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Genetic Polymorphisms Involved in Mitochondrial Metabolism and Pancreatic Cancer Risk

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Genetic Polymorphisms Involved in Mitochondrial Metabolism and Pancreatic Cancer Risk. / Peduzzi, Giulia; Gentiluomo, Manuel; Tavano, Francesca; Arcidiacono, Paolo Giorgio; Ermini, Stefano; Vodicka, Pavel; Boggi, Ugo; Cavestro, Giulia Martina; Capurso, Gabriele; Morelli, Luca; Milanetto, Anna Caterina; Pezzilli, Raffaele; Lawlor, Rita T; Carrara, Silvia; Lovecek, Martin; Souček, Pavel; Guo, Feng; Hackert, Thilo; Uzunoğlu, Faik G; Gazouli, Maria; Párniczky, Andrea; Kupcinskas, Juozas; Bijlsma, Maarten F; Bueno-de-Mesquita, Bas; Vermeulen, Roel; van Eijck, Casper H J; Jamroziak, Krzysztof; Talar-Wojnarowska, Renata; Greenhalf, William; Gioffreda, Domenica; Petrone, Maria C; Landi, Stefano; Archibugi, Livia; Puzzono, Marta; Funel, Niccola; Sperti, Cosimo; Piredda, Maria L; Mohelnikova-Duchonova, Beatrice; Lu, Ye; Hlaváč, Viktor; Gao, Xin; Schneider, Martin; Izbicki, Jakob R; Theodoropoulos, George; Bunduc, Stefania; Kreivenaite, Edita; Busch, Olivier R; Małecka-Panas, Ewa; Costello, Eithne; Perri, Francesco; Testoni, Sabrina Gloria Giulia; Vanella, Giuseppe; Pasquali, Claudio; Oliverius, Martin; Brenner, Hermann; Loos, Martin; Götz, Mara; Georgiou, Konstantinos; Erőss, Bálint; Maiello, Evaristo; Szentesi, Andrea; Bazzocchi, Francesca; Basso, Daniela; Neoptolemos, John P; Hegyi, Péter; Kiudelis, Vytautas; Canzian, Federico; Campa, Daniele.

In: CANCER EPIDEM BIOMAR, Vol. 30, No. 12, 12.2021, p. 2342-2345.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Peduzzi, G, Gentiluomo, M, Tavano, F, Arcidiacono, PG, Ermini, S, Vodicka, P, Boggi, U, Cavestro, GM, Capurso, G, Morelli, L, Milanetto, AC, Pezzilli, R, Lawlor, RT, Carrara, S, Lovecek, M, Souček, P, Guo, F, Hackert, T, Uzunoğlu, FG, Gazouli, M, Párniczky, A, Kupcinskas, J, Bijlsma, MF, Bueno-de-Mesquita, B, Vermeulen, R, van Eijck, CHJ, Jamroziak, K, Talar-Wojnarowska, R, Greenhalf, W, Gioffreda, D, Petrone, MC, Landi, S, Archibugi, L, Puzzono, M, Funel, N, Sperti, C, Piredda, ML, Mohelnikova-Duchonova, B, Lu, Y, Hlaváč, V, Gao, X, Schneider, M, Izbicki, JR, Theodoropoulos, G, Bunduc, S, Kreivenaite, E, Busch, OR, Małecka-Panas, E, Costello, E, Perri, F, Testoni, SGG, Vanella, G, Pasquali, C, Oliverius, M, Brenner, H, Loos, M, Götz, M, Georgiou, K, Erőss, B, Maiello, E, Szentesi, A, Bazzocchi, F, Basso, D, Neoptolemos, JP, Hegyi, P, Kiudelis, V, Canzian, F & Campa, D 2021, 'Genetic Polymorphisms Involved in Mitochondrial Metabolism and Pancreatic Cancer Risk', CANCER EPIDEM BIOMAR, vol. 30, no. 12, pp. 2342-2345. https://doi.org/10.1158/1055-9965.EPI-21-0353

