163 results on '"Mariosa, Daniela"'
Search Results
2. Association between circulating inflammatory markers and adult cancer risk: a Mendelian randomization analysis
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Landi, Maria Teresa, Stevens, Victoria, Wang, Ying, Albanes, Demetrios, Caporaso, Neil, Brennan, Paul, Amos, Christopher I., Shete, Sanjay, Hung, Rayjean J., Bickeböller, Heike, Risch, Angela, Houlston, Richard, Lam, Stephen, Tardon, Adonina, Chen, Chu, Bojesen, Stig E., Johansson, Mattias, Wichmann, H-Erich, Christiani, David, Rennert, Gadi, Arnold, Susanne, Field, John K., Le Marchand, Loic, Melander, Olle, Brunnström, Hans, Liu, Geoffrey, Andrew, Angeline, Kiemeney, Lambertus A., Shen, Hongbing, Zienolddiny, Shan, Grankvist, Kjell, Johansson, Mikael, Teare, M. Dawn, Hong, Yun-Chul, Yuan, Jian-Min, Lazarus, Philip, Schabath, Matthew B., Aldrich, Melinda C., Eeles, Rosalind A., Haiman, Christopher A., Kote-Jarai, Zsofia, Schumacher, Fredrick R., Benlloch, Sara, Al Olama, Ali Amin, Muir, Kenneth R., Berndt, Sonja I., Conti, David V., Wiklund, Fredrik, Chanock, Stephen, Tangen, Catherine M., Batra, Jyotsna, Clements, Judith A., Grönberg, Henrik, Pashayan, Nora, Schleutker, Johanna, Albanes, Demetrius, Weinstein, Stephanie J., Wolk, Alicja, West, Catharine M.L., Mucci, Lorelei A., Cancel-Tassin, Géraldine, Koutros, Stella, Sørensen, Karina Dalsgaard, Grindedal, Eli Marie, Neal, David E., Hamdy, Freddie C., Donovan, Jenny L., Travis, Ruth C., Hamilton, Robert J., Ingles, Sue Ann, Rosenstein, Barry S., Lu, Yong-Jie, Giles, Graham G., MacInnis, Robert J., Kibel, Adam S., Vega, Ana, Kogevinas, Manolis, Penney, Kathryn L., Park, Jong Y., Stanfrod, Janet L., Cybulski, Cezary, Nordestgaard, Børge G., Nielsen, Sune F., Brenner, Hermann, Maier, Christiane, Logothetis, Christopher J., John, Esther M., Teixeira, Manuel R., Neuhausen, Susan L., De Ruyck, Kim, Razack, Azad, Newcomb, Lisa F., Lessel, Davor, Kaneva, Radka, Usmani, Nawaid, Claessens, Frank, Townsend, Paul A., Castelao, Jose Esteban, Roobol, Monique J., Menegaux, Florence, Khaw, Kay-Tee, Cannon-Albright, Lisa, Pandha, Hardev, Thibodeau, Stephen N., Hunter, David J., Kraft, Peter, Blot, William J., Riboli, Elio, Yarmolinsky, James, Robinson, Jamie W., Mariosa, Daniela, Karhunen, Ville, Huang, Jian, Dimou, Niki, Murphy, Neil, Burrows, Kimberley, Bouras, Emmanouil, Smith-Byrne, Karl, Lewis, Sarah J., Galesloot, Tessel E., Vermeulen, Sita, Martin, Paul, Hou, Lifang, Newcomb, Polly A., White, Emily, Wu, Anna H., Le Marchand, Loïc, Phipps, Amanda I., Buchanan, Daniel D., Zhao, Sizheng Steven, Gill, Dipender, Chanock, Stephen J., Purdue, Mark P., Davey Smith, George, Herzig, Karl-Heinz, Järvelin, Marjo-Riitta, Amos, Chris I., Dehghan, Abbas, Gunter, Marc J., Tsilidis, Kostas K., and Martin, Richard M.
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- 2024
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3. Genetically proxied impaired GIPR signaling and risk of 6 cancers
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Rogers, Miranda, Gill, Dipender, Ahlqvist, Emma, Robinson, Tim, Mariosa, Daniela, Johansson, Mattias, Cortez Cardoso Penha, Ricardo, Dossus, Laure, Gunter, Marc J., Moreno, Victor, Davey Smith, George, Martin, Richard M., and Yarmolinsky, James
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- 2023
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4. The association between genetically elevated polyunsaturated fatty acids and risk of cancer
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Tintle, Nathan, Rice, Terri, Cheng, Iona, Jenkins, Mark, Gallinger, Steve, Cornish, Alex J., Sud, Amit, Vijayakrishnan, Jayaram, Wrensch, Margaret, Johansson, Mattias, Norman, Aaron D., Klein, Alison, Clay-Gilmour, Alyssa, Franke, Andre, Ardisson Korat, Andres V., Wheeler, Bill, Nilsson, Björn, Smith, Caren, Heng, Chew-Kiat, Song, Ci, Riadi, David, Claus, Elizabeth B., Ellinghaus, Eva, Ostroumova, Evgenia, Hosnijeh, de Vathaire, Florent, Cugliari, Giovanni, Matullo, Giuseppe, Oi-Lin Ng, Irene, Passow, Jeanette E., Foo, Jia Nee, Han, Jiali, Liu, Jianjun, Barnholtz-Sloan, Jill, Schildkraut, Joellen M., Maris, John, Wiemels, Joseph L., Hemminki, Kari, Yang, Keming, Kiemeney, Lambertus A., Wu, Lang, Amundadottir, Laufey, Stern, Marc-Henri, Boutron, Marie-Christine, Iles, Mark Martin, Purdue, Mark P., Stanulla, Martin, Bondy, Melissa, Gaudet, Mia, Mobuchon, Lenha, Camp, Nicola J., Sham, Pak Chung, Guénel, Pascal, Brennan, Paul, Taylor, Philip R., Ostrom, Quinn, Stolzenberg-Solomon, Rachael, Dorajoo, Rajkumar, Houlston, Richard, Jenkins, Robert B., Diskin, Sharon, Berndt, Sonja I., Tsavachidis, Spiridon, Channock, Stephen J., Harrison, Tabitha, Galesloot, Tessel, Gyllensten, Ulf, Joseph, Vijai, Shi, Y., Yang, Wenjian, Lin, Yi, Van Den Eeden, Stephen K., Haycock, Philip C., Borges, Maria Carolina, Burrows, Kimberley, Lemaitre, Rozenn N., Burgess, Stephen, Khankari, Nikhil K., Tsilidis, Konstantinos K., Gaunt, Tom R., Hemani, Gibran, Zheng, Jie, Truong, Therese, Birmann, Brenda M., OMara, Tracy, Spurdle, Amanda B., Iles, Mark M., Law, Matthew H., Slager, Susan L., Saberi Hosnijeh, Fatemeh, Mariosa, Daniela, Cotterchio, Michelle, Cerhan, James R., Peters, Ulrike, Enroth, Stefan, Gharahkhani, Puya, Le Marchand, Loic, Williams, Ann C., Block, Robert C., Amos, Christopher I., Hung, Rayjean J., Zheng, Wei, Gunter, Marc J., Smith, George Davey, Relton, Caroline, and Martin, Richard M.
