype had worse OS (11 versus 16 months (HR 1.49, 95 per cent c.i. 1.03 to 2.15; P = 0.035)) than patients with a classical subtype. In multivariable Cox regression analysis, including only clinical variables, the basal-like subtype was a statistically significant predictor for poor OS (HR 1.61, 95 per cent c.i. 1.11 to 2.34; P = 0.013). When histopathological variables were added to this model, the prognostic value of subtyping decreased (HR 1.49, 95 per cent c.i. 1.01 to 2.19; P = 0.045). Conclusion The basal-like subtype was associated with worse OS in patients with resected pancreatic cancer. Adding molecular classification to inform on tumor biology may be used in patient stratification.

Published
2022
Full Text
View/download PDF

7. The serrated polyp: getting it right!

Author

Ensari, A., Bosman, F.T., and Offerhaus, G.J.A.

Subjects
Colorectal cancer -- Diagnosis, Colorectal cancer -- Genetic aspects, Polyps (Pathology) -- Genetic aspects, Gene expression -- Analysis, Health, World Health Organization -- Powers and duties
Published
2010

9. Large genomic deletions of SMAD4, BMPR1A and PTEN in juvenile polyposis

Author

van Hattem, W.A., Brosens, L.A.A., de Leng, W.W.J., Morsink, F.H., Lens, S., Carvalho, R., Giardiello, F.M., and Offerhaus, G.J.A.

Subjects
Polyposis, Familial -- Genetic aspects, Polyposis, Familial -- Development and progression, Chromosome deletion -- Analysis, Chromosome deletion -- Research, Health
Published
2008

11. Associations of non-pedunculated T1 colorectal adenocarcinoma outcome with consensus molecular subtypes, immunoscore, and microsatellite status: a multicenter case-cohort study

Author

Haasnoot, K.J.C., Backes, Y., Moons, L.M.G., Kranenburg, O., Trinh, A., Vermeulen, L., Noe, M., Tuynman, J.B., Lent, A.U.G. van, Ginneken, R. van, Seldenrijk, C.A., Raicu, M.G., Trumpi, K., Ubink, I., Milne, A.N., Boonstra, J.J., Groen, J.N., Schwartz, M.P., Wolfhagen, F.H.J., Geesing, J.M.J., Borg, F. ter, Brosens, L.A.A., Bergeijk, J. van, Spanier, B.W.M., Cappel, W.H.D.T.N., Kessels, K., Seerden, T.C.J., Vleggaar, F.P., Offerhaus, G.J.A., Siersema, P.D., Elias, S.G., Lacle, M.M., Dutch T1 CRC Working Grp, Internal medicine, Amsterdam Gastroenterology Endocrinology Metabolism, Surgery, and CCA - Cancer biology and immunology

Subjects
Male, 0301 basic medicine, Oncology, medicine.medical_specialty, Pathology, Time Factors, Adenocarcinoma, Lower risk, Pathology and Forensic Medicine, 03 medical and health sciences, Tumours of the digestive tract Radboud Institute for Health Sciences [Radboudumc 14], 0302 clinical medicine, Predictive Value of Tests, Internal medicine, Biomarkers, Tumor, medicine, Tumours of the digestive tract Radboud Institute for Molecular Life Sciences [Radboudumc 14], Humans, Genetic Predisposition to Disease, Colorectal adenocarcinoma, Lymph node, Aged, Neoplasm Staging, Netherlands, Tissue microarray, business.industry, Hazard ratio, Microsatellite instability, Middle Aged, medicine.disease, Immunohistochemistry, digestive system diseases, DNA Repair Enzymes, Phenotype, Treatment Outcome, 030104 developmental biology, medicine.anatomical_structure, Tissue Array Analysis, Case-Control Studies, 030220 oncology & carcinogenesis, Microsatellite, Female, Microsatellite Instability, Neoplasm Recurrence, Local, Colorectal Neoplasms, business, Cohort study
Abstract

Contains fulltext : 229364.pdf (Publisher’s version ) (Closed access) Advanced colorectal cancer (CRC) consensus molecular subtype 4 (CMS4) or CRC with a low immunoscore is associated with shorter survival times. Non-metastatic CRC with microsatellite instability (MSI) is associated with a lower risk of recurrence. We evaluated outcome (lymph node metastases [LNM] or cancer recurrence) in these tumor subtypes in patients with surgically-removed non-pedunculated T1 CRC by performing a multicenter case-cohort study. We included all patients in 13 hospitals in the Netherlands from 2000-2014 (n = 651). We randomly selected a subgroup of patients (n = 223) and all patients with LNM or recurrence (n = 63), and median follow-up of 44 months. We centrally reviewed tumor-slides, and constructed and immunostained tissue microarrays determining MSI, CMS (MSI/CMS1, CMS2/3, or CMS4), and immunoscore (I-low/I-high). We used weighted Cox proportional hazard models to evaluate the association of MSI, CMS, and immunoscore with LNM or recurrence, adjusting for conventional histologic risk factors. In the randomly selected subgroup of patients, 7.1% of tumors were MSI/CMS1, 91.0% CMS2/3, 1.8% CMS4, and 25% I-low. In the case-cohort, patients with CMS4 tumors had an increased risk for LNM or recurrence compared with patients with tumors of other CMSs (adjusted hazard ratio [HR], 3.97; 95% CI, 1.12-14.06; P = 0.03). Albeit not significant, tumors with MSI had a lower risk for LNM or recurrence than other tumor subtypes (adjusted HR, 0.52; 95% CI, 0.12-2.30; P = 0.39), whereas tumors with a low immunoscore had an increased risk for LNM or recurrence (adjusted HR, 1.30; 95% CI, 0.68-2.48; P = 0.43). In conclusion, in a case-cohort study of patients with non-pedunculated T1 CRC, MSI, and immunoscore were not significantly associated with adverse outcome after surgery. CMS4 substantially increased the risk of adverse outcome. However, CMS4 is rare in T1 CRCs, limiting its value for determining the risk in patients.

Published
2020
Full Text
View/download PDF

12. Significant variation in histopathological assessment of endoscopic resections for Barrett's neoplasia suggests need for consensus reporting: propositions for improvement

Author

Wel, M.J.C. van der, Klaver, E., Pouw, R.E., Brosens, L.A.A., Biermann, K., Doukas, M., Huysentruyt, C., Karrenbeld, A., Kate, F.J. ten, Kats-Ugurlu, G., Laan, J. van der, Lijnschoten, I. Van, Moll, F.C.P., Offerhaus, G.J.A., Ooms, A., Seldenrijk, C.A., Visser, M. de, Tijssen, J.G., Meijer, S.L., Bergman, J., Wel, M.J.C. van der, Klaver, E., Pouw, R.E., Brosens, L.A.A., Biermann, K., Doukas, M., Huysentruyt, C., Karrenbeld, A., Kate, F.J. ten, Kats-Ugurlu, G., Laan, J. van der, Lijnschoten, I. Van, Moll, F.C.P., Offerhaus, G.J.A., Ooms, A., Seldenrijk, C.A., Visser, M. de, Tijssen, J.G., Meijer, S.L., and Bergman, J.

