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1. Methylation-based markers of aging and lifestyle-related factors and risk of breast cancer: a pooled analysis of four prospective studies

Author

Dugue, P-A, Bodelon, C, Chung, FF, Brewer, HR, Ambatipudi, S, Sampson, JN, Cuenin, C, Chajes, V, Romieu, I, Fiorito, G, Sacerdote, C, Krogh, V, Panico, S, Tumino, R, Vineis, P, Polidoro, S, Baglietto, L, English, D, Severi, G, Giles, GG, Milne, RL, Herceg, Z, Garcia-Closas, M, Flanagan, JM, Southey, MC, Dugue, P-A, Bodelon, C, Chung, FF, Brewer, HR, Ambatipudi, S, Sampson, JN, Cuenin, C, Chajes, V, Romieu, I, Fiorito, G, Sacerdote, C, Krogh, V, Panico, S, Tumino, R, Vineis, P, Polidoro, S, Baglietto, L, English, D, Severi, G, Giles, GG, Milne, RL, Herceg, Z, Garcia-Closas, M, Flanagan, JM, and Southey, MC

Abstract

BACKGROUND: DNA methylation in blood may reflect adverse exposures accumulated over the lifetime and could therefore provide potential improvements in the prediction of cancer risk. A substantial body of research has shown associations between epigenetic aging and risk of disease, including cancer. Here we aimed to study epigenetic measures of aging and lifestyle-related factors in association with risk of breast cancer. METHODS: Using data from four prospective case-control studies nested in three cohorts of European ancestry participants, including a total of 1,655 breast cancer cases, we calculated three methylation-based measures of lifestyle factors (body mass index [BMI], tobacco smoking and alcohol consumption) and seven measures of epigenetic aging (Horvath-based, Hannum-based, PhenoAge and GrimAge). All measures were regression-adjusted for their respective risk factors and expressed per standard deviation (SD). Odds ratios (OR) and 95% confidence intervals (CI) were calculated using conditional or unconditional logistic regression and pooled using fixed-effects meta-analysis. Subgroup analyses were conducted by age at blood draw, time from blood sample to diagnosis, oestrogen receptor-positivity status and tumour stage. RESULTS: None of the measures of epigenetic aging were associated with risk of breast cancer in the pooled analysis: Horvath 'age acceleration' (AA): OR per SD = 1.02, 95%CI: 0.95-1.10; AA-Hannum: OR = 1.03, 95%CI:0.95-1.12; PhenoAge: OR = 1.01, 95%CI: 0.94-1.09 and GrimAge: OR = 1.03, 95%CI: 0.94-1.12, in models adjusting for white blood cell proportions, body mass index, smoking and alcohol consumption. The BMI-adjusted predictor of BMI was associated with breast cancer risk, OR per SD = 1.09, 95%CI: 1.01-1.17. The results for the alcohol and smoking methylation-based predictors were consistent with a null association. Risk did not appear to substantially vary by age at blood draw, time to diagnosis or tumour characteristics. CONCLUSION

Published
2022

2. Epigenome-wide association study for lifetime estrogen exposure identifies an epigenetic signature associated with breast cancer risk.

Author

Chajes V., Dugue P.-A., Southey M.C., Giles G.G., English D.R., Milne R.L., Severi G., Ambatipudi S., Cuenin C., Romieu I., Herceg Z., Swerdlow A.J., Vineis P., Flanagan J.M., Johansson A., Palli D., Masala G., Grioni S., Agnoli C., Tumino R., Giurdanella M.C., Fasanelli F., Sacerdote C., Panico S., Mattiello A., Polidoro S., Jones M.E., Schoemaker M.J., Orr N., Tomczyk K., Johnson N., Fletcher O., Perduca V., Baglietto L., Chajes V., Dugue P.-A., Southey M.C., Giles G.G., English D.R., Milne R.L., Severi G., Ambatipudi S., Cuenin C., Romieu I., Herceg Z., Swerdlow A.J., Vineis P., Flanagan J.M., Johansson A., Palli D., Masala G., Grioni S., Agnoli C., Tumino R., Giurdanella M.C., Fasanelli F., Sacerdote C., Panico S., Mattiello A., Polidoro S., Jones M.E., Schoemaker M.J., Orr N., Tomczyk K., Johnson N., Fletcher O., Perduca V., and Baglietto L.