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- 2023
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5. Applying Mendelian randomization to appraise causality in relationships between nutrition and cancer
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Wade, Kaitlin H., Yarmolinsky, James, Giovannucci, Edward, Lewis, Sarah J., Millwood, Iona Y., Munafò, Marcus R., Meddens, Fleur, Burrows, Kimberley, Bell, Joshua A., Davies, Neil M., Mariosa, Daniela, Kanerva, Noora, Vincent, Emma E., Smith-Byrne, Karl, Guida, Florence, Gunter, Marc J., Sanderson, Eleanor, Dudbridge, Frank, Burgess, Stephen, Cornelis, Marilyn C., Richardson, Tom G., Borges, Maria Carolina, Bowden, Jack, Hemani, Gibran, Cho, Yoonsu, Spiller, Wes, Richmond, Rebecca C., Carter, Alice R., Langdon, Ryan, Lawlor, Deborah A., Walters, Robin G., Vimaleswaran, Karani Santhanakrishnan, Anderson, Annie, Sandu, Meda R., Tilling, Kate, Davey Smith, George, Martin, Richard M., and Relton, Caroline L.
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- 2022
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6. Association between circulating inflammatory markers and adult cancer risk: a Mendelian randomization analysis
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Yarmolinsky, James, primary, Robinson, Jamie W., additional, Mariosa, Daniela, additional, Karhunen, Ville, additional, Huang, Jian, additional, Dimou, Niki, additional, Murphy, Neil, additional, Burrows, Kimberley, additional, Bouras, Emmanouil, additional, Smith-Byrne, Karl, additional, Lewis, Sarah J., additional, Galesloot, Tessel E., additional, Kiemeney, Lambertus A., additional, Vermeulen, Sita, additional, Martin, Paul, additional, Albanes, Demetrius, additional, Hou, Lifang, additional, Newcomb, Polly A., additional, White, Emily, additional, Wolk, Alicja, additional, Wu, Anna H., additional, Le Marchand, Loïc, additional, Phipps, Amanda I., additional, Buchanan, Daniel D., additional, Zhao, Sizheng Steven, additional, Gill, Dipender, additional, Chanock, Stephen J., additional, Purdue, Mark P., additional, Davey Smith, George, additional, Brennan, Paul, additional, Herzig, Karl-Heinz, additional, Järvelin, Marjo-Riitta, additional, Amos, Chris I., additional, Hung, Rayjean J., additional, Dehghan, Abbas, additional, Johansson, Mattias, additional, Gunter, Marc J., additional, Tsilidis, Kostas K., additional, Martin, Richard M., additional, Landi, Maria Teresa, additional, Stevens, Victoria, additional, Wang, Ying, additional, Albanes, Demetrios, additional, Caporaso, Neil, additional, Amos, Christopher I., additional, Shete, Sanjay, additional, Bickeböller, Heike, additional, Risch, Angela, additional, Houlston, Richard, additional, Lam, Stephen, additional, Tardon, Adonina, additional, Chen, Chu, additional, Bojesen, Stig E., additional, Wichmann, H-Erich, additional, Christiani, David, additional, Rennert, Gadi, additional, Arnold, Susanne, additional, Field, John K., additional, Le Marchand, Loic, additional, Melander, Olle, additional, Brunnström, Hans, additional, Liu, Geoffrey, additional, Andrew, Angeline, additional, Shen, Hongbing, additional, Zienolddiny, Shan, additional, Grankvist, Kjell, additional, Johansson, Mikael, additional, Teare, M. Dawn, additional, Hong, Yun-Chul, additional, Yuan, Jian-Min, additional, Lazarus, Philip, additional, Schabath, Matthew B., additional, Aldrich, Melinda C., additional, Eeles, Rosalind A., additional, Haiman, Christopher A., additional, Kote-Jarai, Zsofia, additional, Schumacher, Fredrick R., additional, Benlloch, Sara, additional, Al Olama, Ali Amin, additional, Muir, Kenneth R., additional, Berndt, Sonja I., additional, Conti, David V., additional, Wiklund, Fredrik, additional, Chanock, Stephen, additional, Tangen, Catherine M., additional, Batra, Jyotsna, additional, Clements, Judith A., additional, Grönberg, Henrik, additional, Pashayan, Nora, additional, Schleutker, Johanna, additional, Weinstein, Stephanie J., additional, West, Catharine M.L., additional, Mucci, Lorelei A., additional, Cancel-Tassin, Géraldine, additional, Koutros, Stella, additional, Sørensen, Karina Dalsgaard, additional, Grindedal, Eli Marie, additional, Neal, David E., additional, Hamdy, Freddie C., additional, Donovan, Jenny L., additional, Travis, Ruth C., additional, Hamilton, Robert J., additional, Ingles, Sue Ann, additional, Rosenstein, Barry S., additional, Lu, Yong-Jie, additional, Giles, Graham G., additional, MacInnis, Robert J., additional, Kibel, Adam S., additional, Vega, Ana, additional, Kogevinas, Manolis, additional, Penney, Kathryn L., additional, Park, Jong Y., additional, Stanfrod, Janet L., additional, Cybulski, Cezary, additional, Nordestgaard, Børge G., additional, Nielsen, Sune F., additional, Brenner, Hermann, additional, Maier, Christiane, additional, Logothetis, Christopher J., additional, John, Esther M., additional, Teixeira, Manuel R., additional, Neuhausen, Susan L., additional, De Ruyck, Kim, additional, Razack, Azad, additional, Newcomb, Lisa F., additional, Lessel, Davor, additional, Kaneva, Radka, additional, Usmani, Nawaid, additional, Claessens, Frank, additional, Townsend, Paul A., additional, Castelao, Jose Esteban, additional, Roobol, Monique J., additional, Menegaux, Florence, additional, Khaw, Kay-Tee, additional, Cannon-Albright, Lisa, additional, Pandha, Hardev, additional, Thibodeau, Stephen N., additional, Hunter, David J., additional, Kraft, Peter, additional, Blot, William J., additional, and Riboli, Elio, additional
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- 2024
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7. The role of genomics in global cancer prevention
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Ginsburg, Ophira, Ashton-Prolla, Patricia, Cantor, Anna, Mariosa, Daniela, and Brennan, Paul
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- 2021
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8. Germline determinants of humoral immune response to HPV-16 protect against oropharyngeal cancer
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Ferreiro-Iglesias, Aida, McKay, James D., Brenner, Nicole, Virani, Shama, Lesseur, Corina, Gaborieau, Valerie, Ness, Andy R., Hung, Rayjean J., Liu, Geoffrey, Diergaarde, Brenda, Olshan, Andrew F., Hayes, Neil, Weissler, Mark C., Schroeder, Lea, Bender, Noemi, Pawlita, Michael, Thomas, Steve, Pring, Miranda, Dudding, Tom, Kanterewicz, Beatriz, Ferris, Robert, Thomas, Sera, Brhane, Yonathan, Díez-Obrero, Virginia, Milojevic, Maja, Smith-Byrne, Karl, Mariosa, Daniela, Johansson, Mattias J., Herrero, Rolando, Boccia, Stefania, Cadoni, Gabriella, Lacko, Martin, Holcátová, Ivana, Ahrens, Wolfgang, Lagiou, Pagona, Lagiou, Areti, Polesel, Jerry, Simonato, Lorenzo, Merletti, Franco, Healy, Claire M., Hansen, Bo T., Nygård, Mari, Conway, David I., Wright, Sylvia, Macfarlane, Tatiana V., Robinson, Max, Alemany, Laia, Agudo, Antonio, Znaor, Ariana, Amos, Christopher I., Waterboer, Tim, and Brennan, Paul
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- 2021
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9. Causal relationships between risk of venous thromboembolism and 18 cancers: a bidirectional Mendelian randomization analysis.