Abstract

Item does not contain fulltext, Endoscopic resection (ER) is an important diagnostic step in management of patients with early Barrett's esophagus (BE) neoplasia. Based on ER specimens, an accurate histological diagnosis can be made, which guides further treatment. Based on depth of tumor invasion, differentiation grade, lymphovascular invasion, and margin status, the risk of lymph node metastases and local recurrence is judged to be low enough to justify endoscopic management, or high enough to warrant invasive surgical esophagectomy. Adequate assessment of these histological risk factors is therefore of the utmost importance. Aim of this study was to assess pathologist concordance on these histological features on ER specimens and evaluate causes of discrepancy. Of 62 challenging ER cases, one representative H&E slide and matching desmin and endothelial marker were digitalized and independently assessed by 13 dedicated GI pathologists from 8 Dutch BE expert centers, using an online assessment module. For each histological feature, concordance and discordance were calculated. Clinically relevant discordances were observed for all criteria. Grouping depth of invasion categories according to expanded endoscopic treatment criteria (T1a and T1sm1 vs. T1sm2/3), ≥1 pathologist was discrepant in 21% of cases, increasing to 45% when grouping diagnoses according to the traditional T1a versus T1b classification. For differentiation grade, lymphovascular invasion, and margin status, discordances were substantial with 27%, 42%, and 32% of cases having ≥1 discrepant pathologist, respectively. In conclusion, histological assessment of ER specimens of early BE cancer by dedicated GI pathologists shows significant discordances for all relevant histological features. We present propositions to improve definitions of diagnostic criteria.

Published
2021

13. Extension of early esophageal squamous cell neoplasia into ducts and submucosal glands and the role of endoscopic ablation therapy

Author

Overwater, A., Munster, S.N. van, Offerhaus, G.J.A., Seldenrijk, C.A., Raicu, G.M., Koch, A.D., Bergman, J., Pouw, R.E., Brosens, L.A.A., Jansen, M., Weusten, B., Overwater, A., Munster, S.N. van, Offerhaus, G.J.A., Seldenrijk, C.A., Raicu, G.M., Koch, A.D., Bergman, J., Pouw, R.E., Brosens, L.A.A., Jansen, M., and Weusten, B.

Abstract

Item does not contain fulltext, BACKGROUND AND AIMS: Early esophageal squamous cell neoplasia (ESCN) is preferably treated with en-bloc endoscopic resection. Ablation might be an alternative for flat ESCN, but ESCN extension along the epithelial lining of ducts and submucosal glands (SMGs) might jeopardize ablation efficacy. Clinical studies suggest that local recurrence might arise from such buried ESCN niches after ablation. We studied human endoscopic resection specimens of ESCN to quantify ESCN extension into ducts/SMGs and performed a prospective porcine study to evaluate the depth of radiofrequency ablation (RFA) and CryoBalloon ablation (CBA) into ducts/SMGs. METHODS: Endoscopic submucosal dissection specimens of flat-type ESCN from a Japanese (n = 65) and Dutch cohort (n = 14) were evaluated for presence and neoplastic involvement of ducts/SMGs. Twenty-seven pigs were treated with circumferential RFA (c-RFA; n = 4), focal CBA (n = 20), and focal RFA (n = 3) with 4, 60, and 9 treatment areas, respectively. After prespecified survival periods (0 hours, 8 hours, 2 days, 5 days, and 28 days), treatment areas were evaluated for uniformity and depth of ablation and affected SMGs. RESULTS: Neoplastic extension in ducts/SMGs was observed in most lesions: 58% (38/65) in the Japanese and 64% (9/14) in the Dutch cohort. In the animal study, 33% of SMGs (95% confidence interval, 28-50) were not affected after c-RFA, although the overlying epithelium was ablated. Focal RFA and CBA resulted in uniform ablations with effective treatment of all SMGs. CONCLUSIONS: ESCN extends into ducts/SMGs in most patients. In an animal model, focal RFA and CBA effectively ablated SMGs, whereas c-RFA inadequately ablated SMGs. Given this potential reason for recurrence, endoscopic resection should remain the standard of care.

Published
2021

14. A Parathyroid-Gut Axis: Hypercalcemia and the Pathogenesis of Gastrinoma in Multiple Endocrine Neoplasia 1

Author

Hackeng, W.M., Dreijerink, K.M.A., Offerhaus, G.J.A., Brosens, L.A.A., Hackeng, W.M., Dreijerink, K.M.A., Offerhaus, G.J.A., and Brosens, L.A.A.

Abstract

Item does not contain fulltext, Patients with multiple endocrine neoplasia 1 (MEN1) syndrome have a germline mutation in the MEN1 gene. Loss of the wild-type allele can initiate endocrine tumorigenesis. Microscopic and macroscopic pituitary, parathyroid, and pancreatic tumors (referred to as the 3 P's) show loss of the wild-type MEN1 allele up to 100%. In contrast, the duodenal gastrinoma pathogenesis in MEN1 syndrome follows a hyperplasia-to-neoplasia sequence. Gastrinomas have loss of heterozygosity of the MEN1 locus in <50%, and invariably coincide with linear, diffuse, or micronodular gastrin-cell hyperplasia. The factor initiating the gastrin-cell hyperplasia-to-neoplasia sequence is unknown. In this perspective, we argue that hypercalcemia may promote the gastrin-cell hyperplasia-to-neoplasia sequence through the calcium sensing receptor. Hypercalcemia is present in almost all patients with MEN1 syndrome due to parathyroid adenomas. We propose a parathyroid-gut axis, which could well explain why patients with MEN1 syndrome are regularly cured of duodenal gastrinoma after parathyroid surgery, and might cause MEN1 syndrome phenocopies in MEN1-mutation negative individuals with parathyroid adenomas. This perspective on the pathogenesis of the gastrin-cell hyperplasia and neoplasia sequence sheds new light on tumorigenic mechanisms in neuroendocrine tumors and might open up novel areas of gastrinoma research. It may also shift focus in the treatment of MEN1 syndrome-related gastrinoma to biochemical prevention.

Published
2021

15. Genome Methylation Accurately Predicts Neuroendocrine Tumor Origin: An Online Tool

Author

Hackeng, W.M., Dreijerink, K.M.A., Leng, W.W.J. de, Morsink, F.H., Valk, G.D., Vriens, M.R., Offerhaus, G.J.A., Geisenberger, C., Brosens, L.A.A., Hackeng, W.M., Dreijerink, K.M.A., Leng, W.W.J. de, Morsink, F.H., Valk, G.D., Vriens, M.R., Offerhaus, G.J.A., Geisenberger, C., and Brosens, L.A.A.

Abstract

Item does not contain fulltext, PURPOSE: The primary origin of neuroendocrine tumor metastases can be difficult to determine by histopathology alone, but is critical for therapeutic decision making. DNA methylation-based profiling is now routinely used in the diagnostic workup of brain tumors. This has been enabled by the availability of cost-efficient array-based platforms. We have extended these efforts to augment histopathologic diagnosis in neuroendocrine tumors. EXPERIMENTAL DESIGN: Methylation data was compiled for 69 small intestinal, pulmonary, and pancreatic neuroendocrine tumors. These data were used to build a ridge regression calibrated random forest classification algorithm (neuroendocrine neoplasm identifier, NEN-ID). The model was validated during 3 × 3 nested cross-validation and tested in a local and an external cohort (n = 198 cases). RESULTS: NEN-ID predicted the origin of tumor samples with high accuracy (>95%). In addition, the diagnostic approach was determined to be robust across a range of possible confounding experimental parameters, such as tumor purity and array quality. A software infrastructure and online user interface were built to make the model available to the scientific community. CONCLUSIONS: This DNA methylation-based prediction model can be used in the workup for patients with neuroendocrine tumors of unknown primary. To facilitate validation and clinical implementation, we provide a user-friendly, publicly available web-based version of NEN-ID.