Abstract

Background: It is well established that estrogens and other hormonal factors influence breast cancer susceptibility. We hypothesized that a woman's total lifetime estrogen exposure accumulates changes in DNA methylation, detectable in the blood, which could be used in risk assessment for breast cancer. Method(s): An estimated lifetime estrogen exposure (ELEE) model was defined using epidemiological data from EPIC-Italy (n = 31,864). An epigenome-wide association study (EWAS) of ELEE was performed using existing Illumina HumanMethylation450K Beadchip (HM450K) methylation data obtained from EPIC-Italy blood DNA samples (n = 216). A methylation index (MI) of ELEE based on 31 CpG sites was developed using HM450K data from EPIC-Italy and the Generations Study and evaluated for association with breast cancer risk in an independent dataset from the Generations Study (n = 440 incident breast cancer cases matched to 440 healthy controls) using targeted bisulfite sequencing. Lastly, a meta-analysis was conducted including three additional cohorts, consisting of 1187 case-control pairs. Result(s): We observed an estimated 5% increase in breast cancer risk per 1-year longer ELEE (OR = 1.05, 95% CI 1.04-1.07, P = 3 x 10-12) in EPIC-Italy. The EWAS identified 694 CpG sites associated with ELEE (FDR Q < 0.05). We report a DNA methylation index (MI) associated with breast cancer risk that is validated in the Generations Study targeted bisulfite sequencing data (ORQ4-vs-Q1 = 1.77, 95% CI 1.07-2.93, P = 0.027) and in the meta-analysis (ORQ4-vs-Q1 = 1.43, 95% CI 1.05-2.00, P = 0.024); however, the correlation between the MI and ELEE was not validated across study cohorts. Conclusion(s): We have identified a blood DNA methylation signature associated with breast cancer risk in this study. Further investigation is required to confirm the interaction between estrogen exposure and DNA methylation in the blood.Copyright © 2019 The Author(s).

Published
2019

3. Epigenome-wide association study for lifetime estrogen exposure identifies an epigenetic signature associated with breast cancer risk.

Author

Chajes V., Dugue P.-A., Southey M.C., Giles G.G., English D.R., Milne R.L., Severi G., Ambatipudi S., Cuenin C., Romieu I., Herceg Z., Swerdlow A.J., Vineis P., Flanagan J.M., Johansson A., Palli D., Masala G., Grioni S., Agnoli C., Tumino R., Giurdanella M.C., Fasanelli F., Sacerdote C., Panico S., Mattiello A., Polidoro S., Jones M.E., Schoemaker M.J., Orr N., Tomczyk K., Johnson N., Fletcher O., Perduca V., Baglietto L., Chajes V., Dugue P.-A., Southey M.C., Giles G.G., English D.R., Milne R.L., Severi G., Ambatipudi S., Cuenin C., Romieu I., Herceg Z., Swerdlow A.J., Vineis P., Flanagan J.M., Johansson A., Palli D., Masala G., Grioni S., Agnoli C., Tumino R., Giurdanella M.C., Fasanelli F., Sacerdote C., Panico S., Mattiello A., Polidoro S., Jones M.E., Schoemaker M.J., Orr N., Tomczyk K., Johnson N., Fletcher O., Perduca V., and Baglietto L.