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Cornish, Naomi, Haycock, Philip, Brenner, Hermann, Figueiredo, Jane C, Galesloot, Tessel E, Grant, Robert C, Johansson, Mattias, Mariosa, Daniela, McKay, James, Pai, Rish, Pellatt, Andrew J, Samadder, N Jewel, Shi, Jianxin, Thibord, Florian, Trégouët, David-Alexandre, Voegele, Catherine, Thirlwell, Chrissie, Mumford, Andrew, Langdon, Ryan, and Consortium, InterLymph
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THROMBOEMBOLISM ,ODDS ratio ,GENOME-wide association studies ,DISEASE risk factors ,RANDOMIZATION (Statistics) ,PANCREATIC cancer ,VENOUS thrombosis ,ABO blood group system - Abstract
Background People with cancer experience high rates of venous thromboembolism (VTE). Risk of subsequent cancer is also increased in people experiencing their first VTE. The causal mechanisms underlying this association are not completely understood, and it is unknown whether VTE is itself a risk factor for cancer. Methods We used data from large genome-wide association study meta-analyses to perform bidirectional Mendelian randomization analyses to estimate causal associations between genetic liability to VTE and risk of 18 different cancers. Results We found no conclusive evidence that genetic liability to VTE was causally associated with an increased incidence of cancer, or vice versa. We observed an association between liability to VTE and pancreatic cancer risk [odds ratio for pancreatic cancer: 1.23 (95% confidence interval: 1.08–1.40) per log-odds increase in VTE risk, P = 0.002]. However, sensitivity analyses revealed this association was predominantly driven by a variant proxying non-O blood group, with inadequate evidence to suggest a causal relationship. Conclusions These findings do not support the hypothesis that genetic liability to VTE is a cause of cancer. Existing observational epidemiological associations between VTE and cancer are therefore more likely to be driven by pathophysiological changes which occur in the setting of active cancer and anti-cancer treatments. Further work is required to explore and synthesize evidence for these mechanisms. [ABSTRACT FROM AUTHOR]
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- 2024
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10. Table S3 from Cholesterol Auxotrophy as a Targetable Vulnerability in Clear Cell Renal Cell Carcinoma
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Riscal, Romain, primary, Bull, Caroline J., primary, Mesaros, Clementina, primary, Finan, Jennifer M., primary, Carens, Madeleine, primary, Ho, Elaine S., primary, Xu, Jimmy P., primary, Godfrey, Jason, primary, Brennan, Paul, primary, Johansson, Mattias, primary, Purdue, Mark P., primary, Chanock, Stephen J., primary, Mariosa, Daniela, primary, Timpson, Nicholas J., primary, Vincent, Emma E., primary, Keith, Brian, primary, Blair, Ian A., primary, Skuli, Nicolas, primary, and Simon, M. Celeste, primary
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- 2023
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11. Figure S6 from Cholesterol Auxotrophy as a Targetable Vulnerability in Clear Cell Renal Cell Carcinoma
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Riscal, Romain, primary, Bull, Caroline J., primary, Mesaros, Clementina, primary, Finan, Jennifer M., primary, Carens, Madeleine, primary, Ho, Elaine S., primary, Xu, Jimmy P., primary, Godfrey, Jason, primary, Brennan, Paul, primary, Johansson, Mattias, primary, Purdue, Mark P., primary, Chanock, Stephen J., primary, Mariosa, Daniela, primary, Timpson, Nicholas J., primary, Vincent, Emma E., primary, Keith, Brian, primary, Blair, Ian A., primary, Skuli, Nicolas, primary, and Simon, M. Celeste, primary
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- 2023
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12. Data from Cholesterol Auxotrophy as a Targetable Vulnerability in Clear Cell Renal Cell Carcinoma
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Riscal, Romain, primary, Bull, Caroline J., primary, Mesaros, Clementina, primary, Finan, Jennifer M., primary, Carens, Madeleine, primary, Ho, Elaine S., primary, Xu, Jimmy P., primary, Godfrey, Jason, primary, Brennan, Paul, primary, Johansson, Mattias, primary, Purdue, Mark P., primary, Chanock, Stephen J., primary, Mariosa, Daniela, primary, Timpson, Nicholas J., primary, Vincent, Emma E., primary, Keith, Brian, primary, Blair, Ian A., primary, Skuli, Nicolas, primary, and Simon, M. Celeste, primary
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- 2023
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13. Causal relationships between risk of venous thromboembolism and 18 cancers: a bidirectional Mendelian randomisation analysis
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Cornish, Naomi, Haycock, Philip, Brenner, Hermann, Figueiredo, Jane C., Galesloot, Tessel, Grant, Robert C, Johansson, Mattias, Mariosa, Daniela, McKay, James, Pai, Rish, Pellatt, Andrew J, Samadder N., Jewel, Shi, Jianxin, Thibord, Florian, Trégouët, David-Alexandre, Voegele, Catherine, Thirlwell, Chrissie, Mumford, Andrew, and Langdon, Ryan
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Article - Abstract
Background: People with cancer experience high rates of venous thromboembolism (VTE). Additionally, risk of subsequent cancer is increased in people experiencing their first VTE. The causal mechanisms underlying this association are not completely understood, and it is unknown whether VTE is itself a risk factor for cancer. Methods: We used data from large genome-wide association study meta-analyses to perform bi-directional Mendelian randomisation analyses to estimate causal associations between genetically-proxied lifetime risk of VTE and risk of 18 different cancers. Results: We found no conclusive evidence that genetically-proxied lifetime risk of VTE was causally associated with an increased incidence of cancer, or vice-versa. We observed an association between VTE and pancreatic cancer risk (odds ratio for pancreatic cancer 1.23 (95% confidence interval 1.08 - 1.40) per log-odds increase in risk of VTE, P = 0.002). However, sensitivity analyses revealed this association was predominantly driven by a variant proxying non-O blood group, with inadequate evidence from Mendelian randomisation to suggest a causal relationship. Conclusions: These findings do not support the hypothesis that genetically-proxied lifetime risk of VTE is a cause of cancer. Existing observational epidemiological associations between VTE and cancer are therefore more likely to be driven by pathophysiological changes which occur in the setting of active cancer and anti-cancer treatments. Further work is required to explore and synthesise evidence for these mechanisms. KEY MESSAGES: 1) There is strong observational evidence that active cancer is associated with venous thromboembolism. 2) It is currently unknown whether venous thromboembolism is a risk factor for cancer. 3) We applied a bi-directional Mendelian randomisation framework to appraise the causal relationships between genetically-proxied risk of venous thromboembolism and 18 different cancers. 4) Overall, there was no clear evidence from Mendelian randomisation that lifetime-elevated risk of venous thromboembolism is causally associated with an increased risk of cancer, or visa versa.
