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1. Impact of TP53 mutation status on systemic treatment outcome in ALK-rearranged non-small-cell lung cancer

Author

Kron, A., Alidousty, C., Scheffler, M., Merkelbach-Bruse, S., Seidel, D., Riedel, R., Ihle, M.A., Michels, S., Nogova, L., Fassunke, J., Heydt, C., Kron, F., Ueckeroth, F., Serke, M., Krüger, S., Grohe, C., Koschel, D., Benedikter, J., Kaminsky, B., Schaaf, B., Braess, J., Sebastian, M., Kambartel, K -O, Thomas, R., Zander, T., Schultheis, A.M., Büttner, R., and Wolf, J.

Published
2018
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5. Prevalence and potential biological role of TERT amplifications in ALK translocated adenocarcinoma of the lung.

Author

Wolf J., Kron A., Schultheis A.M., Buettner R., Alidousty C., Duerbaum N., Wagener-Ryczek S., Baar T., Martelotto L.G., Heydt C., Siemanowski J., Holz B., Binot E., Fassunke J., Merkelbach-Bruse S., Wolf J., Kron A., Schultheis A.M., Buettner R., Alidousty C., Duerbaum N., Wagener-Ryczek S., Baar T., Martelotto L.G., Heydt C., Siemanowski J., Holz B., Binot E., Fassunke J., and Merkelbach-Bruse S.

Abstract

Aims: The advent of specific ALK-targeting drugs has radically changed the outcome of patients with ALK translocated non-small-cell lung cancer (NSCLC). However, emerging resistance to treatment with ALK inhibitors in these patients remains a major concern. In previous studies, we analysed two ALK+ patient cohorts (TP53 wild-type/TP53 mutated) in terms of copy number alterations. All patients belonging to the TP53 wild-type group had mainly genetically stable genomes, with one exception showing chromosomal instability and amplifications of several gene loci, including TERT. Here, we aimed to determine the prevalence of TERT amplifications in these ALK+ lung cancer patients by analysing an independent cohort of 109 ALK translocated cases. We further analysed the copy numbers of numerous cancer-relevant genes and other genetic aberrations. Methods and Results: The prevalence of TERT amplifications was determined by means of FISH analyses. Copy numbers of 87 cancer-relevant genes were determined by NanoString nCounter technology, FoundationOne and lung-specific NGS panels in some of these TERT-amplified samples, and clinical data on patients with TERT-amplified tumours were collected. Our data revealed that five (4.6%) of all 109 analysed ALK+ patients harboured amplification of TERT and that these patients had genetically unstable genomes. Conclusion(s): Our preliminary study shows that ALK+ adenocarcinomas should be evaluated in the context of their genomic background in order to more clearly understand and predict patients' individual course of disease.Copyright © 2020 The Authors. Histopathology published by John Wiley & Sons Ltd

Published
2021

6. FP14.04 Resistance to MET Inhibition in MET Driven NSCLC and Response after Switching from Type I to Type II MET Inhibitors

Author

Riedel, R., primary, Heydt, C., additional, Scheel, A., additional, Tumbrink, H., additional, Brägelmann, J., additional, Fassunke, J., additional, Nogova, L., additional, Michels, S., additional, Scheffler, M., additional, Fischer, R., additional, Koleczko, S., additional, Weber, J., additional, Westphal, T., additional, Abdulla, D., additional, Merkelbach-Bruse, S., additional, Sos, M., additional, Büttner, R., additional, and Wolf, J., additional

Published
2021
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8. KRAS mutations in never-smoker NSCLC patients: Defining a new patient subgroup

Author

Scheffler, M., Nogova, L., Michels, S., Holzem, A., Chanra, T., Abdulla, D. S. Y., Koleczko, S., Merkelbach-Bruse, S., Fassunke, J., Kron, A., Scheel, A. H., Ihle, M. A., Heydt, C., Westphal, T., Weber, J. -P., Fischer, R. N., Riedel, R., Kaminsky, B., Draube, A., Rothe, A., Kambartel, K. -O., Hillmer, A., Buettner, R., Wolf, J., Scheffler, M., Nogova, L., Michels, S., Holzem, A., Chanra, T., Abdulla, D. S. Y., Koleczko, S., Merkelbach-Bruse, S., Fassunke, J., Kron, A., Scheel, A. H., Ihle, M. A., Heydt, C., Westphal, T., Weber, J. -P., Fischer, R. N., Riedel, R., Kaminsky, B., Draube, A., Rothe, A., Kambartel, K. -O., Hillmer, A., Buettner, R., and Wolf, J.