Abstract

Background: It is well established that estrogens and other hormonal factors influence breast cancer susceptibility. We hypothesized that a woman's total lifetime estrogen exposure accumulates changes in DNA methylation, detectable in the blood, which could be used in risk assessment for breast cancer. Method(s): An estimated lifetime estrogen exposure (ELEE) model was defined using epidemiological data from EPIC-Italy (n = 31,864). An epigenome-wide association study (EWAS) of ELEE was performed using existing Illumina HumanMethylation450K Beadchip (HM450K) methylation data obtained from EPIC-Italy blood DNA samples (n = 216). A methylation index (MI) of ELEE based on 31 CpG sites was developed using HM450K data from EPIC-Italy and the Generations Study and evaluated for association with breast cancer risk in an independent dataset from the Generations Study (n = 440 incident breast cancer cases matched to 440 healthy controls) using targeted bisulfite sequencing. Lastly, a meta-analysis was conducted including three additional cohorts, consisting of 1187 case-control pairs. Result(s): We observed an estimated 5% increase in breast cancer risk per 1-year longer ELEE (OR = 1.05, 95% CI 1.04-1.07, P = 3 x 10-12) in EPIC-Italy. The EWAS identified 694 CpG sites associated with ELEE (FDR Q < 0.05). We report a DNA methylation index (MI) associated with breast cancer risk that is validated in the Generations Study targeted bisulfite sequencing data (ORQ4-vs-Q1 = 1.77, 95% CI 1.07-2.93, P = 0.027) and in the meta-analysis (ORQ4-vs-Q1 = 1.43, 95% CI 1.05-2.00, P = 0.024); however, the correlation between the MI and ELEE was not validated across study cohorts. Conclusion(s): We have identified a blood DNA methylation signature associated with breast cancer risk in this study. Further investigation is required to confirm the interaction between estrogen exposure and DNA methylation in the blood.Copyright © 2019 The Author(s).

Published
2019

4. 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

5. Epigenome-wide association study for lifetime estrogen exposure identifies an epigenetic signature associated with breast cancer risk

Author

Johansson, A, Palli, D, Masala, G, Grioni, S, Agnoli, C, Tumino, R, Giurdanella, MC, Fasanelli, F, Sacerdote, C, Panico, S, Mattiello, A, Polidoro, S, Jones, ME, Schoemaker, MJ, Orr, N, Tomczyk, K, Johnson, N, Fletcher, O, Perduca, V, Baglietto, L, Dugue, P-A, Southey, MC, Giles, GG, English, DR, Milne, RL, Severi, G, Ambatipudi, S, Cuenin, C, Chajes, V, Romieu, I, Herceg, Z, Swerdlow, AJ, Vineis, P, Flanagan, JM, Johansson, A, Palli, D, Masala, G, Grioni, S, Agnoli, C, Tumino, R, Giurdanella, MC, Fasanelli, F, Sacerdote, C, Panico, S, Mattiello, A, Polidoro, S, Jones, ME, Schoemaker, MJ, Orr, N, Tomczyk, K, Johnson, N, Fletcher, O, Perduca, V, Baglietto, L, Dugue, P-A, Southey, MC, Giles, GG, English, DR, Milne, RL, Severi, G, Ambatipudi, S, Cuenin, C, Chajes, V, Romieu, I, Herceg, Z, Swerdlow, AJ, Vineis, P, and Flanagan, JM

Abstract

BACKGROUND: It is well established that estrogens and other hormonal factors influence breast cancer susceptibility. We hypothesized that a woman's total lifetime estrogen exposure accumulates changes in DNA methylation, detectable in the blood, which could be used in risk assessment for breast cancer. METHODS: An estimated lifetime estrogen exposure (ELEE) model was defined using epidemiological data from EPIC-Italy (n = 31,864). An epigenome-wide association study (EWAS) of ELEE was performed using existing Illumina HumanMethylation450K Beadchip (HM450K) methylation data obtained from EPIC-Italy blood DNA samples (n = 216). A methylation index (MI) of ELEE based on 31 CpG sites was developed using HM450K data from EPIC-Italy and the Generations Study and evaluated for association with breast cancer risk in an independent dataset from the Generations Study (n = 440 incident breast cancer cases matched to 440 healthy controls) using targeted bisulfite sequencing. Lastly, a meta-analysis was conducted including three additional cohorts, consisting of 1187 case-control pairs. RESULTS: We observed an estimated 5% increase in breast cancer risk per 1-year longer ELEE (OR = 1.05, 95% CI 1.04-1.07, P = 3 × 10-12) in EPIC-Italy. The EWAS identified 694 CpG sites associated with ELEE (FDR Q < 0.05). We report a DNA methylation index (MI) associated with breast cancer risk that is validated in the Generations Study targeted bisulfite sequencing data (ORQ4_vs_Q1 = 1.77, 95% CI 1.07-2.93, P = 0.027) and in the meta-analysis (ORQ4_vs_Q1 = 1.43, 95% CI 1.05-2.00, P = 0.024); however, the correlation between the MI and ELEE was not validated across study cohorts. CONCLUSION: We have identified a blood DNA methylation signature associated with breast cancer risk in this study. Further investigation is required to confirm the interaction between estrogen exposure and DNA methylation in the blood.