APA

Peduzzi, G., Gentiluomo, M., Tavano, F., Arcidiacono, P. G., Ermini, S., Vodicka, P., Boggi, U., Cavestro, G. M., Capurso, G., Morelli, L., Milanetto, A. C., Pezzilli, R., Lawlor, R. T., Carrara, S., Lovecek, M., Souček, P., Guo, F., Hackert, T., Uzunoğlu, F. G., ... Campa, D. (2021). Genetic Polymorphisms Involved in Mitochondrial Metabolism and Pancreatic Cancer Risk. CANCER EPIDEM BIOMAR, 30(12), 2342-2345. https://doi.org/10.1158/1055-9965.EPI-21-0353

Vancouver

Peduzzi G, Gentiluomo M, Tavano F, Arcidiacono PG, Ermini S, Vodicka P et al. Genetic Polymorphisms Involved in Mitochondrial Metabolism and Pancreatic Cancer Risk. CANCER EPIDEM BIOMAR. 2021 Dec;30(12):2342-2345. https://doi.org/10.1158/1055-9965.EPI-21-0353

Bibtex

@article{62c5f34bff5e4e33b5c0d3239004f3b6,
title = "Genetic Polymorphisms Involved in Mitochondrial Metabolism and Pancreatic Cancer Risk",
abstract = "BACKGROUND: The mitochondrial metabolism has been associated with pancreatic ductal adenocarcinoma (PDAC) risk. Recent evidence also suggests the involvement of the genetic variability of the mitochondrial function in several traits involved in PDAC etiology. However, a systematic investigation of the genetic variability of mitochondrial genome (mtSNP) and of all the nuclear genes involved in its functioning (n-mtSNPs) has never been reported.METHODS: We conducted a two-phase association study of mtSNPs and n-mtSNPs to assess their effect on PDAC risk. We analyzed 35,297 n-mtSNPs and 101 mtSNPs in up to 55,870 individuals (12,884 PDAC cases and 42,986 controls). In addition, we also conducted a gene-based analysis on 1,588 genes involved in mitochondrial metabolism using Multi-marker Analysis of GenoMic Annotation (MAGMA) software.RESULTS: In the discovery phase, we identified 49 n-mtSNPs and no mtSNPs associated with PDAC risk (P < 0.05). In the second phase, none of the findings were replicated. In the gene-level analysis, we observed that three genes (TERT, SUGCT, and SURF1) involved in the mitochondrial metabolism showed an association below the Bonferroni-corrected threshold of statistical significance (P = 0.05/1588 = 3.1 × 10-5).CONCLUSIONS: Even though the mitochondrial metabolism might be involved in PDAC etiology, our results, obtained in a study with one of the largest sample sizes to date, show that neither n-mtSNPs nor mtSNPs are associated with PDAC risk.IMPACT: This large case-control study does not support a role of the genetic variability of the mitochondrial function in PDAC risk.",
author = "Giulia Peduzzi and Manuel Gentiluomo and Francesca Tavano and Arcidiacono, {Paolo Giorgio} and Stefano Ermini and Pavel Vodicka and Ugo Boggi and Cavestro, {Giulia Martina} and Gabriele Capurso and Luca Morelli and Milanetto, {Anna Caterina} and Raffaele Pezzilli and Lawlor, {Rita T} and Silvia Carrara and Martin Lovecek and Pavel Sou{\v c}ek and Feng Guo and Thilo Hackert and Uzunoğlu, {Faik G} and Maria Gazouli and Andrea P{\'a}rniczky and Juozas Kupcinskas and Bijlsma, {Maarten F} and Bas Bueno-de-Mesquita and Roel Vermeulen and {van Eijck}, {Casper H J} and Krzysztof Jamroziak and Renata Talar-Wojnarowska and William Greenhalf and Domenica Gioffreda and Petrone, {Maria C} and Stefano Landi and Livia Archibugi and Marta Puzzono and Niccola Funel and Cosimo Sperti and Piredda, {Maria L} and Beatrice Mohelnikova-Duchonova and Ye Lu and Viktor Hlav{\'a}{\v c} and Xin Gao and Martin Schneider and Izbicki, {Jakob R} and George Theodoropoulos and Stefania Bunduc and Edita Kreivenaite and Busch, {Olivier R} and Ewa Ma{\l}ecka-Panas and Eithne Costello and Francesco Perri and Testoni, {Sabrina Gloria Giulia} and Giuseppe Vanella and Claudio Pasquali and Martin Oliverius and Hermann Brenner and Martin Loos and Mara G{\"o}tz and Konstantinos Georgiou and B{\'a}lint Er{\H o}ss and Evaristo Maiello and Andrea Szentesi and Francesca Bazzocchi and Daniela Basso and Neoptolemos, {John P} and P{\'e}ter Hegyi and Vytautas Kiudelis and Federico Canzian and Daniele Campa",
note = "{\textcopyright}2021 American Association for Cancer Research.",
year = "2021",
month = dec,
doi = "10.1158/1055-9965.EPI-21-0353",
language = "English",
volume = "30",
pages = "2342--2345",
journal = "CANCER EPIDEM BIOMAR",
issn = "1055-9965",
publisher = "American Association for Cancer Research Inc.",
number = "12",