Published
2020

11. Comparative proteomics reveals a diagnostic signature for pulmonary head-and-neck cancer metastasis

Author

Bohnenberger, H., Kaderali, L., Ströbel, P., Yepes, D., Pleßmann, U., Dharia, N., Yao, S., Heydt, C., Merkelbach‐Bruse, S., Emmert, A., Hoffmann, J., Bodemeyer, J., Reuter‐Jessen, K., Lois, A., Dröge, L., Baumeister, P., Walz, C., Biggemann, L., Walter, R., Häupl, B., Comoglio, F., Pan, K., Scheich, S., Lenz, C., Küffer, S., Bremmer, F., Kitz, J., Sitte, M., Beißbarth, T., Hinterthaner, M., Sebastian, M., Lotz, J., Schildhaus, H., Wolff, H., Danner, B., Brandts, C., Büttner, R., Canis, M., Stegmaier, K., Serve, H., Urlaub, H., and Oellerich, T.

Subjects
stomatognathic diseases
Abstract

Patients with head‐and‐neck cancer can develop both lung metastasis and primary lung cancer during the course of their disease. Despite the clinical importance of discrimination, reliable diagnostic biomarkers are still lacking. Here, we have characterised a cohort of squamous cell lung (SQCLC) and head‐and‐neck (HNSCC) carcinomas by quantitative proteomics. In a training cohort, we quantified 4,957 proteins in 44 SQCLC and 30 HNSCC tumours. A total of 518 proteins were found to be differentially expressed between SQCLC and HNSCC, and some of these were identified as genetic dependencies in either of the two tumour types. Using supervised machine learning, we inferred a proteomic signature for the classification of squamous cell carcinomas as either SQCLC or HNSCC, with diagnostic accuracies of 90.5% and 86.8% in cross‐ and independent validations, respectively. Furthermore, application of this signature to a cohort of pulmonary squamous cell carcinomas of unknown origin leads to a significant prognostic separation. This study not only provides a diagnostic proteomic signature for classification of secondary lung tumours in HNSCC patients, but also represents a proteomic resource for HNSCC and SQCLC.

Published
2018

13. New insights into acquired resistance mechanisms to third-generation EGFR tyrosine kinase inhibitor therapy in lung cancer

Author

Fassunke, J., primary, Heydt, C., additional, Michels, S., additional, Van Veggel, B., additional, Müller, F., additional, Keul, M., additional, Dammert, M.A., additional, Schmitt, A., additional, Smit, E.F., additional, Kast, S., additional, Wolf, J., additional, Buettner, R., additional, Sos, M.L., additional, Rauh, D., additional, and Merkelbach-Bruse, S., additional

Published
2019
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15. Genetic instability and recurrent MYC amplification in ALK-translocated NSCLC: a central role of TP53 mutations.

Author

Buettner R., Kron A., Merkelbach-Bruse S., Ihle M.A., Wolf J., Schultheis A.M., Alidousty C., Baar T., Martelotto L.G., Heydt C., Wagener S., Fassunke J., Duerbaum N., Scheel A.H., Frank S., Holz B., Binot E., Buettner R., Kron A., Merkelbach-Bruse S., Ihle M.A., Wolf J., Schultheis A.M., Alidousty C., Baar T., Martelotto L.G., Heydt C., Wagener S., Fassunke J., Duerbaum N., Scheel A.H., Frank S., Holz B., and Binot E.