Published
2019

6. Association of leukocyte DNA methylation changes with dietary folate and alcohol intake in the EPIC study

Author

Perrier, F, Viallon, V, Ambatipudi, S, Ghantous, A, Cuenin, C, Hernandez-Vargas, H, Chajes, V, Baglietto, L, Matejcic, M, Moreno-Macias, H, Kuehn, T, Boeing, H, Karakatsani, A, Kotanidou, A, Trichopoulou, A, Sieri, S, Panico, S, Fasanelli, F, Dolle, M, Onland-Moret, C, Sluijs, I, Weiderpass, E, Quiros, JR, Agudo, A, Huerta, JM, Ardanaz, E, Dorronsoro, M, Tong, TYN, Tsilidis, K, Riboli, E, Gunter, MJ, Herceg, Z, Ferrari, P, Romieu, I, Perrier, F, Viallon, V, Ambatipudi, S, Ghantous, A, Cuenin, C, Hernandez-Vargas, H, Chajes, V, Baglietto, L, Matejcic, M, Moreno-Macias, H, Kuehn, T, Boeing, H, Karakatsani, A, Kotanidou, A, Trichopoulou, A, Sieri, S, Panico, S, Fasanelli, F, Dolle, M, Onland-Moret, C, Sluijs, I, Weiderpass, E, Quiros, JR, Agudo, A, Huerta, JM, Ardanaz, E, Dorronsoro, M, Tong, TYN, Tsilidis, K, Riboli, E, Gunter, MJ, Herceg, Z, Ferrari, P, and Romieu, I

Abstract

BACKGROUND: There is increasing evidence that folate, an important component of one-carbon metabolism, modulates the epigenome. Alcohol, which can disrupt folate absorption, is also known to affect the epigenome. We investigated the association of dietary folate and alcohol intake on leukocyte DNA methylation levels in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Leukocyte genome-wide DNA methylation profiles on approximately 450,000 CpG sites were acquired with Illumina HumanMethylation 450K BeadChip measured among 450 women control participants of a case-control study on breast cancer nested within the EPIC cohort. After data preprocessing using surrogate variable analysis to reduce systematic variation, associations of DNA methylation with dietary folate and alcohol intake, assessed with dietary questionnaires, were investigated using CpG site-specific linear models. Specific regions of the methylome were explored using differentially methylated region (DMR) analysis and fused lasso (FL) regressions. The DMR analysis combined results from the feature-specific analysis for a specific chromosome and using distances between features as weights whereas FL regression combined two penalties to encourage sparsity of single features and the difference between two consecutive features. RESULTS: After correction for multiple testing, intake of dietary folate was not associated with methylation level at any DNA methylation site, while weak associations were observed between alcohol intake and methylation level at CpG sites cg03199996 and cg07382687, with qval = 0.029 and qval = 0.048, respectively. Interestingly, the DMR analysis revealed a total of 24 and 90 regions associated with dietary folate and alcohol, respectively. For alcohol intake, 6 of the 15 most significant DMRs were identified through FL. CONCLUSIONS: Alcohol intake was associated with methylation levels at two CpG sites. Evidence from DMR and FL analyses indicated that diet

Published
2019

7. Blood DNA methylation and breast cancer risk: a meta-analysis of four prospective cohort studies

Author

Bodelon, C, Ambatipudi, S, Dugue, P-A, Johansson, A, Sampson, JN, Hicks, B, Karlins, E, Hutchinson, A, Cuenin, C, Chajes, V, Southey, MC, Romieu, I, Giles, GG, English, D, Polidoro, S, Assumma, M, Baglietto, L, Vineis, P, Severi, G, Herceg, Z, Flanagan, JM, Milne, RL, Garcia-Closas, M, Bodelon, C, Ambatipudi, S, Dugue, P-A, Johansson, A, Sampson, JN, Hicks, B, Karlins, E, Hutchinson, A, Cuenin, C, Chajes, V, Southey, MC, Romieu, I, Giles, GG, English, D, Polidoro, S, Assumma, M, Baglietto, L, Vineis, P, Severi, G, Herceg, Z, Flanagan, JM, Milne, RL, and Garcia-Closas, M