Published
2021

17. Contributors

Author

Abbasi, S., primary, Adolphi, N.L., additional, Aikawa, E., additional, Akbar, H., additional, Akilesh, S., additional, Aladjem, M.I., additional, Allocca, M., additional, Alpini, G., additional, Alroy, J., additional, Altman, B.J., additional, Andujar, P., additional, Antonello, Z.A., additional, Antsiferova, M., additional, Apica, B.S., additional, Ariel, I., additional, Aronow, B.J., additional, Ashley, J.W., additional, Badell, I.R., additional, Bagg, A., additional, Bajaj, M., additional, Banerjee, S., additional, Barbieri, J.S., additional, Bardes, E.E., additional, Barisoni, L., additional, Barletta, J.A., additional, Baskin, D.G., additional, Bastarrachea, R.A., additional, Bayat, A., additional, Bayrak-Toydemir, P., additional, Beck, A.H., additional, Beebe, D.C., additional, Beltran, H., additional, Benichou, G., additional, Bergman, M., additional, Bernard, S.A., additional, Bernardi, P., additional, Best, D.H., additional, Blair, H.C., additional, Bonaldo, P., additional, Bondy, J., additional, Bosman, F.T., additional, Bouma, B.E., additional, Brandi, M.L., additional, Bresler, S.C., additional, Brewer, M.T., additional, Britto, C.J., additional, Brock, J.E., additional, Brosens, L.A.A., additional, Budge, H., additional, Burd, E.M., additional, Burness, M.L., additional, Bushnell, T., additional, Byrd, J., additional, Calderone, A., additional, Campbell, M.J., additional, Cao, D., additional, Capell, W., additional, Cardigan, R., additional, Carey, P.M., additional, Carneiro, F., additional, Carp, S.A., additional, Carter, A.M., additional, Cascio, M.J., additional, Castellani, R.J., additional, Castellanos, J., additional, Caviglia, J.M., additional, Cecconi, F., additional, Chamarthy, S., additional, Chamma, E., additional, Chang, A., additional, Chang, A.Y., additional, Chang, N.C., additional, Chapman, D.G., additional, Charles, A.K., additional, Chen, D., additional, Chen, D.F., additional, Chen, P., additional, Cheng, J., additional, Chernock, R.D., additional, Cheruvu, S., additional, Chiang, J., additional, Childs, G.V., additional, Cho, Y.-B., additional, Choi, A.M.K., additional, Choi, J.K., additional, Cipriani, N.A., additional, Cleary, J.O.S.H., additional, Clementi, E., additional, Clines, G.A., additional, Cohen, M.L., additional, Coleman, W.B., additional, Coletta, D.K., additional, Collie, A.M.B., additional, Cooling, L., additional, Coron, E., additional, Côté, D., additional, Coussens, L.M., additional, Crielaard, B.J., additional, Cron, R.Q., additional, Crum, C.P., additional, Cruz, N.M., additional, Dairkee, S.H., additional, Daly, C.A., additional, Dang, C.V., additional, Danila, M.I., additional, Daradich, A., additional, Darnell, C.M., additional, Dartt, D.A., additional, Das, A., additional, D’Asta, F., additional, DeFronzo, R., additional, De Hertogh, G., additional, Dela Cruz, C.S., additional, de la Cruz-Merino, L., additional, De Palma, C., additional, Demetris, A.J., additional, DeMorrow, S., additional, Denechaud, P.-D., additional, Di Carli, M.F., additional, DiCarlo, E.F., additional, Dikic, I., additional, Dimberg, A., additional, Dowell, M.L., additional, Doyle, L.A., additional, Drachenberg, C.B., additional, Driskell, E., additional, Duda, D.G., additional, Duker, J., additional, Dyck, J.R.B., additional, Ecker, C., additional, Elifritz, J.M., additional, Elsheikh, T.M., additional, Ensari, A., additional, Ernst, L.M., additional, Esch, K.J., additional, Fajas-Coll, L., additional, Fang, Q., additional, Farhat, N.A., additional, Farshid, G., additional, Faye-Petersen, O.M., additional, Fehlings, M.G., additional, Fend, F., additional, Feng, X., additional, Fernandes, H., additional, Fernandez-Checa, J.C., additional, Ferreira, B.P., additional, Fidler, I.J., additional, Finn, J.A., additional, Fischer, A., additional, Fishbein, M.C., additional, Fleit, H.B., additional, Flomenbaum, M., additional, Folkins, A., additional, Francis, H., additional, Frank, K.M., additional, Frevert, C.W., additional, Frias, A.E., additional, Friedman, J.R., additional, Fukumura, D., additional, Furie, M.B., additional, Gaffo, A.L., additional, Galateau-Sallé, F., additional, Gallegos-Cabriales, E.C., additional, Gandhi, C.R., additional, Gannon, M., additional, García-Moliner, M.L., additional, Gardner, J.M., additional, Gasper, C.A., additional, Gaulard, P., additional, Gaut, J.P., additional, Gavia-García, G., additional, Gerrard, C., additional, Ghosh, A.P., additional, Giersch, A.B.S, additional, Gilbert, S.R., additional, Gill, J.R., additional, Giusti, F., additional, Glorioso, J.M., additional, González-Torres, M.C., additional, Goolsby, C.L., additional, Gora, M.J., additional, Gordon, I.O., additional, Gotlieb, A.I., additional, Gouw, A.M., additional, Goyal, A., additional, Grégoire, M., additional, Graham, B.B., additional, Granger, D.N., additional, Greene, A.K., additional, Greenlee, J.J., additional, Griffiths, R., additional, Guimarães, A.R., additional, Gulati, M., additional, Gullet, A., additional, Gupta, S., additional, Haider, N.B., additional, Halushka, M.K., additional, Hambuch, T.M., additional, Hamza, S.M., additional, Han, Y., additional, Hansen, W.P., additional, Hard, R., additional, Harris, B.T., additional, Harris, J.E., additional, Hartnett, M.E., additional, Hasserjian, R.P., additional, Hatch, G.M., additional, Hefti, M.M., additional, Heller, D.S., additional, Hemminger, J.A., additional, Hendrickson, J.E., additional, Henley, K.D., additional, Herzog, E., additional, Hess, J.R., additional, Hill, C.E., additional, Hipp, J., additional, Hobbs, R., additional, Höller, D., additional, Hodges, R.R., additional, Homer, R.J., additional, Horowitz, N., additional, Hsi, E.D., additional, Hsieh, A.L., additional, Hunt, J.M., additional, Hure, S., additional, Husain, A.N., additional, Hussey, S., additional, Hutcheson, J.D., additional, Hutson, R.M., additional, Illescas-Vacas, A., additional, Irvin, C.G., additional, Jaffer, F.A., additional, Jäger, R., additional, Jain, R.K., additional, Jain, S., additional, James, J., additional, Jansen, M., additional, Jarzembowski, J.A., additional, Jaurand, M.-C., additional, Jean, D., additional, Jegga, A.G., additional, Jellinger, K.A., additional, Jen, K.-Y., additional, Jo, V.Y., additional, Johnson, B., additional, Jones, R.L., additional, Kalfa, T.A., additional, Kamionek, M., additional, Kang, D., additional, Kantari, C., additional, Kantor, P.F., additional, Kanzaki, G., additional, Karns, R., additional, Katzman, P.J., additional, Kawai, T., additional, Kelley, T.W., additional, Kent, J.W., additional, Kerr, E.H., additional, Kew, R.R., additional, Khalighi, M., additional, Khanh Vu, T.H., additional, Khong, T.Y., additional, Kim, B.S., additional, Kim, J., additional, Klein, M.J., additional, Knechtle, S.J., additional, Konkle, B.A., additional, Kowalewska, J., additional, Kricka, L.J., additional, Krishnan, B., additional, Kumar, A., additional, Kumar, S., additional, Kvietys, P., additional, Kwong, R.Y., additional, Lafont, E., additional, Laga, A.C., additional, Lagarrigue, S., additional, Lakin, A., additional, Laszik, Z.G., additional, Lauwers, G.Y., additional, Laver, N.V., additional, Lawlor, M.W., additional, Lederer, J.A., additional, Lee, R.E., additional, Lee, W.M., additional, LeGallo, R., additional, Leich, E., additional, Lemmens, B., additional, Le Pimpec-Barthes, F., additional, Leval, L., additional, Levy, B.D., additional, Lewis, J.S., additional, Lewis, T.L., additional, Leyva-Illades, D., additional, Li, L., additional, Li, Y.