Abstract

The anaplastic lymphoma kinase (ALK) rearrangement defines a distinct molecular subtype of non-small cell lung cancer (NSCLC). Despite the excellent initial efficacy of ALK inhibitors in patients with ALK+ lung cancer, resistance occurs almost inevitably. To date, there is no reliable biomarker allowing the identification of patients at higher risk of relapse. Here, we analysed a subset of 53 ALK+ tumours with and without TP53 mutation and ALK+ NSCLC cell lines by NanoString nCounter technology. We found that the co-occurrence of early TP53 mutations in ALK+ NSCLC can lead to chromosomal instability: 24% of TP53-mutated patients showed amplifications of known cancer genes such as MYC (14%), CCND1 (10%), TERT (5%), BIRC2 (5%), ORAOV1 (5%), and YAP1 (5%). MYC-overexpressing ALK+ TP53-mutated cells had a proliferative advantage compared to wild-type cells. ChIP-Seq data revealed MYC-binding sites within the promoter region of EML4, and MYC overexpression in ALK+ TP53-mutated cells resulted in an upregulation of EML4-ALK, indicating a potential MYC-dependent resistance mechanism in patients with increased MYC copy number. Our study reveals that ALK+ NSCLC represents a more heterogeneous subgroup of tumours than initially thought, and that TP53 mutations in that particular cancer type define a subset of tumours that harbour chromosomal instability, leading to the co-occurrence of pathogenic aberrations. © 2018 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.

Published
2018

19. Genetic instability and recurrent MYC amplification in ALK-translocated NSCLC; a central role of TP53 mutations

Author

Alidousty, C., Baar, T., Martelotto, L. G., Heydt, C., Wagener, S., Fassunke, J., Duerbaum, N., Scheel, A., Frank, S., Holz, B., Binot, E., Kron, A., Merkelbach-Bruse, S., Ihle, M., Wolf, J., Buettner, R., Schultheis, A. M., Alidousty, C., Baar, T., Martelotto, L. G., Heydt, C., Wagener, S., Fassunke, J., Duerbaum, N., Scheel, A., Frank, S., Holz, B., Binot, E., Kron, A., Merkelbach-Bruse, S., Ihle, M., Wolf, J., Buettner, R., and Schultheis, A. M.

Published
2018

23. An evaluation of the challenges to developing tumor BRCA1 and BRCA2 testing methodologies for clinical practice

Author

Ellison, G, Ahdesmaki, M, Luke, S, Waring, PM, Wallace, A, Wright, R, Rothlisberger, B, Ludin, K, Merkelbach-Bruse, S, Heydt, C, Ligtenberg, MJL, Mensenkamp, AR, de Castro, DG, Jones, T, Vivancos, A, Kondrashova, O, Pauwels, P, Weyn, C, Hahnen, E, Hauke, J, Soong, R, Lai, Z, Dougherty, B, Carr, TH, Johnson, J, Mills, J, Barrett, JC, Ellison, G, Ahdesmaki, M, Luke, S, Waring, PM, Wallace, A, Wright, R, Rothlisberger, B, Ludin, K, Merkelbach-Bruse, S, Heydt, C, Ligtenberg, MJL, Mensenkamp, AR, de Castro, DG, Jones, T, Vivancos, A, Kondrashova, O, Pauwels, P, Weyn, C, Hahnen, E, Hauke, J, Soong, R, Lai, Z, Dougherty, B, Carr, TH, Johnson, J, Mills, J, and Barrett, JC

Abstract

Ovarian cancer patients with germline or somatic pathogenic variants benefit from treatment with poly ADP ribose polymerase (PARP) inhibitors. Tumor BRCA1/2 testing is more challenging than germline testing as the majority of samples are formalin-fixed paraffin embedded (FFPE), the tumor genome is complex, and the allelic fraction of somatic variants can be low. We collaborated with 10 laboratories testing BRCA1/2 in tumors to compare different approaches to identify clinically important variants within FFPE tumor DNA samples. This was not a proficiency study but an inter-laboratory comparison to identify common issues. Each laboratory received the same tumor DNA samples ranging in genotype, quantity, quality, and variant allele frequency (VAF). Each laboratory performed their preferred next-generation sequencing method to report on the variants. No false positive results were reported in this small study and the majority of methods detected the low VAF variants. A number of variants were not detected due to the bioinformatics analysis, variant classification, or insufficient DNA. The use of hybridization capture or short amplicon methods are recommended based on a bioinformatic assessment of the data. The study highlights the importance of establishing standards and standardization for tBRCA testing particularly when the test results dictate clinical decisions regarding life extending therapies.