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- 2023
14. Association between circulating inflammatory markers and adult cancer risk: a Mendelian randomization analysis
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Yarmolinsky, James, Robinson, Jamie W, Mariosa, Daniela, Karhunen, Ville, Huang, Jian, Dimou, Niki, Murphy, Neil, Burrows, Kimberley, Bouras, Emmanouil, Smith-Byrne, Karl, Lewis, Sarah J, Galesloot, Tessel E, Kiemeney, Lambertus A, Vermeulen, Sita, Martin, Paul, Albanes, Demetrius, Hou, Lifang, Newcomb, Polly A, White, Emily, Wolk, Alicja, Wu, Anna H, Marchand, Loïc Le, Phipps, Amanda I, Buchanan, Daniel D, Zhao, Sizheng Steven, Gill, Dipender, Chanock, Stephen J, Purdue, Mark P, Smith, George Davey, Brennan, Paul, Herzig, Karl-Heinz, Jarvelin, Marjo-Riitta, Dehghan, Abbas, Johansson, Mattias, Gunter, Marc J, Tsilidis, Kostas K, and Martin, Richard M
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Article - Abstract
BACKGROUND: Tumour-promoting inflammation is a “hallmark” of cancer and conventional epidemiological studies have reported links between various inflammatory markers and cancer risk. The causal nature of these relationships and, thus, the suitability of these markers as intervention targets for cancer prevention is unclear. METHODS: We meta-analysed 6 genome-wide association studies of circulating inflammatory markers comprising 59,969 participants of European ancestry. We then used combined cis -Mendelian randomization and colocalisation analysis to evaluate the causal role of 66 circulating inflammatory markers in risk of 30 adult cancers in 338,162 cancer cases and up to 824,556 controls. Genetic instruments for inflammatory markers were constructed using genome-wide significant ( P < 5.0 x 10 (-8) ) cis -acting SNPs (i.e. in or ±250 kb from the gene encoding the relevant protein) in weak linkage disequilibrium (LD, r (2) < 0.10). Effect estimates were generated using inverse-variance weighted random-effects models and standard errors were inflated to account for weak LD between variants with reference to the 1000 Genomes Phase 3 CEU panel. A false discovery rate (FDR)-corrected P -value (“ q -value”) < 0.05 was used as a threshold to define “strong evidence” to support associations and 0.05 ≤ q -value < 0.20 to define “suggestive evidence”. A colocalisation posterior probability (PPH (4) ) > 70% was employed to indicate support for shared causal variants across inflammatory markers and cancer outcomes. RESULTS: We found strong evidence to support an association of genetically-proxied circulating pro-adrenomedullin concentrations with increased breast cancer risk (OR 1.19, 95% CI 1.10-1.29, q -value=0.033, PPH (4) =84.3%) and suggestive evidence to support associations of interleukin-23 receptor concentrations with increased pancreatic cancer risk (OR 1.42, 95% CI 1.20-1.69, q -value=0.055, PPH (4) =73.9%), prothrombin concentrations with decreased basal cell carcinoma risk (OR 0.66, 95% CI 0.53-0.81, q -value=0.067, PPH (4) =81.8%), macrophage migration inhibitory factor concentrations with increased bladder cancer risk (OR 1.14, 95% CI 1.05-1.23, q -value=0.072, PPH (4) =76.1%), and interleukin-1 receptor-like 1 concentrations with decreased triple-negative breast cancer risk (OR 0.92, 95% CI 0.88-0.97, q -value=0.15), PPH (4) =85.6%). For 22 of 30 cancer outcomes examined, there was little evidence ( q -value ≥ 0.20) that any of the 66 circulating inflammatory markers examined were associated with cancer risk. CONCLUSION: Our comprehensive joint Mendelian randomization and colocalisation analysis of the role of circulating inflammatory markers in cancer risk identified potential roles for 5 circulating inflammatory markers in risk of 5 site-specific cancers. Contrary to reports from some prior conventional epidemiological studies, we found little evidence of association of circulating inflammatory markers with the majority of site-specific cancers evaluated.
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- 2023
15. The association between genetically elevated polyunsaturated fatty acids and risk of cancer
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Haycock, Philip C, Borges, Maria Carolina, Burrows, Kimberley, Lemaitre, Rozenn N, Burgess, Stephen, Khankari, Nikhil K, Tsilidis, Konstantinos K, Gaunt, Tom R, Hemani, Gibran, Zheng, Jie, Truong, Therese, Birmann, Brenda M, OMara, Tracy, Spurdle, Amanda B, Iles, Mark M, Law, Matthew H, Slager, Susan L, Saberi Hosnijeh, Fatemeh, Mariosa, Daniela, Cotterchio, Michelle, Cerhan, James R, Peters, Ulrike, Enroth, Stefan, Gharahkhani, Puya, Le Marchand, Loic, Williams, Ann C, Block, Robert C, ACCC, CCFR-CORECT-GECCO, EPITHYR, InterLymph, MMAC, ECAC, ILCCO, PRACTICAL Consortium, PanScan, PanC4, Amos, Christopher I, Hung, Rayjean J, Zheng, Wei, Gunter, Marc J, Smith, George Davey, Relton, Caroline, Martin, Richard M, Fatty Acids in Cancer Mendelian Randomization Collaboration, Burgess, Stephen [0000-0001-5365-8760], and Apollo - University of Cambridge Repository
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Fatty Acid Desaturases ,Esophageal Neoplasms ,Delta-5 desaturase ,Inflammatory Bowel Diseases ,Polymorphism, Single Nucleotide ,Omega 6 ,Cancer risk ,Omega 3 ,Fatty Acids, Omega-3 ,Mendelian randomization ,Fatty Acids, Unsaturated ,Delta-6 desaturase ,Humans ,Polyunsaturated fatty acids ,Esophageal Squamous Cell Carcinoma ,Colorectal Neoplasms - Abstract
BACKGROUND: The causal relevance of polyunsaturated fatty acids (PUFAs) for risk of site-specific cancers remains uncertain. METHODS: Using a Mendelian randomization (MR) framework, we assessed the causal relevance of PUFAs for risk of cancer in European and East Asian ancestry individuals. We defined the primary exposure as PUFA desaturase activity, proxied by rs174546 at the FADS locus. Secondary exposures were defined as omega 3 and omega 6 PUFAs that could be proxied by genetic polymorphisms outside the FADS region. Our study used summary genetic data on 10 PUFAs and 67 cancers, corresponding to 562,871 cases and 1,619,465 controls, collected by the Fatty Acids in Cancer Mendelian Randomization Collaboration. We estimated odds ratios (ORs) for cancer per standard deviation increase in genetically proxied PUFA exposures. FINDINGS: Genetically elevated PUFA desaturase activity was associated (P
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- 2023
16. Opioid medications: an emerging cancer risk factor?
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Sheikh, Mahdi, primary, Brennan, Paul, additional, Mariosa, Daniela, additional, and Robbins, Hilary A., additional
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- 2023
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17. Blood levels of trace metals and amyotrophic lateral sclerosis
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Peters, Tracy L., Beard, John D., Umbach, David M., Allen, Kelli, Keller, Jean, Mariosa, Daniela, Sandler, Dale P., Schmidt, Silke, Fang, Fang, Ye, Weimin, and Kamel, Freya
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- 2016
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18. A prospective cohort study of the combined effects of physical activity and anthropometric measures on the risk of post-menopausal breast cancer
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Bellocco, Rino, Marrone, Gaetano, Ye, Weimin, Nyrén, Olof, Adami, Hans-Olov, Mariosa, Daniela, and Lagerros, Ylva Trolle
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- 2016
19. Additional file 1 of Separating the effects of early and later life adiposity on colorectal cancer risk: a Mendelian randomization study
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Papadimitriou, Nikos, Bull, Caroline J., Jenab, Mazda, Hughes, David J., Bell, Joshua A., Sanderson, Eleanor, Timpson, Nicholas J., Smith, George Davey, Albanes, Demetrius, Campbell, Peter T., Küry, Sébastien, Le Marchand, Loic, Ulrich, Cornelia M., Visvanathan, Kala, Figueiredo, Jane C., Newcomb, Polly A., Pai, Rish K., Peters, Ulrike, Tsilidis, Kostas K., Boer, Jolanda M. A., Vincent, Emma E., Mariosa, Daniela, Gunter, Marc J., Richardson, Tom G., and Murphy, Neil
- Abstract
Additional file 1: Table S1. Beta estimates for genome-wide significant SNPs for early/adult life body size in UK Biobank (overall, men, women). Table S2. Summary information on colorectal cancer risk for the SNPs used in the analysis. Table S3. Number of cancer cases by sex and subsite. Table S4. Sample size and power calculations for each phenotype and group in the Mendelian randomization study of early and adult life body size and risk of colorectal cancer. Table S5. Beta estimates for early/adult life body size in UK Biobank for the SNPs included in the MVMR analysis (overall, men, women). Table S6. STROBE-MR checklist of recommended items to address in reports of Mendelian randomization studies. Table S7. Univariable Mendelian randomization estimates between early and adult body size and colorectal cancer risk. Table S8. Fearly life body size, Fadult body size and Qa in the multivariable MR between early, adult body size and colorectal cancer. Table S9. Multivariable MR Egger analysis to assess the effect of both predicted early life and adult body size on colorectal cancer.