-P., additional, Lianidou, E.S., additional, Liao, L., additional, Liapis, H., additional, Lin, J.B., additional, Lin, A.-L., additional, Lindsay, M.E., additional, Liu, E., additional, Longacre, T., additional, Lopez-Alvarenga, J.C., additional, Lopez-Mejía, I., additional, Lozanski, G., additional, Lucia, M.S., additional, Luk, E., additional, Lutty, G.A., additional, Maclellan, R.A., additional, Madabhushi, A., additional, Mahindra, A., additional, Malek, E., additional, Mammucari, C., additional, Mani, H., additional, Mao, S.A., additional, Marboe, C.C., additional, Marí, M., additional, Marini, F., additional, Markou, A., additional, Marshall, A.H., additional, Martin, S.J., additional, Marzioni, M., additional, Masli, S., additional, Matsukuma, K.E., additional, Matulonis, U.A., additional, Mayfield, J., additional, McCoy, J.P., additional, McDougle, C.J., additional, McGinnis, M.R., additional, McGuire, A., additional, McKinstry, K.K., additional, McManus, B.M., additional, Means, A.L., additional, Meny, G.M., additional, Merchant, N., additional, Meserve, E.E.K, additional, Mess, A.M., additional, Minervini, M.I., additional, Mitchell, R.N., additional, Monaco, S.E., additional, Monga, S.P., additional, Monica Way, H.-Y., additional, Montecucco, C., additional, Montone, K.T., additional, Morgan, E.A., additional, Morgan, T.K., additional, Morrissey, K., additional, Mortensen, R.M., additional, Moser, S.A., additional, Mosquera, J.M., additional, Mossman, B.T., additional, Motta, A.C.F., additional, Mullins, E., additional, Murphy, G.F., additional, Murray, L., additional, Mysorekar, I.U., additional, Nadel, B., additional, Nadon, A.S., additional, Nagathihalli, N., additional, Nájera-Medina, O., additional, Nalesnik, M.A., additional, Nast, C.C., additional, Natkunam, Y., additional, Nault, J.C., additional, Nava-González, E.J., additional, Nayar, R., additional, Nerenz, R.D., additional, Neumann, H., additional, Ni, H., additional, Nolte, K.B., additional, Norton, L., additional, Nowak, J., additional, Nucera, C., additional, Nyberg, S.L., additional, Oakes, S.A., additional, Offerhaus, G.J.A., additional, Ojha, S., additional, Okabe, H., additional, Oliveira, A.M., additional, Osborn, E.A., additional, O'Tierney-Ginn, P., additional, Ott, G., additional, Ozcan, A., additional, Padera, R.F., additional, Pagano, M.B., additional, Page, E.K., additional, Paintal, A.S., additional, Pairon, J.-C., additional, Papadimitriou, J.C., additional, Park, H.-J., additional, Park, J.Y., additional, Parsons, L.N., additional, Patra, D., additional, Peclovits, A., additional, Peeters, P.M., additional, Perkins, T.N., additional, Perry, G., additional, Perumbeti, A., additional, Petersen, C.A., additional, Petrache, I., additional, Petroff, M.G., additional, Pettus, J.R., additional, Picken, M.M., additional, Pierson, C.R., additional, Pittman, M.E., additional, Pogoriler, J., additional, Politi, K., additional, Pollack, S.M., additional, Quintanilla-Martínez, L., additional, Rai, M.F., additional, Ramkissoon, S., additional, Randhawa, P.S., additional, Rangel, J.R., additional, Rasola, A., additional, Reeves, B., additional, Reheman, A., additional, Remick, D.G., additional, Reynaert, N.L., additional, Richmond, J.M., additional, Rivella, S., additional, Rivenbark, A.G., additional, Rizzuto, R., additional, Roberts, K.A., additional, Robin, D.A., additional, Robinson, L.J., additional, Rockey, D.C., additional, Rosenwald, A., additional, Rossetto, O., additional, Roth, K.A., additional, Roy-Chowdhury, J., additional, Roy-Chowdhury, N., additional, Rubin, M.A., additional, Rudnicki, M.A., additional, Russell, D.S., additional, Ryter, S.W., additional, Saban, D.R., additional, Sacher, R.A., additional, Sacks, D.B., additional, Sagaert, X., additional, Sagdeo, A., additional, Sahay, B., additional, Sahin, A., additional, Samali, A., additional, Sampson, B., additional, Sánchez-Escribano, R., additional, Sandri, M., additional, Sanyal, A., additional, Sasatomi, E., additional, Sauer, V., additional, Scherpereel, A., additional, Schmidt, E.P., additional, Schwabe, R.F., additional, Scorrano, L., additional, Scott, M.G., additional, Scull, J.C., additional, Seidman, M.A., additional, Seki, A., additional, Sellati, T.J., additional, Serban, K., additional, Serhan, C.N., additional, Seshan, S.V., additional, Seth, A., additional, Seykora, J.T., additional, Sharma, N., additional, Shi, C., additional, Shi, S.-R., additional, Shimada, M., additional, Shimizu, A., additional, Singer, D.B., additional, Sitko, K., additional, Smallwood, R.F., additional, Smiraglia, D.J., additional, Smith, B.R., additional, Smola, H., additional, Soubeyrand, M., additional, Stahl, W.L., additional, Stajić, M., additional, Stanworth, S.J., additional, Stathatos, N., additional, Stemler, K.M., additional, Stevens, T.M., additional, Stine, Z.E., additional, Stoll, M.L., additional, Strati, A., additional, Strutt, T.M., additional, Sund, M., additional, Sung, M.M., additional, Symonds, M.E., additional, Tabar, S., additional, Takahashi, N., additional, Talmadge, J.E., additional, Tang, V., additional, Tangrea, M., additional, Tarango, C., additional, Tario, J.D., additional, Taylor, C.R., additional, Taylor, R., additional, Tearney, G.J., additional, Tefera, K., additional, Thomas, S., additional, Thornburg, K.L., additional, Tirado, C.A., additional, Tobian, A.A.R., additional, Tomaszewski, J.E., additional, Tormey, C.A., additional, Torres, R., additional, Tran, M.-H., additional, Tredget, E.E., additional, Treister, N.S., additional, Trotter, J., additional, Troyer, D., additional, Truong, L., additional, Tubbs, R.R., additional, Turakhia, S., additional, Unglert, C.I., additional, Utheim, T., additional, Vahabzadeh, A., additional, van Bokhoven, A., additional, Vanden Berghe, T., additional, Vandenabeele, P., additional, van der Klei, I.J., additional, Vanguri, V.K., additional, Van Noorden, C.J.F, additional, Van Poznak, C., additional, Vassallo, R.R., additional, Vawda, R., additional, Vieth, M., additional, Visscher, D.W., additional, Volk, S.W., additional, Vyas, G.N., additional, Waggoner, S.N., additional, Walczak, H., additional, Walker, D.H., additional, Wallace, P.K., additional, Wanat, K.A., additional, Wang, J., additional, Wang, Y., additional, Wang, Y.X., additional, Warger, W.C., additional, Wei, S., additional, Weinman, S.A., additional, Wenig, B.M., additional, Wentz, S.C., additional, Werner, S., additional, Wertheim, G., additional, Whitley, E.M., additional, Wooderchak-Donahue, W., additional, Woods, K., additional, Wouters, E.F.M., additional, Wu, Y., additional, Xing, W., additional, Yachimski, P., additional, Yan, P., additional, Yang, J., additional, Yang, L., additional, Yoshizawa, S., additional, Yuan, J., additional, Yun, S.-H., additional, Yvon, A., additional, Zhang, H., additional, Zhang, P., additional, Zhao, Z., additional, Zhu, G., additional, Zhu, R., additional, Zordoky, B.N., additional, Zou, J., additional, Zuccato, J.A., additional, and Zucman-Rossi, J., additional