Published
2018

29. Analysis of Clinical Relevant Mutations by the Novel Gene Reader NGS System

Author

Koitzsch, U., Heydt, C., Divakar, K., Attig, H., Fassunke, J., Merkelbach-Bruse, S., Fammartino, A. Alessandro, Buettner, R., Kong, Y., Odenthal, M., Koitzsch, U., Heydt, C., Divakar, K., Attig, H., Fassunke, J., Merkelbach-Bruse, S., Fammartino, A. Alessandro, Buettner, R., Kong, Y., and Odenthal, M.

Published
2017

30. BRCA diagnostics of ovarian cancer. Molecular tumor testing since the introduction of PARP inhibitor therapy

Author

Loeser, H., Heydt, C., Buettner, R., Markiefka, B., Loeser, H., Heydt, C., Buettner, R., and Markiefka, B.

Abstract

Approximately 9000 women are diagnosed with ovarian cancer in Germany each year. The most common subtype is high-grade serous ovarian cancer. A relevant proportion of these tumors are associated with mutations in the breast and ovarian cancer susceptibility genes (BRCA1 and BRCA2) representing highly penetrant tumor suppressor genes with autosomal inheritance and play a crucial role in DNA repair mechanisms. These patients have predominantly germline mutations and less frequently have somatic BRCA mutations. Tumors harboring BRCA mutations show a significant improvement in progression-free survival under therapy with poly(adenosine diphosphate ribose) polymerase (PARP) inhibitors. In 2015 the first PARP inhibitor was approved for the therapy of high-grade serous ovarian cancer with BRCA mutations. Mutation analysis can be performed on formalin-fixed paraffin-embedded (FFPE) tumor tissue within a few days.

Published
2017

31. Impact of co-occurring genomic alterations on overall survival of BRAF mutated lung cancer patients: results of the Network Genomic Medicine

Author

Kron, A., Riedel, R., Michels, S., Fassunke, J., Merkelbach-Bruse, S., Scheffler, M., Ueckeroth, F., Schueller, M., Pauli, B., Grohe, C., Kaminsky, B., Braess, J., Graeven, U., Krueger, S., Nogova, L., Abdulla, D., Fischer, R., Heydt, C., Buettner, R., Wolf, J., Kron, A., Riedel, R., Michels, S., Fassunke, J., Merkelbach-Bruse, S., Scheffler, M., Ueckeroth, F., Schueller, M., Pauli, B., Grohe, C., Kaminsky, B., Braess, J., Graeven, U., Krueger, S., Nogova, L., Abdulla, D., Fischer, R., Heydt, C., Buettner, R., and Wolf, J.

Published
2017

32. Molecular panel sequencing of pre-treatment samples reveals mechanisms of innate resistance to 3rd generation EGFR TKI treatment in T790M-positive NSCLC patients

Author

Michels, S., Heydt, C., Deschler-Baier, B., Ruesseler, V., Stratmann, J., Steinhauser, S., Fischer, R., Scheffler, M., Fassunke, J., Kron, A., Griesinger, F., Gautschi, O., Sebastian, M., Hellmich, M., Heukamp, L., Merkelbach-Bruse, S., Bttner, R., Wolf, J., Michels, S., Heydt, C., Deschler-Baier, B., Ruesseler, V., Stratmann, J., Steinhauser, S., Fischer, R., Scheffler, M., Fassunke, J., Kron, A., Griesinger, F., Gautschi, O., Sebastian, M., Hellmich, M., Heukamp, L., Merkelbach-Bruse, S., Bttner, R., and Wolf, J.

Published
2017

33. Impact of next generation TKI and co-occurring mutations in ALK-positive NSCLC patients: Results of the Network Genomic Medicine

Author

Riedel, R., Kron, A., Michels, S., Fassunke, J., Scheffler, M., Fischer, R., Nogova, L., Abdulla, D., Heydt, C., Ueckeroth, F., Pauli, B., Serke, M., Krueger, S., Grohe, C., Sebastian, M., Koschel, D., Kambartel, K-O., Zander, T., Buettner, R., Wolf, J., Riedel, R., Kron, A., Michels, S., Fassunke, J., Scheffler, M., Fischer, R., Nogova, L., Abdulla, D., Heydt, C., Ueckeroth, F., Pauli, B., Serke, M., Krueger, S., Grohe, C., Sebastian, M., Koschel, D., Kambartel, K-O., Zander, T., Buettner, R., and Wolf, J.