}

RIS

TY - JOUR

T1 - Genetic Polymorphisms Involved in Mitochondrial Metabolism and Pancreatic Cancer Risk

AU - Peduzzi, Giulia

AU - Gentiluomo, Manuel

AU - Tavano, Francesca

AU - Arcidiacono, Paolo Giorgio

AU - Ermini, Stefano

AU - Vodicka, Pavel

AU - Boggi, Ugo

AU - Cavestro, Giulia Martina

AU - Capurso, Gabriele

AU - Morelli, Luca

AU - Milanetto, Anna Caterina

AU - Pezzilli, Raffaele

AU - Lawlor, Rita T

AU - Carrara, Silvia

AU - Lovecek, Martin

AU - Souček, Pavel

AU - Guo, Feng

AU - Hackert, Thilo

AU - Uzunoğlu, Faik G

AU - Gazouli, Maria

AU - Párniczky, Andrea

AU - Kupcinskas, Juozas

AU - Bijlsma, Maarten F

AU - Bueno-de-Mesquita, Bas

AU - Vermeulen, Roel

AU - van Eijck, Casper H J

AU - Jamroziak, Krzysztof

AU - Talar-Wojnarowska, Renata

AU - Greenhalf, William

AU - Gioffreda, Domenica

AU - Petrone, Maria C

AU - Landi, Stefano

AU - Archibugi, Livia

AU - Puzzono, Marta

AU - Funel, Niccola

AU - Sperti, Cosimo

AU - Piredda, Maria L

AU - Mohelnikova-Duchonova, Beatrice

AU - Lu, Ye

AU - Hlaváč, Viktor

AU - Gao, Xin

AU - Schneider, Martin

AU - Izbicki, Jakob R

AU - Theodoropoulos, George

AU - Bunduc, Stefania

AU - Kreivenaite, Edita

AU - Busch, Olivier R

AU - Małecka-Panas, Ewa

AU - Costello, Eithne

AU - Perri, Francesco

AU - Testoni, Sabrina Gloria Giulia

AU - Vanella, Giuseppe

AU - Pasquali, Claudio

AU - Oliverius, Martin

AU - Brenner, Hermann

AU - Loos, Martin

AU - Götz, Mara

AU - Georgiou, Konstantinos

AU - Erőss, Bálint

AU - Maiello, Evaristo

AU - Szentesi, Andrea

AU - Bazzocchi, Francesca

AU - Basso, Daniela

AU - Neoptolemos, John P

AU - Hegyi, Péter

AU - Kiudelis, Vytautas

AU - Canzian, Federico

AU - Campa, Daniele

N1 - ©2021 American Association for Cancer Research.