Published
2014
Full Text
View/download PDF

18. Mucosal prolapse in the pathogenesis of Peutz-Jeghers polyposis

Author

Jansen, M., de Leng, W.W.J., Baas, A.F., Myoshi, H., Mathus-Vliegen, L., Taketo, M.M., Clevers, H., Giardiello, F.M., and Offerhaus, G.J.A.

Subjects
Intestinal mucosa -- Abnormalities, Intestinal mucosa -- Research, Prolapse -- Genetic aspects, Prolapse -- Research, Peutz-Jeghers syndrome -- Development and progression, Epithelial cells -- Genetic aspects, Gene mutations -- Analysis, Health
Published
2006

19. Comparison of the novel quantitative ARMS assay and an enriched PCR-ASO assay for K-ras mutations with conventional cytology on endobiliary brush cytology from 312 consecutive extrahepatic biliary stenoses

Author

van Heek, N.T., Clayton, S.J., Sturm, P.D.J., Walker, J., Gouma, D.J., Noorduyn, L.A., Offerhaus, G.J.A., and Fox, J.C.

Subjects
Biliary tract diseases -- Genetic aspects, Pancreatic cancer -- Risk factors, Gene mutations -- Analysis, Polymerase chain reaction -- Analysis, Allelomorphism -- Analysis, Health
Published
2005

20. STRAD in Peutz-Jeghers syndrome and sporadic cancers

Author

de Leng, W.W.J., Keller, J.J., Luiten, S., Musler, A.R., Jansen, M., Baas, A.F., de Rooij, F.W.M., Gille, J.J.P., Menko, F.H., Offerhaus, G.J.A, and Weterman, M.A.J.

Subjects
Peutz-Jeghers syndrome -- Physiological aspects, Tumor suppressor genes -- Analysis, Health
Published
2005

22. Epstein-Barr virus in gastric carcinomas and gastric stump carcinomas: a late event in gastric carcinogenesis

Author

Zur Hausen, A., Van Rees, B.P., Van Beek, J., Craanen, M.E., Bloemena, E., Offerhaus, G.J.A., Meijer, C.J.L.M., and Van den Brule, A.J.C.

Subjects
Carcinogenesis -- Research, Stomach cancer -- Research, Epstein-Barr virus -- Research, Epstein-Barr virus -- Risk factors, Health
Abstract

The Epstein-Barr virus (EBV) encoded RNA 1/2 (EBER1/2) transcripts were absent in preneoplastic gastric lesions but present in gastric carcinomas of the intact stomach (GCIS) and gastric stump carcinoma (GSC). This suggests that EBV infects only neoplastic gastric cells and thus is a late event in gastric carcinogenesis.

Published
2004

23. Comparison of cyclooxygenase 2 expression in adenocarcinomas of the gastric cardia and distal oesophagus

Author

Buskens, C.J., Sivula, A., van Rees, B.P., Haglund, C., Offerhaus, G.J.A., van Lanschot, J.J.B., and Ristimaki, A.

Subjects
American Joint Committee on Cancer -- Reports, Care and treatment, Physiological aspects, Genetic aspects, Research, Reports, Comparative analysis, Methods, Health aspects, Causes of, Genotypes -- Physiological aspects -- Reports -- Health aspects -- Research -- Genetic aspects -- Comparative analysis -- Methods, Cyclooxygenases -- Genetic aspects -- Physiological aspects -- Health aspects -- Comparative analysis -- Reports -- Research -- Methods, Stomach cancer -- Genetic aspects -- Health aspects -- Care and treatment -- Research, Adenocarcinoma -- Health aspects -- Care and treatment -- Genetic aspects -- Research, Intestinal diseases -- Research -- Causes of -- Health aspects -- Comparative analysis -- Care and treatment -- Genetic aspects, Pathogenic microorganisms -- Genetic aspects -- Research -- Health aspects -- Methods -- Physiological aspects -- Reports -- Comparative analysis, Medical research -- Methods -- Health aspects -- Comparative analysis -- Physiological aspects -- Reports, Patients -- Health aspects -- Care and treatment -- Physiological aspects -- Research -- Methods -- Reports -- Comparative analysis, Gene expression -- Physiological aspects -- Research -- Reports -- Methods -- Comparative analysis -- Genetic aspects -- Health aspects, Medicine, Experimental -- Methods -- Health aspects -- Comparative analysis -- Physiological aspects -- Reports, Colorectal diseases -- Research -- Causes of -- Health aspects -- Comparative analysis -- Care and treatment -- Genetic aspects, Genotype -- Physiological aspects -- Reports -- Health aspects -- Research -- Genetic aspects -- Comparative analysis -- Methods, Gastrointestinal diseases -- Research -- Causes of -- Health aspects -- Comparative analysis -- Care and treatment -- Genetic aspects
Abstract

Gut 2003;52:1678-1683 Background: Adenocarcinomas of the gastric cardia and distal oesophagus are at present often considered as one clinical entity because of their comparable increasing incidence, prognosis, and optimal treatment [...]

Published
2003

24. Routine morphometrical analysis can improve reproducibility of dysplasia grade in Barrett's oesorhagus surveillance biopsies. (Original Article)

Author

Baak, J.P.A., Kate, F.J.W. ten, Offerhaus, G.J.A., Lanschot, J.J. van, and Meijer, G.A.

Subjects
Statistics, Care and treatment, Evaluation, Physiological aspects, Methods, Dysplasia -- Care and treatment, Biopsy -- Statistics -- Evaluation -- Physiological aspects -- Methods, Barrett esophagus -- Physiological aspects -- Care and treatment, Pathological physiology -- Methods -- Physiological aspects -- Statistics, Physiology, Pathological -- Methods -- Physiological aspects -- Statistics, Barrett's esophagus -- Physiological aspects -- Care and treatment
Abstract

Background: The grade of dysplasia found in Barrett's oesophagus surveillance biopsies is a major factor to determine follow up and treatment. However, it has been reported that the reproducibility of [...]

Published
2002

25. A tumour with a neuroendocrine and papillary serous component: two or a pair? (Case Report)

Author

Eeden, S. van, Nederlof, P.M., Taal, B.G., Offerhaus, G.J.A., and Velthuysen, M-L F. van

Subjects
Analysis, Development and progression, Endocrine gland tumors -- Analysis -- Development and progression, Endocrine gland cancer -- Development and progression -- Analysis
Abstract

Aims: To examine the clonal origin of a tumour, made up of a neuroendocrine component and a papillary serous component by comparing the pattern of loss of heterozygosity (LOH) and [...]