Published
2017

34. Impact of next generation tyrosine kinase inhibitors (TKI) and co-occurring mutations in ALK-positive NSCLC patients: results of the Network Genomic Medicine

Author

Kron, A., Riedel, R., Michels, S., Heydt, C., Fassunke, J., Merkelbach-Bruse, S., Scheffler, M., Fischer, R., Abdulla, D., Nogova, L., Ueckeroth, F., Pauli, B., Schueller, M., Serke, M., Koschel, D., Krueger, S., Grohe, C., Kambartel, K., Sebastian, M., Zander, T., Buettner, R., Wolf, J., Kron, A., Riedel, R., Michels, S., Heydt, C., Fassunke, J., Merkelbach-Bruse, S., Scheffler, M., Fischer, R., Abdulla, D., Nogova, L., Ueckeroth, F., Pauli, B., Schueller, M., Serke, M., Koschel, D., Krueger, S., Grohe, C., Kambartel, K., Sebastian, M., Zander, T., Buettner, R., and Wolf, J.

Published
2017

35. Molecular characterisation of sinunasal carcinomas

Author

Castiglione, R., Ihle, M. A., Heydt, C., Alidousty, C., Schultheis, A., Merkelbach-Bruse, S., Hermsen, M., Buettner, R., Franchi, A., Castiglione, R., Ihle, M. A., Heydt, C., Alidousty, C., Schultheis, A., Merkelbach-Bruse, S., Hermsen, M., Buettner, R., and Franchi, A.

Published
2017

36. Impact of next generation TKI and co-occurring mutations in ALK-positive NSCLC patients: Results of the Network Genomic Medicine

Author

Riedel, R., primary, Kron, A., additional, Michels, S., additional, Fassunke, J., additional, Scheffler, M., additional, Fischer, R., additional, Nogova, L., additional, Abdulla, D., additional, Heydt, C., additional, Ueckeroth, F., additional, Pauli, B., additional, Serke, M., additional, Krueger, S., additional, Grohe, C., additional, Sebastian, M., additional, Koschel, D., additional, Kambartel, K.-O., additional, Zander, T., additional, Büttner, R., additional, and Wolf, J., additional

Published
2017
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37. ALK evaluation in the world of multiplex testing: Network Genomic Medicine (NGM): the Cologne model for implementing personalised oncology

Author

Heydt, C., Kostenko, A., Merkelbach-Bruse, S., Wolf, J., Buttner, R., Heydt, C., Kostenko, A., Merkelbach-Bruse, S., Wolf, J., and Buttner, R.

Abstract

The Network Genomic Medicine (NGM) has established the first paradigm model for central molecular testing and clinical trial platforms enabling the delivery of decentralised therapies in a patient-oriented setting. Here we describe the structures of the network and give a summary of technologies to identify patients with anaplastic lymphoma kinase (ALK) fusion positive lung adenocarcinomas.Comprehensive molecular genotyping of lung cancers has become a key requirement for guiding therapeutic decisions. As a paradigm model of implementing next-generation comprehensive diagnostics, Network Genomic Medicine (NGM) has established central diagnostic and clinical trial platforms for centralised testing and decentralised personalised treatment in clinical practice. Here, we describe the structures of the NGM network and give a summary of technologies to identify patients with anaplastic lymphoma kinase (ALK) fusion-positive lung adenocarcinomas. As unifying test platforms will become increasingly important for delivering reliable, quick and affordable tests, the NGM diagnostic platform is currently implementing a comprehensive hybrid capture-based parallel sequencing pan-cancer assay.

Published
2016

38. Improved overall survival following implementation of next generation sequencing in routine diagnostics of advanced lung cancer in Germany: results of the Network Genomic Medicine

Author

Kostenko, A., Michels, S., Kron, F., Brandes, V, Fischer, R., Nogova, L., Scheffler, M., Fassunke, J., Merkelbach-Bruse, S., Scheel, A., Ueckeroth, F., Sueptitz, J., Gerigk, M., Heydt, C., Glossmann, J. -P, Buettner, R., Wolf, J., Kostenko, A., Michels, S., Kron, F., Brandes, V, Fischer, R., Nogova, L., Scheffler, M., Fassunke, J., Merkelbach-Bruse, S., Scheel, A., Ueckeroth, F., Sueptitz, J., Gerigk, M., Heydt, C., Glossmann, J. -P, Buettner, R., and Wolf, J.

