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1. Integrative and comparative genomic analyses identify clinically relevant pulmonary carcinoid groups and unveil the supra-carcinoids

Author

Alcala, N., Leblay, N., Gabriel, A. A. G., Mangiante, L., Hervas, D., Giffon, T., Sertier, A. S., Ferrari, A., Derks, J., Ghantous, A., Delhomme, T. M., Chabrier, A., Cuenin, C., Abedi-Ardekani, B., Boland, A., Olaso, R., Meyer, V, Altmuller, J., Le Calvez-Kelm, F., Durand, G., Voegele, C., Boyault, S., Moonen, L., Lemaitre, N., Lorimier, P., Toffart, A. C., Soltermann, A., Clement, J. H., Saenger, J., Field, J. K., Brevet, M., Blanc-Fournier, C., Galateau-Salle, F., Le Stang, N., Russell, P. A., Wright, G., Sozzi, G., Pastorino, U., Lacomme, S., Vignaud, J. M., Hofman, V, Hofman, P., Brustugun, O. T., Lund-Iversen, M., de Montpreville, V. Thomas, Muscarella, L. A., Graziano, P., Popper, H., Stojsic, J., Deleuze, J. F., Herceg, Z., Viari, A., Nuernberg, P., Pelosi, G., Dingemans, A. M. C., Milione, M., Roz, L., Brcic, L., Volante, M., Papotti, M. G., Caux, C., Sandoval, J., Hernandez-Vargas, H., Brambilla, E., Speel, E. J. M., Girard, N., Lantuejoul, S., McKay, J. D., Foll, M., Fernandez-Cuesta, L., Alcala, N., Leblay, N., Gabriel, A. A. G., Mangiante, L., Hervas, D., Giffon, T., Sertier, A. S., Ferrari, A., Derks, J., Ghantous, A., Delhomme, T. M., Chabrier, A., Cuenin, C., Abedi-Ardekani, B., Boland, A., Olaso, R., Meyer, V, Altmuller, J., Le Calvez-Kelm, F., Durand, G., Voegele, C., Boyault, S., Moonen, L., Lemaitre, N., Lorimier, P., Toffart, A. C., Soltermann, A., Clement, J. H., Saenger, J., Field, J. K., Brevet, M., Blanc-Fournier, C., Galateau-Salle, F., Le Stang, N., Russell, P. A., Wright, G., Sozzi, G., Pastorino, U., Lacomme, S., Vignaud, J. M., Hofman, V, Hofman, P., Brustugun, O. T., Lund-Iversen, M., de Montpreville, V. Thomas, Muscarella, L. A., Graziano, P., Popper, H., Stojsic, J., Deleuze, J. F., Herceg, Z., Viari, A., Nuernberg, P., Pelosi, G., Dingemans, A. M. C., Milione, M., Roz, L., Brcic, L., Volante, M., Papotti, M. G., Caux, C., Sandoval, J., Hernandez-Vargas, H., Brambilla, E., Speel, E. J. M., Girard, N., Lantuejoul, S., McKay, J. D., Foll, M., and Fernandez-Cuesta, L.

Abstract

The worldwide incidence of pulmonary carcinoids is increasing, but little is known about their molecular characteristics. Through machine learning and multi-omics factor analysis, we compare and contrast the genomic profiles of 116 pulmonary carcinoids (including 35 atypical), 75 large-cell neuroendocrine carcinomas (LCNEC), and 66 small-cell lung cancers. Here we report that the integrative analyses on 257 lung neuroendocrine neoplasms stratify atypical carcinoids into two prognostic groups with a 10-year overall survival of 88% and 27%, respectively. We identify therapeutically relevant molecular groups of pulmonary carcinoids, suggesting DLL3 and the immune system as candidate therapeutic targets; we confirm the value of OTP expression levels for the prognosis and diagnosis of these diseases, and we unveil the group of supra-carcinoids. This group comprises samples with carcinoid-like morphology yet the molecular and clinical features of the deadly LCNEC, further supporting the previously proposed molecular link between the low-and high-grade lung neuroendocrine neoplasms.