PY - 2021/12

Y1 - 2021/12

N2 - BACKGROUND: The mitochondrial metabolism has been associated with pancreatic ductal adenocarcinoma (PDAC) risk. Recent evidence also suggests the involvement of the genetic variability of the mitochondrial function in several traits involved in PDAC etiology. However, a systematic investigation of the genetic variability of mitochondrial genome (mtSNP) and of all the nuclear genes involved in its functioning (n-mtSNPs) has never been reported.METHODS: We conducted a two-phase association study of mtSNPs and n-mtSNPs to assess their effect on PDAC risk. We analyzed 35,297 n-mtSNPs and 101 mtSNPs in up to 55,870 individuals (12,884 PDAC cases and 42,986 controls). In addition, we also conducted a gene-based analysis on 1,588 genes involved in mitochondrial metabolism using Multi-marker Analysis of GenoMic Annotation (MAGMA) software.RESULTS: In the discovery phase, we identified 49 n-mtSNPs and no mtSNPs associated with PDAC risk (P < 0.05). In the second phase, none of the findings were replicated. In the gene-level analysis, we observed that three genes (TERT, SUGCT, and SURF1) involved in the mitochondrial metabolism showed an association below the Bonferroni-corrected threshold of statistical significance (P = 0.05/1588 = 3.1 × 10-5).CONCLUSIONS: Even though the mitochondrial metabolism might be involved in PDAC etiology, our results, obtained in a study with one of the largest sample sizes to date, show that neither n-mtSNPs nor mtSNPs are associated with PDAC risk.IMPACT: This large case-control study does not support a role of the genetic variability of the mitochondrial function in PDAC risk.

AB - BACKGROUND: The mitochondrial metabolism has been associated with pancreatic ductal adenocarcinoma (PDAC) risk. Recent evidence also suggests the involvement of the genetic variability of the mitochondrial function in several traits involved in PDAC etiology. However, a systematic investigation of the genetic variability of mitochondrial genome (mtSNP) and of all the nuclear genes involved in its functioning (n-mtSNPs) has never been reported.METHODS: We conducted a two-phase association study of mtSNPs and n-mtSNPs to assess their effect on PDAC risk. We analyzed 35,297 n-mtSNPs and 101 mtSNPs in up to 55,870 individuals (12,884 PDAC cases and 42,986 controls). In addition, we also conducted a gene-based analysis on 1,588 genes involved in mitochondrial metabolism using Multi-marker Analysis of GenoMic Annotation (MAGMA) software.RESULTS: In the discovery phase, we identified 49 n-mtSNPs and no mtSNPs associated with PDAC risk (P < 0.05). In the second phase, none of the findings were replicated. In the gene-level analysis, we observed that three genes (TERT, SUGCT, and SURF1) involved in the mitochondrial metabolism showed an association below the Bonferroni-corrected threshold of statistical significance (P = 0.05/1588 = 3.1 × 10-5).CONCLUSIONS: Even though the mitochondrial metabolism might be involved in PDAC etiology, our results, obtained in a study with one of the largest sample sizes to date, show that neither n-mtSNPs nor mtSNPs are associated with PDAC risk.IMPACT: This large case-control study does not support a role of the genetic variability of the mitochondrial function in PDAC risk.

U2 - 10.1158/1055-9965.EPI-21-0353

DO - 10.1158/1055-9965.EPI-21-0353

M3 - SCORING: Journal article

C2 - 34526302

VL - 30

SP - 2342

EP - 2345

JO - CANCER EPIDEM BIOMAR

JF - CANCER EPIDEM BIOMAR

SN - 1055-9965

IS - 12

ER -