Published
2002

26. Pancreatic cancer after remote peptic ulcer surgery. (Original Article)

Author

Tascilar, M., Rees, B.P. Van, Sturm, P.D.J., Tytgat, G.N.J., Hruban, R.H., Goodman, S.N., Giardiello, F.M., Offerhaus, G.J.A., and Tersmette, A.C.

Subjects
Risk factors, Surgery, Pancreatic cancer -- Risk factors, Peptic ulcer -- Risk factors
Abstract

Background: Peptic ulcer surgery may carry an increased risk for pancreatic cancer development. Molecular analysis of K-ras codon 12, frequently mutated in conventional pancreatic cancers, might provide insight into the [...]

Published
2002

27. Increased prevalence of Barrett's esophagus in patients with MUTYH-associated polyposis (MAP)

Author

Daans, C.G., Ghorbanoghli, Z., Velthuizen, M.E., Vasen, H.F., Offerhaus, G.J.A., Lacle, M.M., Siersema, P.D., Ausems, M., Boonstra, J.J., Daans, C.G., Ghorbanoghli, Z., Velthuizen, M.E., Vasen, H.F., Offerhaus, G.J.A., Lacle, M.M., Siersema, P.D., Ausems, M., and Boonstra, J.J.

Abstract

Contains fulltext : 220097.pdf (Publisher’s version ) (Open Access), Barrett's oesophagus (BE) has been associated with an increased risk of both colorectal adenomas and colorectal cancer. A recent investigation reported a high frequency of BE in patients with adenomatous polyposis coli (APC)-associated polyposis (FAP). The aim of the present study is to evaluate the prevalence of BE in a large cohort of patients with MUTYH-associated polyposis (MAP) and APC-associated adenomatous polyposis. Patients with a genetically confirmed diagnosis of familial adenomatous polyposis (FAP) or MAP were selected and upper gastrointestinal (GI) endoscopy reports, pathology reports of upper GI biopsies were reviewed to determine the prevalence of BE in these patients. Histologically confirmed BE was found in 7 (9.7%) of 72 patients with MAP. The mean age of diagnosis was 60.2 years (range 54.1-72.4 years). Two patients initially diagnosed with low grade dysplasia showed fast progression into high grade dysplasia and esophageal cancer, respectively. Only 4 (1.4%) of 365 patients with FAP were found to have pathologically confirmed BE. The prevalence of BE in patients with MAP is much higher than reported in the general population. We recommend that upper GI surveillance of patients with MAP should not only focus on the detection of gastric and duodenal adenomas but also on the presence of BE.

Published
2020

31. Homozygous disruption of the murine mdr2 P-glycoprotein gene leads to a complete absence of phospholipid from bile and liver disease

Author

Smit, J.J.M., Schinkel, A.H., Elferink, R.P.J. Oude, Groen, A.K., Wagenaar, E., Deemter L. van, Mol, C.A.A.M., Ottenhoff, R., Lugt, N.M.T. van der, Roon, M.A. van, Valk, M.A. van der, Offerhaus, G.J.A., Berns, A.J.M., and Borst, P.

Subjects
Glycoproteins -- Genetic aspects, Phospholipids -- Analysis, Bile -- Abnormalities, Liver diseases -- Analysis, Biological sciences
Abstract

mdr2 P-glycoprotein is vital for the secretion of phosphatidylcholine into bile, which suggests that it might be either a phospholipid transport protein or a phospholipid flippase. Mammals possess two varieties of P-glycoprotein. One type transports drugs while the second variety, encoded by mouse mdr2 and human MDR3 genes, is unable to transport hydrophobic anticancer drugs.

Published
1993

32. Mucosal prolapse syndrome presenting as rectal polyposis

Author

Brosens, L.A.A., Montgomery, E.A., Bhagavan, B.S., Offerhaus, G.J.A., and Giardiello, F.M.

Subjects
Rectal polyps -- Diagnosis, Rectal polyps -- Care and treatment, Rectal polyps -- Case studies, Rectum -- Prolapse, Rectum -- Diagnosis, Rectum -- Care and treatment, Rectum -- Case studies, Health
Published
2009

33. Value of combined phenotypic markers in identifying inheritance of familial adenomatous polyposis

Author

Giardiello, F.M., Offerhaus, G.J.A., Graboulsi, E.I., Graybeal, J.C., Maumenee, I.H., Krush, A.J., Levins, L.S., Booker, S.V., and Hamilton, S.R.

Subjects
Polyposis, Familial -- Diagnosis, Colorectal cancer -- Risk factors, Polyps (Pathology) -- Complications, Health
Abstract

Familial adenomatous polyposis is an inherited disorder characterized by the occurrence of many adenomas (tumors) in the colon and rectum during adolescence and young adulthood. Most individuals with this condition must undergo prophylactic removal of the colon (colectomy) to prevent the otherwise almost inevitable development of colorectal cancer before the age of 50. Familial adenomatous polyposis is frequently associated with nongastrointestinal symptoms such as retinal disorders, benign soft tissue and bony tumors, nonintestinal lesions, and various types of cancer. To evaluate the utility of using two of these nongastrointestinal markers (occult radiopaque jaw lesions, a disorder of bone development, and retinal lesions) in the diagnosis of familial adenomatous polyposis, a study was carried out involving 43 affected patients and 12 unaffected first-degree relatives from 24 families with a history of polyposis. Seventy-seven percent of the patients with polyposis were positive for both of the nongastrointestinal markers. Only eight percent of the unaffected first-degree relatives were positive for both markers. The predictive value of both markers was significantly greater than for either one alone. Patients who exhibit both of the indices correlated with familial adenomatous polyposis should be evaluated with particular care to determine whether a prophylactic colectomy should be performed, inasmuch as they have a high probability of developing both polyposis and, at a more advanced age, colorectal cancer. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1991

34. Pedunculated Morphology of T1 Colorectal Tumors Associates With Reduced Risk of Adverse Outcome

Author

Kessels, K., Backes, Y., Elias, S.G., Blink, A. van den, Offerhaus, G.J.A., Bergeijk, J.D. van, Groen, J.N., Seerden, T.C.J., Schwartz, M.P., Cappel, W.H.D.T.N., Spanier, B.W.M., Geesing, J.M.J., Kerkhof, M., Siersema, P.D., Didden, P., Boonstra, J.J., Herrero, L.A., Wolfhagen, F.H.J., Borg, F. ter, Lent, A.U. van, Droste, J.S.T.S., Hazen, W.L., Schrauwen, R.W.M., Vleggaar, F.P., Lacle, M.M., Moons, L.M.G., Dutch T1 Colorectal Canc Working, and Anesthesiology

Subjects
Male, medicine.medical_specialty, Time Factors, Endoscopic Mucosal Resection, Population, Endoscopic mucosal resection, Gastroenterology, Risk Assessment, Metastasis, 03 medical and health sciences, Tumours of the digestive tract Radboud Institute for Health Sciences [Radboudumc 14], 0302 clinical medicine, All institutes and research themes of the Radboud University Medical Center, Interquartile range, Risk Factors, Internal medicine, Medicine, Humans, Neoplasm Metastasis, education, Adverse effect, Aged, Neoplasm Staging, Netherlands, Retrospective Studies, education.field_of_study, Hepatology, Colon Cancer, business.industry, Incidence, Prognostic Factor, Hazard ratio, Retrospective cohort study, Odds ratio, Colonoscopy, Middle Aged, medicine.disease, Prognosis, Survival Rate, 030220 oncology & carcinogenesis, 030211 gastroenterology & hepatology, Female, Neoplasm Recurrence, Local, business, Colorectal Neoplasms, Follow-Up Studies
Abstract