Abstract

BACKGROUND: Environmental and genetic factors play an important role in the etiology of breast cancer. Several small blood-based DNA methylation studies have reported risk associations with methylation at individual CpGs and average methylation levels; however, these findings require validation in larger prospective cohort studies. To investigate the role of blood DNA methylation on breast cancer risk, we conducted a meta-analysis of four prospective cohort studies, including a total of 1663 incident cases and 1885 controls, the largest study of blood DNA methylation and breast cancer risk to date. METHODS: We assessed associations with methylation at 365,145 CpGs present in the HumanMethylation450 (HM450K) Beadchip, after excluding CpGs that did not pass quality controls in all studies. Each of the four cohorts estimated odds ratios (ORs) and 95% confidence intervals (CI) for the association between each individual CpG and breast cancer risk. In addition, each study assessed the association between average methylation measures and breast cancer risk, adjusted and unadjusted for cell-type composition. Study-specific ORs were combined using fixed-effect meta-analysis with inverse variance weights. Stratified analyses were conducted by age at diagnosis (< 50, ≥ 50), estrogen receptor (ER) status (+/-), and time since blood collection (< 5, 5-10, > 10 years). The false discovery rate (q value) was used to account for multiple testing. RESULTS: The average age at blood draw ranged from 52.2 to 62.2 years across the four cohorts. Median follow-up time ranged from 6.6 to 8.4 years. The methylation measured at individual CpGs was not associated with breast cancer risk (q value > 0.59). In addition, higher average methylation level was not associated with risk of breast cancer (OR = 0.94, 95% CI = 0.85, 1.05; P = 0.26; P for study heterogeneity = 0.86). We found no evidence of modification of this association by age at diagnosis (P = 0.17), ER status (P = 0.88), time since

Published
2019

8. 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

9. 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., Thomas de Montpreville, V., 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., Thomas de Montpreville, V., 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

10. 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

30. Quantitative analysis of DNA methylation after whole bisulfitome amplification of a minute amount of DNA from body fluids.

Author

Risk Assessment of Toxic and Immunomodulatory Agents, Dep IRAS, Vaissiere, T., Cuenin, C., Paliwal, A., Vineis, P., Hoek, G., Krzyzanowski, M., Airoldi, L., Dunning, A., Garte, S., Malaveille, C., Overvad, K., Clavel-Chapelon, F., Linseisen, J., Boeing, H., Trichopoulou, A., Trichopoulous, D., Kaladidi, A., Palli, D., Krogh, V., Tumino, R., Panico, S., Bueno de Mesquita, H.B., Peeters, P.H.M., Kumle, M., Gonzalez, C.A., Martinez, C., Dorronsoro, M., Barricarte, A., Navarro, C., Quiros, J.R., Berglund, B., Janzon, L., Jarvholm, B., Day, N.E., Key, T.J., Saracci, R., Kaaks, R., Riboli, E., Hainaut, P., Herceg, Z., Risk Assessment of Toxic and Immunomodulatory Agents, Dep IRAS, Vaissiere, T., Cuenin, C., Paliwal, A., Vineis, P., Hoek, G., Krzyzanowski, M., Airoldi, L., Dunning, A., Garte, S., Malaveille, C., Overvad, K., Clavel-Chapelon, F., Linseisen, J., Boeing, H., Trichopoulou, A., Trichopoulous, D., Kaladidi, A., Palli, D., Krogh, V., Tumino, R., Panico, S., Bueno de Mesquita, H.B., Peeters, P.H.M., Kumle, M., Gonzalez, C.A., Martinez, C., Dorronsoro, M., Barricarte, A., Navarro, C., Quiros, J.R., Berglund, B., Janzon, L., Jarvholm, B., Day, N.E., Key, T.J., Saracci, R., Kaaks, R., Riboli, E., Hainaut, P., and Herceg, Z.