Published
2016

42. Genetic heterogeneity and lack of prognostic impact of patients with non-small cell lung cancer (NSCLC) harboring PIK3CA mutation

Author

Scheffler, M., Gardizi, M., Bos, M., Koenig, K., Michels, S., Fassunke, J., Heydt, C., Kuenstlinger, H., Ihle, M. A., Ueckeroth, F., Albus, K., Serke, M., Gerigk, U., Schulte, W., Toepelt, K., Nogova, L., Zander, T., Engel-Riedel, W., Stoelben, E., Ko, Y. -D., Randerath, W. J., Kaminsky, B., Panse, J., Becker, C., Hellmich, M., Merkelbach-Bruse, S., Buettner, R., Heukamp, L. C., Wolf, J., Scheffler, M., Gardizi, M., Bos, M., Koenig, K., Michels, S., Fassunke, J., Heydt, C., Kuenstlinger, H., Ihle, M. A., Ueckeroth, F., Albus, K., Serke, M., Gerigk, U., Schulte, W., Toepelt, K., Nogova, L., Zander, T., Engel-Riedel, W., Stoelben, E., Ko, Y. -D., Randerath, W. J., Kaminsky, B., Panse, J., Becker, C., Hellmich, M., Merkelbach-Bruse, S., Buettner, R., Heukamp, L. C., and Wolf, J.

Published
2014

44. Biomarker analysis from a pathologist's view. Founding the rationale for personalised treatment of lung cancer

Author

Buettner, R., Heydt, C., Buettner, R., and Heydt, C.

Abstract

The advent of genomic medicine and sequencing analysis of entire cancer genomes has rapidly improved our understanding of cancer genomics and has defined pathogenetic lesions initiating and driving cancer phenotypes in a causative manner. Moreover rapid development of small molecule inhibitors and highly selective biologicals provided effective tools to intervene with oncogenic signalling resulting from such lesions in the cancer genome. Thereby, the pathologist is now in the position to diagnose causative lesions in the cancer genome as molecular biomarkers directing the selection of patients for effective and highly selective therapies. If oncogenic driver lesions are vigorously validated preclinically and a useful diagnostic test is available, it is possible to provide a proof-of-concept at a very early stage of clinical drug development with the possibility of immediate personal benefit for participants in such phase I/II studies. This approach has significantly changed clinical testing and avoids testing proof for efficacy in large stage III clinical trials at a high failure rate. Therefore, our review summarises recent and paradigmatic progress in lung cancer biomarker diagnostics and defines academic and regulatory requirements for biomarker analysis and selective personalised therapies.

Published
2013

47. Molecular Profiling of Odontogenic Tumors - Pilot Study

Author

Gültekin Sibel Elif, Sengüven Burcu, Aziz Reemitcha, Heydt Carina, and Buettner Reinhard

Subjects
odontogenic tumors, next generation sequencing, mutation, Dentistry, RK1-715
Abstract

Background/Aim: In the pathogenesis of odontogenic tumors which arise from the rests of the dental apparatus in the jaw, several molecular pathways have been shown to play critical roles such as genetic alterations in the hedgehog, BRAF/Ras/MAPK, epidermal growth factor receptor. Next generation genomic sequencing has identified gene mutations in many different tumors. Materials and Methods: Here we report four types of odontogenic tumor including six cases in which five had mutation according to next generation sequencing analysis from archival paraffin blocks that diagnosed previously as ameloblastoma (solid), amloblastoma (unicystic-mural), ameloblastic fibroma, squamous odontogenic tumor, and adenomatoid odontogenic tumor. Results: All ameloblastomatic tumors were shown BRAF mutation and adenomatoid odontogenic tumors were KRAS mutation. Conclusion: This evidence may highlight the poorly understood pathogenesis of odontogenic tumors. Further comparisons need to be made with other benign and malignant odontogenic tumors so that unique odontogenic features may be found.

Published
2017
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