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- 2023
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20. Additional file 2 of Separating the effects of early and later life adiposity on colorectal cancer risk: a Mendelian randomization study
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Papadimitriou, Nikos, Bull, Caroline J., Jenab, Mazda, Hughes, David J., Bell, Joshua A., Sanderson, Eleanor, Timpson, Nicholas J., Smith, George Davey, Albanes, Demetrius, Campbell, Peter T., Küry, Sébastien, Le Marchand, Loic, Ulrich, Cornelia M., Visvanathan, Kala, Figueiredo, Jane C., Newcomb, Polly A., Pai, Rish K., Peters, Ulrike, Tsilidis, Kostas K., Boer, Jolanda M. A., Vincent, Emma E., Mariosa, Daniela, Gunter, Marc J., Richardson, Tom G., and Murphy, Neil
- Abstract
Additional file 2. Funding, acknowledgements. Funding – Information on consortia funding. Acknowledgements – Information on consortia acknowledgements.
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- 2023
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21. Lipids, Apolipoproteins, and the Risk of Parkinson Disease: A Prospective Cohort Study and a Mendelian Randomization Analysis
- Author
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Fang, Fang, Zhan, Yiqiang, Hammar, Niklas, Shen, Xia, Wirdefeldt, Karin, Walldius, Göran, and Mariosa, Daniela
- Published
- 2019
- Full Text
- View/download PDF
22. A systematic review and meta-analysis comparing partial stomach partitioning gastrojejunostomy versus conventional gastrojejunostomy for malignant gastroduodenal obstruction
- Author
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Kumagai, Koshi, Rouvelas, Ioannis, Ernberg, Annika, Persson, Saga, Analatos, Apostolos, Mariosa, Daniela, Lindblad, Mats, Nilsson, Magnus, Ye, Weimin, Lundell, Lars, and Tsai, Jon A.
- Published
- 2016
- Full Text
- View/download PDF
23. The relationship between blood pressure and risk of renal cell carcinoma
- Author
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Alcala, Karine, Mariosa, Daniela, Smith-Byrne, Karl, Nasrollahzadeh Nesheli, Dariush, Carreras-Torres, Robert, Ardanaz Aicua, Eva, Bondonno, Nicola P, Bonet, Catalina, Brunström, Mattias, Bueno-De-Mesquita, Bas, Chirlaque, María-Dolores, Christakoudi, Sofia, Heath, Alicia K, Kaaks, Rudolf, Katzke, Verena, Krogh, Vittorio, Ljungberg, Börje, Martin, Richard M, May, Anne, Melander, Olle, Palli, Domenico, Rodriguez-Barranco, Miguel, Sacerdote, Carlotta, Stocks, Tanja, Tjønneland, Anne, Travis, Ruth C., Vermeulen, Roel, Chanock, Stephen, Purdue, Mark, Weiderpass, Elisabete, Muller, David, Brennan, Paul, Johansson, Mattias, and IRAS OH Epidemiology Chemical Agents
- Subjects
systolic blood pressure ,Mendelian randomization ,diastolic blood pressure ,kidney cancer ,RCC - Abstract
Background: The relation between blood pressure and kidney cancer risk is well established but complex and different study designs have reported discrepant findings on the relative importance of diastolic blood pressure (DBP) and systolic blood pressure (SBP). In this study, we sought to describe the temporal relation between diastolic and SBP with renal cell carcinoma (RCC) risk in detail. Methods: Our study involved two prospective cohorts: the European Prospective Investigation into Cancer and Nutrition study and UK Biobank, including >700 000 participants and 1692 incident RCC cases. Risk analyses were conducted using flexible parametric survival models for DBP and SBP both separately as well as with mutuality adjustment and then adjustment for extended risk factors. We also carried out univariable and multivariable Mendelian randomization (MR) analyses (DBP: ninstruments = 251, SBP: ninstruments = 213) to complement the analyses of measured DBP and SBP. Results: In the univariable analysis, we observed clear positive associations with RCC risk for both diastolic and SBP when measured ≥5 years before diagnosis and suggestive evidence for a stronger risk association in the year leading up to diagnosis. In mutually adjusted analysis, the long-term risk association of DBP remained, with a hazard ratio (HR) per standard deviation increment 10 years before diagnosis (HR10y) of 1.20 (95% CI: 1.10-1.30), whereas the association of SBP was attenuated (HR10y: 1.00, 95% CI: 0.91-1.10). In the complementary multivariable MR analysis, we observed an odds ratio for a 1-SD increment (ORsd) of 1.34 (95% CI: 1.08-1.67) for genetically predicted DBP and 0.70 (95% CI: 0.56-0.88) for genetically predicted SBP. Conclusion: The results of this observational and MR study are consistent with an important role of DBP in RCC aetiology. The relation between SBP and RCC risk was less clear but does not appear to be independent of DBP. © 2022 World Health Organization,. All rights reserved. The World Health Organization has granted the Publisher permission for the reproduction of this article.