Published
2009

31. Quantitative analysis of DNA methylation after whole bisulfitome amplification of a minute amount of DNA from body fluids.

Author

Risk Assessment of Toxic and Immunomodulatory Agents, Dep IRAS, Vaissiere, T., Cuenin, C., Paliwal, A., Vineis, P., Hoek, G., Krzyzanowski, M., Airoldi, L., Dunning, A., Garte, S., Malaveille, C., Overvad, K., Clavel-Chapelon, F., Linseisen, J., Boeing, H., Trichopoulou, A., Trichopoulous, D., Kaladidi, A., Palli, D., Krogh, V., Tumino, R., Panico, S., Bueno de Mesquita, H.B., Peeters, P.H.M., Kumle, M., Gonzalez, C.A., Martinez, C., Dorronsoro, M., Barricarte, A., Navarro, C., Quiros, J.R., Berglund, B., Janzon, L., Jarvholm, B., Day, N.E., Key, T.J., Saracci, R., Kaaks, R., Riboli, E., Hainaut, P., Herceg, Z., Risk Assessment of Toxic and Immunomodulatory Agents, Dep IRAS, Vaissiere, T., Cuenin, C., Paliwal, A., Vineis, P., Hoek, G., Krzyzanowski, M., Airoldi, L., Dunning, A., Garte, S., Malaveille, C., Overvad, K., Clavel-Chapelon, F., Linseisen, J., Boeing, H., Trichopoulou, A., Trichopoulous, D., Kaladidi, A., Palli, D., Krogh, V., Tumino, R., Panico, S., Bueno de Mesquita, H.B., Peeters, P.H.M., Kumle, M., Gonzalez, C.A., Martinez, C., Dorronsoro, M., Barricarte, A., Navarro, C., Quiros, J.R., Berglund, B., Janzon, L., Jarvholm, B., Day, N.E., Key, T.J., Saracci, R., Kaaks, R., Riboli, E., Hainaut, P., and Herceg, Z.

Published
2009

32. Quantitative analysis of DNA methylation after whole bisulfitome amplification of a minute amount of DNA from body fluids.

Author

Risk Assessment of Toxic and Immunomodulatory Agents, Dep IRAS, Vaissiere, T., Cuenin, C., Paliwal, A., Vineis, P., Hoek, G., Krzyzanowski, M., Airoldi, L., Dunning, A., Garte, S., Malaveille, C., Overvad, K., Clavel-Chapelon, F., Linseisen, J., Boeing, H., Trichopoulou, A., Trichopoulous, D., Kaladidi, A., Palli, D., Krogh, V., Tumino, R., Panico, S., Bueno de Mesquita, H.B., Peeters, P.H.M., Kumle, M., Gonzalez, C.A., Martinez, C., Dorronsoro, M., Barricarte, A., Navarro, C., Quiros, J.R., Berglund, B., Janzon, L., Jarvholm, B., Day, N.E., Key, T.J., Saracci, R., Kaaks, R., Riboli, E., Hainaut, P., Herceg, Z., Risk Assessment of Toxic and Immunomodulatory Agents, Dep IRAS, Vaissiere, T., Cuenin, C., Paliwal, A., Vineis, P., Hoek, G., Krzyzanowski, M., Airoldi, L., Dunning, A., Garte, S., Malaveille, C., Overvad, K., Clavel-Chapelon, F., Linseisen, J., Boeing, H., Trichopoulou, A., Trichopoulous, D., Kaladidi, A., Palli, D., Krogh, V., Tumino, R., Panico, S., Bueno de Mesquita, H.B., Peeters, P.H.M., Kumle, M., Gonzalez, C.A., Martinez, C., Dorronsoro, M., Barricarte, A., Navarro, C., Quiros, J.R., Berglund, B., Janzon, L., Jarvholm, B., Day, N.E., Key, T.J., Saracci, R., Kaaks, R., Riboli, E., Hainaut, P., and Herceg, Z.

Published
2009

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