Background & Aims Risk stratification for adverse events, such as metastasis to lymph nodes, is based only on histologic features of tumors. We aimed to compare adverse outcomes of pedunculated vs nonpedunculated T1 colorectal cancers (CRC). Methods We performed a retrospective study of 1656 patients diagnosed with T1CRC from 2000 through 2014 at 14 hospitals in The Netherlands. The median follow-up time of patients was 42.5 months (interquartile range, 18.5–77.5 mo). We evaluated the association between tumor morphology and the primary composite end point, adverse outcome, adjusted for clinical variables, histologic variables, resection margins, and treatment approach. Adverse outcome was defined as metastasis to lymph nodes, distant metastases, local recurrence, or residual tissue. Secondary end points were tumor metastasis, recurrence, and incomplete resection. Results Adverse outcome occurred in 67 of 723 patients (9.3%) with pedunculated T1CRCs vs 155 of 933 patients (16.6%) with nonpedunculated T1CRCs. Pedunculated morphology was independently associated with decreased risk of adverse outcome (adjusted odds ratio [OR], 0.59; 95% CI, 0.42–0.83; P = .003). Metastasis, incomplete resection, and recurrence were observed in 5.8%, 4.6%, and 3.9% of pedunculated T1CRCs vs 10.6%, 8.0%, and 6.6% of nonpedunculated T1CRCs, respectively. Pedunculated morphology was independently associated with a reduced risk of metastasis (adjusted OR, 0.62; 95% CI, 0.41–0.94; P = .03), incomplete resection (adjusted OR, 0.57; 95% CI, 0.36–0.91; P = .02), and recurrence (adjusted hazard ratio, 0.52; 95% CI, 0.32–0.85; P = .009). Metastasis, incomplete resection, and recurrence did not differ significantly between low-risk pedunculated vs nonpedunculated T1CRCs (0.8% vs 2.9%, P = .38; 1.5% vs 0%, P = .99; 1.5% vs 0%; P = .99). However, incomplete resection and recurrence were significantly lower for high-risk pedunculated vs nonpedunculated T1CRCs (6.5% vs 12.5%; P = .007; 4.4% vs 8.6%; P = .03). Conclusions In a retrospective study of patients with T1CRC, we found pedunculated morphology to be associated independently with a decreased risk of adverse outcome in a T1CRC population at high risk of adverse outcome. Incorporating morphologic features of tumors in risk assessment could help predict outcomes of patients with T1CRC and help identify the best candidates for surgery.

Published
2019
Full Text
View/download PDF

36. Adherence to pre-set benchmark quality criteria to qualify as expert assessor of dysplasia in Barrett’s esophagus biopsies – towards digital review of Barrett’s esophagus

Author

van der Wel, M.J. (M. J.), Klaver, E. (E.), Duits, L.C. (L. C.), Pouw, R.E. (R. E.), Seldenrijk, K.A. (Kees), Offerhaus, G.J.A. (Johan), Visser, M. (Marjan), ten Kate, F.J.W. (F. J.W.), Biermann, K. (Katharina), Brosens, L.A. (Lodewijk), Doukas, M. (M.), Huysentruyt, C.J. (Clément J.), Karrenbeld, A. (A.), Kats-Ugurlu, G. (Gursah), van der Laan, J.S. (J. S.), Lijnschoten, G. van, Moll, F.C.P., Ooms, A.H.A.G. (Ariadne), Tijssen, J.G.P. (Jan), Bergman, J.J.G.H.M. (Jacques), Meijer, S.L. (Sybren), van der Wel, M.J. (M. J.), Klaver, E. (E.), Duits, L.C. (L. C.), Pouw, R.E. (R. E.), Seldenrijk, K.A. (Kees), Offerhaus, G.J.A. (Johan), Visser, M. (Marjan), ten Kate, F.J.W. (F. J.W.), Biermann, K. (Katharina), Brosens, L.A. (Lodewijk), Doukas, M. (M.), Huysentruyt, C.J. (Clément J.), Karrenbeld, A. (A.), Kats-Ugurlu, G. (Gursah), van der Laan, J.S. (J. S.), Lijnschoten, G. van, Moll, F.C.P., Ooms, A.H.A.G. (Ariadne), Tijssen, J.G.P. (Jan), Bergman, J.J.G.H.M. (Jacques), and Meijer, S.L. (Sybren)

Abstract

Background: Dysplasia assessment of Barrett’s esophagus biopsies is associated with low observer agreement; guidelines advise expert review. We have developed a web-based review panel for dysplastic Barrett’s esophagus biopsies. Objective: The purpose of this study was to test if 10 gastrointestinal pathologists working at Dutch Barrett’s esophagus expert centres met pre-set benchmark scores for quality criteria. Methods: Ten gastrointestinal pathologists twice assessed 60 digitalized Barrett’s esophagus cases, enriched for dysplasia; then r

Published
2019
Full Text
View/download PDF

45. Pathologic evaluation and reporting of intraductal papillary mucinous neoplasms of the pancreas and other tumoral intraepithelial neoplasms of pancreatobiliary tract: Recommendations of verona consensus meeting

Author

Adsay, V. (Volkan), Mino-Kenudson, M. (Mari), Furukawa, T. (Toru), Basturk, O. (Olca), Zamboni, G. (Giuseppe), Marchegiani, G. (Giovanni), Bassi, C. (Claudio), Salvia, R. (Roberto), Malleo, G. (Giuseppe), Paiella, S. (Salvatore), Wolfgang, C.L. (Christopher L.), Matthaei, H. (Hanno), Offerhaus, G.J.A. (Johan), Adham, I.M., Bruno, M.J. (Marco), Reid, M.D. (Michelle D.), Krasinskas, A. (Alyssa), Kloppel, G. (Günter), Ohike, N. (Nobuyuki), Tajiri, T. (Takuma), Jang, K.-T. (Kee-Taek), Roa, J.C. (Juan Carlos), Allen, P.J. (Peter), Fernández-Del Castillo, C. (Carlos), Jang, J.-Y. (Jin-Young), Klimstra, D.S. (David), Hruban, R.H. (Ralph), Adsay, V. (Volkan), Mino-Kenudson, M. (Mari), Furukawa, T. (Toru), Basturk, O. (Olca), Zamboni, G. (Giuseppe), Marchegiani, G. (Giovanni), Bassi, C. (Claudio), Salvia, R. (Roberto), Malleo, G. (Giuseppe), Paiella, S. (Salvatore), Wolfgang, C.L. (Christopher L.), Matthaei, H. (Hanno), Offerhaus, G.J.A. (Johan), Adham, I.M., Bruno, M.J. (Marco), Reid, M.D. (Michelle D.), Krasinskas, A. (Alyssa), Kloppel, G. (Günter), Ohike, N. (Nobuyuki), Tajiri, T. (Takuma), Jang, K.-T. (Kee-Taek), Roa, J.C. (Juan Carlos), Allen, P.J. (Peter), Fernández-Del Castillo, C. (Carlos), Jang, J.-Y. (Jin-Young), Klimstra, D.S. (David), and Hruban, R.H. (Ralph)