- Published
- 2022
24. Genetically-proxied impaired GIPR signalling and risk of 6 cancers
- Author
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Rogers, Miranda, primary, Gill, Dipender, additional, Ahlqvist, Emma, additional, Robinson, Tim, additional, Mariosa, Daniela, additional, Johansson, Mattias, additional, Penha, Ricardo Cortez Cardoso, additional, Dossus, Laure, additional, Gunter, Marc J, additional, Moreno, Victor, additional, Davey Smith, George, additional, Martin, Richard M, additional, and Yarmolinsky, James, additional
- Published
- 2022
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- View/download PDF
25. Separating the effects of early and later life adiposity on colorectal cancer risk: a Mendelian randomization study
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Papadimitriou, Nikos, primary, Bull, Caroline J, additional, Jenab, Mazda, additional, Hughes, David J, additional, Bell, Joshua, additional, Sanderson, Eleanor, additional, Timpson, Nicholas J, additional, Davey Smith, George, additional, Albanes, Demetrius, additional, Campbell, Peter T, additional, Kury, Sebastien, additional, Le Marchand, Loic, additional, Ulrich, Cornelia M, additional, Visvanathan, Kala, additional, Figueiredo, Jane C, additional, Newcomb, Polly A, additional, Pai, Rish K, additional, Peters, Ulrike, additional, Tsilidis, Konstantinos K, additional, Boer, Jolanda MA, additional, Vincent, Emma E, additional, Mariosa, Daniela, additional, Gunter, Marc J, additional, Richardson, Tom G, additional, and Murphy, Neil, additional
- Published
- 2022
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26. Blood Lead, Bone Turnover, and Survival in Amyotrophic Lateral Sclerosis
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Fang, Fang, Peters, Tracy L, Beard, John D, Umbach, David M, Keller, Jean, Mariosa, Daniela, Allen, Kelli D, Ye, Weimin, Sandler, Dale P, Schmidt, Silke, and Kamel, Freya
- Published
- 2017
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27. Physical activity and body mass index as predictors of prostate cancer risk
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Grotta, Alessandra, Bottai, Matteo, Adami, Hans-Olov, Adams, Swann Arp, Akre, Olof, Blair, Steven Noel, Mariosa, Daniela, Nyrén, Olof, Ye, Weimin, Stattin, Pär, Bellocco, Rino, and Trolle Lagerros, Ylva
- Published
- 2015
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28. Body Size at Different Ages and Risk of 6 Cancers: A Mendelian Randomization and Prospective Cohort Study
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Mariosa, Daniela, primary, Smith-Byrne, Karl, additional, Richardson, Tom G, additional, Ferrari, Pietro, additional, Gunter, Marc J, additional, Papadimitriou, Nikos, additional, Murphy, Neil, additional, Christakoudi, Sofia, additional, Tsilidis, Konstantinos K, additional, Riboli, Elio, additional, Muller, David, additional, Purdue, Mark P, additional, Chanock, Stephen J, additional, Hung, Rayjean J, additional, Amos, Christopher I, additional, O’Mara, Tracy A, additional, Amiano, Pilar, additional, Pasanisi, Fabrizio, additional, Rodriguez-Barranco, Miguel, additional, Krogh, Vittorio, additional, Tjønneland, Anne, additional, Halkjær, Jytte, additional, Perez-Cornago, Aurora, additional, Chirlaque, María-Dolores, additional, Skeie, Guri, additional, Rylander, Charlotta, additional, Borch, Kristin Benjaminsen, additional, Aune, Dagfinn, additional, Heath, Alicia K, additional, Ward, Heather A, additional, Schulze, Matthias, additional, Bonet, Catalina, additional, Weiderpass, Elisabete, additional, Davey Smith, George, additional, Brennan, Paul, additional, and Johansson, Mattias, additional
- Published
- 2022
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29. Body Mass Index and Amyotrophic Lateral Sclerosis: A Study of US Military Veterans
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Mariosa, Daniela, Beard, John D., Umbach, David M., Bellocco, Rino, Keller, Jean, Peters, Tracy L., Allen, Kelli D., Ye, Weimin, Sandler, Dale P., Schmidt, Silke, Fang, Fang, and Kamel, Freya
- Published
- 2017
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30. The influence of obesity-related factors in the etiology of renal cell carcinoma-A mendelian randomization study
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Johansson, Mattias, Carreras-Torres, Robert, Scelo, Ghislaine, Purdue, Mark P., Mariosa, Daniela, Muller, David C., Timpson, Nicolas J., Haycock, Philip C., Brown, Kevin M., Wang, Zhaoming, Ye, Yuanqing, Hofmann, Jonathan N., Foll, Matthieu, Gaborieau, Valerie, Machiela, Mitchell J., Colli, Leandro M., Li, Peng, Garnier, Jean-Guillaume, Blanche, Helene, Boland, Anne, Burdette, Laurie, Prokhortchouk, Egor, Skryabin, Konstantin G., Yeager, Meredith, Radojevic-Skodric, Sanja, Ognjanovic, Simona, Foretova, Lenka, Holcatova, Ivana, Janout, Vladimir, Mates, Dana, Mukeriya, Anush, Rascu, Stefan, Zaridze, David, Bencko, Vladimir, Cybulski, Cezary, Fabianova, Eleonora, Jinga, Viorel, Lissowska, Jolanta, Lubinski, Jan, Navratilova, Marie, Rudnai, Peter, Benhamou, Simone, Cancel-Tassin, Geraldine, Cussenot, Olivier, Weiderpass, Elisabete, Ljungberg, Börje, Tumkur Sitaram, Raviprakash, Häggström, Christel, Bruinsma, Fiona, Jordan, Susan J., Severi, Gianluca, Winship, Ingrid, Hveem, Kristian, Vatten, Lars J., Fletcher, Tony, Larsson, Susanna C., Wolk, Alicja, Banks, Rosamonde E., Selby, Peter J., Easton, Douglas F., Andreotti, Gabriella, Beane Freeman, Laura E., Koutros, Stella, Männistö, Satu, Weinstein, Stephanie, Clark, Peter E., Edwards, Todd L., Lipworth, Loren, Gapstur, Susan M., Stevens, Victoria L., Carol, Hallie, Freedman, Matthew L., Pomerantz, Mark M., Cho, Eunyoung, Wilson, Kathryn M., Gaziano, J. Michael, Sesso, Howard D., Freedman, Neal D., Parker, Alexander S., Eckel-Passow, Jeanette E., Huang, Wen-Yi, Kahnoski, Richard J., Lane, Brian R., Noyes, Sabrina L., Petillo, David, Teh, Bin Tean, Peters, Ulrike, White, Emily, Anderson, Garnet L., Johnson, Lisa, Luo, Juhua, Buring, Julie, Lee, I-Min, Chow, Wong-Ho, Moore, Lee E., Eisen, Timothy, Henrion, Marc, Larkin, James, Barman, Poulami, Leibovich, Bradley C., Choueiri, Toni K., Lathrop, G. Mark, Deleuze, Jean-Francois, Gunter, Marc, McKay, James D., Wu, Xifeng, Houlston, Richard S., Chanock, Stephen J., Relton, Caroline, Richards, J. Brent, Martin, Richard M., Davey Smith, George, and Brennan, Paul
- Subjects
Obesity -- Genetic aspects -- Complications and side effects ,Renal cell carcinoma -- Genetic aspects -- Development and progression -- Care and treatment ,Genetic markers -- Health aspects ,Etiology (Medicine) ,Genetics ,Carcinoma ,Cancer ,Type 2 diabetes ,Genomics ,Insulin ,Proxy ,Lipids ,Genomes ,Fasting ,Glucose ,Biological sciences - Abstract
Background Several obesity-related factors have been associated with renal cell carcinoma (RCC), but it is unclear which individual factors directly influence risk. We addressed this question using genetic markers as proxies for putative risk factors and evaluated their relation to RCC risk in a mendelian randomization (MR) framework. This methodology limits bias due to confounding and is not affected by reverse causation. Methods and findings Genetic markers associated with obesity measures, blood pressure, lipids, type 2 diabetes, insulin, and glucose were initially identified as instrumental variables, and their association with RCC risk was subsequently evaluated in a genome-wide association study (GWAS) of 10,784 RCC patients and 20,406 control participants in a 2-sample MR framework. The effect on RCC risk was estimated by calculating odds ratios (OR.sub.SD) for a standard deviation (SD) increment in each risk factor. The MR analysis indicated that higher body mass index increases the risk of RCC (OR.sub.SD : 1.56, 95% confidence interval [CI] 1.44-1.70), with comparable results for waist-to-hip ratio (OR.sub.SD : 1.63, 95% CI 1.40-1.90) and body fat percentage (OR.sub.SD : 1.66, 95% CI 1.44-1.90). This analysis further indicated that higher fasting insulin (OR.sub.SD : 1.82, 95% CI 1.30-2.55) and diastolic blood pressure (DBP; OR.sub.SD : 1.28, 95% CI 1.11-1.47), but not systolic blood pressure (OR.sub.SD : 0.98, 95% CI 0.84-1.14), increase the risk for RCC. No association with RCC risk was seen for lipids, overall type 2 diabetes, or fasting glucose. Conclusions This study provides novel evidence for an etiological role of insulin in RCC, as well as confirmatory evidence that obesity and DBP influence RCC risk., Author(s): Mattias Johansson 1,*, Robert Carreras-Torres 1, Ghislaine Scelo 1, Mark P. Purdue 2, Daniela Mariosa 1, David C. Muller 3, Nicolas J. Timpson 4, Philip C. Haycock 4, Kevin [...]