Published
2019

2. Integrative and comparative genomic analyses identify clinically relevant pulmonary carcinoid groups and unveil the supra-carcinoids

Author

Alcala, N; https://orcid.org/0000-0002-5961-5064, Leblay, N, Gabriel, A A G, Mangiante, L, Hervas, D, Giffon, T; https://orcid.org/0000-0001-8133-6507, Sertier, A S, Ferrari, A, Derks, J; https://orcid.org/0000-0002-0442-1879, Ghantous, A, Delhomme, T M; https://orcid.org/0000-0003-0265-4246, Chabrier, A, Cuenin, C, Abedi-Ardekani, B, Boland, A, Olaso, R, Meyer, V, Altmuller, J, Le Calvez-Kelm, F, Durand, G, Voegele, C, Boyault, S; https://orcid.org/0000-0002-2297-6894, Moonen, L, Lemaitre, N, Lorimier, P, Toffart, A C, Soltermann, A, Clement, J H; https://orcid.org/0000-0002-6601-2456, Saenger, J, Field, J K; https://orcid.org/0000-0003-3951-6365, et al, Alcala, N; https://orcid.org/0000-0002-5961-5064, Leblay, N, Gabriel, A A G, Mangiante, L, Hervas, D, Giffon, T; https://orcid.org/0000-0001-8133-6507, Sertier, A S, Ferrari, A, Derks, J; https://orcid.org/0000-0002-0442-1879, Ghantous, A, Delhomme, T M; https://orcid.org/0000-0003-0265-4246, Chabrier, A, Cuenin, C, Abedi-Ardekani, B, Boland, A, Olaso, R, Meyer, V, Altmuller, J, Le Calvez-Kelm, F, Durand, G, Voegele, C, Boyault, S; https://orcid.org/0000-0002-2297-6894, Moonen, L, Lemaitre, N, Lorimier, P, Toffart, A C, Soltermann, A, Clement, J H; https://orcid.org/0000-0002-6601-2456, Saenger, J, Field, J K; https://orcid.org/0000-0003-3951-6365, and et al

Abstract

The worldwide incidence of pulmonary carcinoids is increasing, but little is known about their molecular characteristics. Through machine learning and multi-omics factor analysis, we compare and contrast the genomic profiles of 116 pulmonary carcinoids (including 35 atypical), 75 large-cell neuroendocrine carcinomas (LCNEC), and 66 small-cell lung cancers. Here we report that the integrative analyses on 257 lung neuroendocrine neoplasms stratify atypical carcinoids into two prognostic groups with a 10-year overall survival of 88% and 27%, respectively. We identify therapeutically relevant molecular groups of pulmonary carcinoids, suggesting DLL3 and the immune system as candidate therapeutic targets; we confirm the value of OTP expression levels for the prognosis and diagnosis of these diseases, and we unveil the group of supra-carcinoids. This group comprises samples with carcinoid-like morphology yet the molecular and clinical features of the deadly LCNEC, further supporting the previously proposed molecular link between the low- and high-grade lung neuroendocrine neoplasms.

Published
2019

3. The methylome of the celiac intestinal epithelium harbours genotype-independent alterations in the HLA region.

Author

Fernandez-Jimenez N, Garcia-Etxebarria K, Plaza-Izurieta L, Romero-Garmendia I, Jauregi-Miguel A, Legarda M, Ecsedi S, Castellanos-Rubio A, Cahais V, Cuenin C, Degli Esposti D, Irastorza I, Hernandez-Vargas H, Herceg Z, and Bilbao JR

Subjects
Biopsy, Celiac Disease metabolism, Celiac Disease pathology, CpG Islands, Female, Gene Expression Profiling, Gene Expression Regulation, Genome-Wide Association Study, HLA Antigens immunology, Humans, Intestinal Mucosa pathology, Male, Promoter Regions, Genetic, Celiac Disease etiology, DNA Methylation, Epigenome, Genotype, HLA Antigens genetics, Intestinal Mucosa immunology, Intestinal Mucosa metabolism
Abstract

The Human Leucocyte Antigen (HLA) locus and other DNA sequence variants identified in Genome-Wide Association (GWA) studies explain around 50% of the heritability of celiac disease (CD). However, the pathogenesis of CD could be driven by other layers of genomic information independent from sequence variation, such as DNA methylation, and it is possible that allele-specific methylation explains part of the SNP associations. Since the DNA methylation landscape is expected to be different among cell types, we analyzed the methylome of the epithelial and immune cell populations of duodenal biopsies in CD patients and controls separately. We found a cell type-specific methylation signature that includes genes mapping to the HLA region, namely TAP1 and HLA-B. We also performed Immunochip SNP genotyping of the same samples and interrogated the expression of some of the affected genes. Our analysis revealed that the epithelial methylome is characterized by the loss of CpG island (CGI) boundaries, often associated to altered gene expression, and by the increased variability of the methylation across the samples. The overlap between differentially methylated positions (DMPs) and CD-associated SNPs or variants contributing to methylation quantitative trait loci (mQTLs) is minimal. In contrast, there is a notable enrichment of mQTLs among the most significant CD-associated SNPs. Our results support the notion that DNA methylation alterations constitute a genotype-independent event and confirm its role in the HLA region (apart from the well-known, DQ allele-specific effect). Finally, we find that a fraction of the CD-associated variants could exert its phenotypic effect through DNA methylation.

Published
2019
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