Abstract

Background: There are no established guidelines for pathologic diagnosis/reporting of intraductal papillary mucinous neoplasms (IPMNs). Design: An international multidisciplinary group, brought together by the Verona Pancreas Group in Italy-2013, was tasked to devise recommendations. Results: (1) Crucial to rule out invasive carcinoma with extensive (if not complete) sampling. (2) Invasive component is to be documented in a full synoptic report including its size, type, grade, and stage. (3) The term "minimally invasive" should be avoided; instead, invasion size with stage and substaging of T1 (1a, b, c; ≤0.5, >0.5-≤1, >1 cm) is to be documented. (4) Largest diameter of the invasion, not the distance from the nearest duct, is to be used. (5) A category of "indeterminate/(suspicious) for invasion" is acceptable for rare cases. (6) The term "malignant" IPMN should be avoided. (7) The highest grade of dysplasia in the non-invasive component is to be documented separately. (8) Lesion size is to be correlated with imaging findings in cysts with rupture. (9) The main duct diameter and, if possible, its involvement are to be documented; however, it is not required to provide main versus branch duct classification in the resected tumor. (10) Subtyping as gastric/intestinal/pancreatobiliary/oncocytic/mixed is of value. (11) Frozen section is to be performed highly selectively, with appreciation of its shortcomings. (12) These principles also apply to other similar tumoral intraepithelial neoplasms (mucinous cystic neoplasms, intra-ampullary, and intrabiliary/cholecystic). Conclusions: These recommendations will ensure proper communication of salient tumor characteristics to the management teams, accurate comparison of data between analyses, and development of more effective management algorithms.

Published
2016
Full Text
View/download PDF

46. Adenomas in Patients with Inflammatory Bowel Disease Are Associated with an Increased Risk of Advanced Neoplasia

Author

Schaik, F.D.M. van, Mooiweer, E., Have, M. van der, Belderbos, T.D.G., Kate, F.J.W. ten, Offerhaus, G.J.A., Schipper, M.E.I., Dijkstra, G., Pierik, M., Stokkers, P.C.F., Ponsioen, C., Jong, D.J. de, Hommes, D.W., Bodegraven, A.A. van, Siersema, P.D., Oijen, M.G.H. van, Oldenburg, B., Dutch Initiative Crohn Colitis ICC, Interne Geneeskunde, RS: NUTRIM - R2 - Gut-liver homeostasis, Gastroenterology and hepatology, CCA - Innovative therapy, Other departments, Pathology, Amsterdam Gastroenterology Endocrinology Metabolism, Gastroenterology and Hepatology, Oncology, Public Health, Gastroenterology & Hepatology, Groningen Institute for Gastro Intestinal Genetics and Immunology (3GI), Translational Immunology Groningen (TRIGR), and Groningen Institute for Organ Transplantation (GIOT)

Subjects
Male, POLYPS, endocrine system diseases, Colorectal cancer, medicine.medical_treatment, Kaplan-Meier Estimate, Inflammatory bowel disease, Gastroenterology, COLORECTAL-CANCER, Immunology and Allergy, POLYPECTOMY, Middle Aged, adenoma, Female, Colorectal Neoplasms, Adult, Risk, DYSPLASTIC LESIONS, medicine.medical_specialty, Adenoma, CARCINOMA, CHRONIC ULCERATIVE-COLITIS, colorectal cancer, Molecular gastro-enterology and hepatology Pathogenesis and modulation of inflammation [IGMD 2], digestive system, dysplasia, inflammatory bowel disease, Internal medicine, SURVEILLANCE, Carcinoma, medicine, Humans, Molecular gastro-enterology and hepatology [IGMD 2], Proportional Hazards Models, Retrospective Studies, Proportional hazards model, business.industry, Retrospective cohort study, ENDOSCOPIC RESECTION, medicine.disease, Inflammatory Bowel Diseases, Polypectomy, digestive system diseases, stomatognathic diseases, Dysplasia, ADEQUATE TREATMENT, Neoplasm Grading, business, FOLLOW-UP, Precancerous Conditions, Follow-Up Studies
Abstract

Background: It is still unclear whether inflammatory bowel disease (IBD) patients with adenomas have a higher risk of developing high-grade dysplasia (HGD) or colorectal cancer (CRC) than non-IBD patients with sporadic adenomas. We compared the risk of advanced neoplasia (AN, defined as HGD or CRC) in IBD patients with adenomas to IBD patients without adenomas and patients without IBD with adenomas.Methods: IBD patients with a histological adenoma diagnosis (IBD + adenoma), age-matched IBD patients without adenoma (IBD-nonadenoma), and adenoma patients without IBD (nonIBD + adenoma) were enrolled in this study. Medical charts were reviewed for adenoma characteristics and development of AN. The endoscopic appearance of the adenomas was characterized as typical (solitary sessile or pedunculated) or atypical (all other descriptions).Results: A total of 110 IBD + adenoma patients, 123 IBD-nonadenoma patients, and 179 nonIBD + adenoma patients were included. Mean duration of follow-up was 88 months (SD +/- 41). The 5-year cumulative risks of AN were 11%, 3%, and 5% in IBD + adenoma, IBD-nonadenoma, and nonIBD + adenoma patients, respectively (P Conclusions: IBD patients with a histological diagnosis of adenoma have a higher risk of developing AN than adenoma patients without IBD and IBD patients without adenomas. The presence of atypical adenomas in particular was associated with this increased risk, although patients with typical adenomas were found to carry an additional risk as well. (Inflamm Bowel Dis 2013; 19: 342-349)

Published
2013
Full Text
View/download PDF

50. Direct visualization of Smad1/5/8-mediated transcriptional activity identifies podocytes and collecting ducts as major targets of BMP signalling in healthy and diseased kidneys

Author

Leeuwis, J.W., Nguyen, T.Q., Lopes, S.M.C.D., Giezen, D.M. van der, Ven, K. van der, Rouw, P.J.H., Offerhaus, G.J.A., Mummery, C.L., and Goldschmeding, R.

Subjects
animal structures, embryonic structures, bone morphogenetic protein kidney GFP SMAD BRE podocytes bone morphogenetic protein-7 growth-factor-beta diabetic-nephropathy osteogenic protein-1 epithelial-cells gene-expression smad1/5 phosphorylation receptor complexes renal fibrosis mouse kidney
Abstract

Bone morphogenetic protein 7 (BMP7) is a key determinant of renal response to injury, exhibiting strong protective as well as regenerative potential in a variety of experimental models. In vitro, beneficial effects of stimulation with BMP7 and other BMPs have been observed in many renal cell types. Still, it remains poorly understood which cells in the native kidney actually respond to BMPs in health and disease. Here, we report the use of BRE:gfp mice expressing green fluorescent protein (GFP) under the control of a pSmad1/5/8-specific BMP-responsive element (BRE) to directly visualize the spatiotemporal distribution of transcriptional activity downstream of canonical BMP signalling in healthy kidneys and in two distinct models of kidney disease. BRE-GFP signal coincided with expression of endogenous BMP target genes but, surprisingly, it was much more restricted than expected from the widespread distribution of pSmad1/5/8, a classical component of canonical BMP signal tranduction. BRE-GFP was mainly present in podocytes and collecting duct cells, and both glomerular and medullary BRE-GFP decreased following ischaemia-reperfusion injury as well as following unilateral ureteric obstruction, together with decreased BMP7, pSmad1/5/8 and BMP target gene expression. Remarkably, however, BRE-GFP was increased in injured proximal tubules in association with up-regulation of BMP receptors ALK2 and ALK3. Thus, native BMP transcriptional activity is much more restricted than previously suggested based on pSmad1/5/8 detection alone, and its response to injury varies according to cell type and nephron segment. Copyright (C) 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Published
2011

Catalog

Books, media, physical & digital resources
See catalog results