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- 2019
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31. Applying Mendelian randomization to appraise causality in relationships between nutrition and cancer
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Wade, Kaitlin, primary, Yarmolinsky, James, additional, Giovannucci, Edward, additional, Lewis, Sarah J., additional, Millwood, Iona Y, additional, Munafo, Marcus Robert, additional, Meddens, Fleur, additional, Burrows, Kimberley, additional, Bell, Joshua A, additional, Davies, Neil Martin, additional, Mariosa, Daniela, additional, Kanerva, Noora, additional, Vincent, Emma E, additional, Smith-Byrne, Karl, additional, Guida, Florence, additional, Gunter, Marc J., additional, Sanderson, Eleanor, additional, Dudbridge, Frank, additional, Burgess, Stephen, additional, Cornelis, Marilyn C, additional, Richardson, Tom, additional, Borges, Maria Carolina, additional, Bowden, Jack, additional, Hemani, Gibran, additional, Cho, Yoonsu, additional, Spiller, Wes, additional, Richmond, Rebecca, additional, Carter, Alice, additional, Langdon, Ryan, additional, Lawlor, Deborah A, additional, Walters, Robin G, additional, Vimaleswaran, Karani Santhanakrishnan, additional, Anderson, Annie, additional, Sandu, Meda, additional, Tilling, Kate, additional, Smith, George Davey, additional, Martin, Richard, additional, Relton, Caroline, additional, and group, in Nutrition and Cancer working, additional
- Published
- 2021
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32. Cholesterol Auxotrophy as a Targetable Vulnerability in Clear Cell Renal Cell Carcinoma
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Riscal, Romain, primary, Bull, Caroline J., additional, Mesaros, Clementina, additional, Finan, Jennifer M., additional, Carens, Madeleine, additional, Ho, Elaine S., additional, Xu, Jimmy P., additional, Godfrey, Jason, additional, Brennan, Paul, additional, Johansson, Mattias, additional, Purdue, Mark P., additional, Chanock, Stephen J., additional, Mariosa, Daniela, additional, Timpson, Nicholas J., additional, Vincent, Emma E., additional, Keith, Brian, additional, Blair, Ian A., additional, Skuli, Nicolas, additional, and Simon, M. Celeste, additional
- Published
- 2021
- Full Text
- View/download PDF
33. Genetically Raised Circulating Bilirubin Levels and Risk of Ten Cancers: A Mendelian Randomization Study
- Author
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Seyed Khoei, Nazlisadat, Carreras Torres, Robert, Murphy, Neil, Gunter, Marc J., Brennan, Paul, Smith-Byrne, Karl, Mariosa, Daniela, McKay, James D., O’Mara, Tracy, Jarrett, Ruth, Hjalgrim, Henrik, Smedby, Karin E., Cozen, Wendy, Onel, Kenan, Diepstra, Arjan, Wagner, Karl-Heinz, Freisling, Heinz, and ECAC Group
- Subjects
Factors de risc en les malalties ,Risk factors in diseases ,Càncer ,Antioxidants ,Cancer - Abstract
Bilirubin, an endogenous antioxidant, may play a protective role in cancer development. We applied two-sample Mendelian randomization to investigate whether genetically raised bilirubin levels are causally associated with the risk of ten cancers (pancreas, kidney, endometrium, ovary, breast, prostate, lung, Hodgkin's lymphoma, melanoma, and neuroblastoma). The number of cases and their matched controls of European descent ranged from 122,977 and 105,974 for breast cancer to 1200 and 6417 for Hodgkin's lymphoma, respectively. A total of 115 single-nucleotide polymorphisms (SNPs) associated (p < 5 × 10-8) with circulating total bilirubin, extracted from a genome-wide association study in the UK Biobank, were used as instrumental variables. One SNP (rs6431625) in the promoter region of the uridine-diphosphoglucuronate glucuronosyltransferase1A1 (UGT1A1) gene explained 16.9% and the remaining 114 SNPs (non-UGT1A1 SNPs) explained 3.1% of phenotypic variance in circulating bilirubin levels. A one-standarddeviation increment in circulating bilirubin (≈ 4.4 µmol/L), predicted by non-UGT1A1 SNPs, was inversely associated with risk of squamous cell lung cancer and Hodgkin's lymphoma (odds ratio (OR) 0.85, 95% confidence interval (CI) 0.73-0.99, P 0.04 and OR 0.64, 95% CI 0.42-0.99, p 0.04, respectively), which was confirmed after removing potential pleiotropic SNPs. In contrast, a positive association was observed with the risk of breast cancer after removing potential pleiotropic SNPs (OR 1.12, 95% CI 1.04-1.20, p 0.002). There was little evidence for robust associations with the other seven cancers investigated. Genetically raised bilirubin levels were inversely associated with risk of squamous cell lung cancer as well as Hodgkin's lymphoma and positively associated with risk of breast cancer. Further studies are required to investigate the utility of bilirubin as a low-cost clinical marker to improve risk prediction for certain cancers.
- Published
- 2021
34. Genetically Raised Circulating Bilirubin Levels and Risk of Ten Cancers: A Mendelian Randomization Study
- Author
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Seyed Khoei, Nazlisadat Seyed, Carreras-Torres, Robert, Murphy, Neil, Gunter, Marc J., Brennan, Paul, Smith-Byrne, Karl, Mariosa, Daniela, Mckay, James, O’Mara, Tracy, Jarrett, Ruth, Hjalgrim, Henrik, Smedby, Karin E., Cozen, Wendy, Onel, Kenan, Diepstra, Arjan, Wagner, Karl-Heinz, Freisling, Heinz, and Stem Cell Aging Leukemia and Lymphoma (SALL)
- Subjects
Breast Neoplasms ,Mendelian Randomization Analysis ,cancer risk ,Polymorphism, Single Nucleotide ,Article ,lcsh:Biology (General) ,Risk Factors ,hemic and lymphatic diseases ,Mendelian randomization ,Humans ,UGT1A1 ,bilirubin ,lcsh:QH301-705.5 ,Biomarkers ,Genome-Wide Association Study - Abstract
Bilirubin, an endogenous antioxidant, may play a protective role in cancer development. We applied two-sample Mendelian randomization to investigate whether genetically raised bilirubin levels are causally associated with the risk of ten cancers (pancreas, kidney, endometrium, ovary, breast, prostate, lung, Hodgkin’s lymphoma, melanoma, and neuroblastoma). The number of cases and their matched controls of European descent ranged from 122,977 and 105,974 for breast cancer to 1200 and 6417 for Hodgkin’s lymphoma, respectively. A total of 115 single-nucleotide polymorphisms (SNPs) associated (p <, 5 × 10−8) with circulating total bilirubin, extracted from a genome-wide association study in the UK Biobank, were used as instrumental variables. One SNP (rs6431625) in the promoter region of the uridine-diphosphoglucuronate glucuronosyltransferase1A1 (UGT1A1) gene explained 16.9% and the remaining 114 SNPs (non-UGT1A1 SNPs) explained 3.1% of phenotypic variance in circulating bilirubin levels. A one-standarddeviation increment in circulating bilirubin (≈ 4.4 µmol/L), predicted by non-UGT1A1 SNPs, was inversely associated with risk of squamous cell lung cancer and Hodgkin’s lymphoma (odds ratio (OR) 0.85, 95% confidence interval (CI) 0.73–0.99, P 0.04 and OR 0.64, 95% CI 0.42–0.99, p 0.04, respectively), which was confirmed after removing potential pleiotropic SNPs. In contrast, a positive association was observed with the risk of breast cancer after removing potential pleiotropic SNPs (OR 1.12, 95% CI 1.04–1.20, p 0.002). There was little evidence for robust associations with the other seven cancers investigated. Genetically raised bilirubin levels were inversely associated with risk of squamous cell lung cancer as well as Hodgkin’s lymphoma and positively associated with risk of breast cancer. Further studies are required to investigate the utility of bilirubin as a low-cost clinical marker to improve risk prediction for certain cancers.
- Published
- 2021
35. Germline Determinants of Humoral Immune Response To HPV-16 Protect Against Oropharyngeal Cancer
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Ferreiro-Iglesias, Aida, primary, McKay, James, additional, Brenner, Nicole, additional, Virani, Shama, additional, Lesseur, Corina, additional, Gaborieau, Valérie, additional, Ness, Andrew, additional, Hung, Rayjean, additional, Liu, Geoffrey, additional, Diergaarde, Brenda, additional, Olshan, Andrew, additional, Hayes, D, additional, Weissler, Mark, additional, Schroeder, Lea, additional, Bender, Noemi, additional, Pawlita, Michael, additional, Thomas, Steven, additional, Pring, Miranda, additional, Dudding, Tom, additional, Kanterewicz, Beatriz, additional, Ferris, Robert, additional, Thomas, Sera, additional, Brhane, Yonathan, additional, Díez-Obrero, Virginia, additional, Milojevic, Maja, additional, Smith-Byrne, Karl, additional, Mariosa, Daniela, additional, Johansson, Mattias, additional, Herrero, Rolando, additional, Boccia, Stefania, additional, Cadoni, Gabriella, additional, Lacko, Martin, additional, Holcátová, Ivana, additional, Ahrens, Wolfgang, additional, Lagiou, Pagona, additional, Lagiou, Areti, additional, Polesel, Jerry, additional, Simonato, Lorenzo, additional, Merletti, Franco, additional, Healy, Claire, additional, Hansen, Bo, additional, Nygård, Mari, additional, Conway, David, additional, Wright, Sylvia, additional, Macfarlane, Tatiana, additional, Robinson, Max, additional, Alemany, Laia, additional, Agudo, Antonio, additional, Znaor, Ariana, additional, Amos, Christopher, additional, Waterboer, Tim, additional, and Brennan, Paul, additional
- Published
- 2020
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36. The role of genomics in global cancer prevention
- Author
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Ginsburg, Ophira, primary, Ashton-Prolla, Patricia, additional, Cantor, Anna, additional, Mariosa, Daniela, additional, and Brennan, Paul, additional
- Published
- 2020
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- View/download PDF
37. Peripheral immune biomarkers and neurodegenerative diseases: A prospective cohort study with 20 years of follow‐up
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Yazdani, Solmaz, primary, Mariosa, Daniela, additional, Hammar, Niklas, additional, Andersson, John, additional, Ingre, Caroline, additional, Walldius, Göran, additional, and Fang, Fang, additional
- Published
- 2019
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- View/download PDF
38. Circulating adipokine concentrations and risk of five obesity‐related cancers: A Mendelian randomization study.
- Author
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Dimou, Niki L., Papadimitriou, Nikos, Mariosa, Daniela, Johansson, Mattias, Brennan, Paul, Peters, Ulrike, Chanock, Stephen J., Purdue, Mark, Bishop, D. Timothy, Gago‐Dominquez, Manuela, Giles, Graham G., Moreno, Victor, Platz, Elizabeth A., Tangen, Catherine M., Wolk, Alicja, Zheng, Wei, Wu, Xifeng, Campbell, Peter T., Giovannucci, Edward, and Lin, Yi
- Subjects
HEREDITARY nonpolyposis colorectal cancer ,LEPTIN receptors ,RENAL cell carcinoma ,ADIPOKINES ,ADIPOSE tissues ,PLASMINOGEN activators ,ENDOMETRIAL tumors - Abstract
Obesity is considered a chronic inflammatory state characterized by continued secretion of adipokines and cytokines. Experimental and epidemiological evidence indicates that circulating adipokines may be associated with the development of obesity‐related cancers, but it is unclear if these associations are causal or confounded. We examined potential causal associations of specific adipokines (adiponectin, leptin, soluble leptin receptor [sOB‐R] and plasminogen activator inhibitor‐1 [PAI‐1]) with five obesity‐related cancers (colorectal, pancreatic, renal cell carcinoma [RCC], ovarian and endometrial) using Mendelian randomization (MR) methods. We used summary‐level data from large genetic consortia for 114 530 cancer cases and 245 284 controls. We constructed genetic instruments using 18 genetic variants for adiponectin, 2 for leptin and 4 for both sOB‐R and PAI‐1 (P value for inclusion<5 × 10−8). Causal estimates were obtained using two‐sample MR methods. In the inverse‐variance weighted models, we found an inverse association between adiponectin and risk of colorectal cancer (odds ratio per 1 μg/mL increment in adiponectin concentration: 0.90 [95% confidence interval = 0.84‐0.97]; P =.01); but, evidence of horizontal pleiotropy was detected and the association was not present when this was taken into consideration. No association was found for adiponectin and risks of pancreatic cancer, RCC, ovarian cancer and endometrial cancer. Leptin, sOB‐R and PAI‐1 were also similarly unrelated to risk of obesity‐related cancers. Despite the large sample size, our MR analyses do not support causal effects of circulating adiponectin, leptin, sOB‐R and PAI‐1 concentrations on the development of five obesity‐related cancers. What's new? Chronic inflammation attributed to obesity may influence cancer development. However, little is known about the relationship between oncogenesis and changes in adipokine secretion stemming from immune cell infiltration in adipose tissue. Here, large‐scale Mendelian randomization analysis was used to assess possible causal associations of adipokine concentrations influenced by genetic variation and risk of five obesity‐related cancers, including renal cell carcinoma and colorectal, pancreatic, ovarian and endometrial cancer. In general, no association was detected between adipokines and the five malignancies, suggesting that adipokine levels have no causal influence on these cancers. [ABSTRACT FROM AUTHOR]
- Published
- 2021
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39. Commentary: What can Mendelian randomization tell us about causes of cancer?
- Author
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Mariosa, Daniela, primary, Carreras-Torres, Robert, additional, Martin, Richard M, additional, Johansson, Mattias, additional, and Brennan, Paul, additional
- Published
- 2019
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- View/download PDF
40. Neurodegenerative and psychiatric diseases among families with amyotrophic lateral sclerosis
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Longinetti, Elisa, primary, Mariosa, Daniela, additional, Larsson, Henrik, additional, Ye, Weimin, additional, Ingre, Caroline, additional, Almqvist, Catarina, additional, Lichtenstein, Paul, additional, Piehl, Fredrik, additional, and Fang, Fang, additional
- Published
- 2017
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- View/download PDF
41. Blood biomarkers of carbohydrate, lipid, and apolipoprotein metabolisms and risk of amyotrophic lateral sclerosis: A more than 20-year follow-up of the Swedish AMORIS cohort
- Author
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Mariosa, Daniela, primary, Hammar, Niklas, additional, Malmström, Håkan, additional, Ingre, Caroline, additional, Jungner, Ingmar, additional, Ye, Weimin, additional, Fang, Fang, additional, and Walldius, Göran, additional
- Published
- 2017
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42. Cohort Profile: The Swedish National March Cohort
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Trolle Lagerros, Ylva, primary, Hantikainen, Essi, additional, Mariosa, Daniela, additional, Ye, Weimin, additional, Adami, Hans-Olov, additional, Grotta, Alessandra, additional, Ghilotti, Francesca, additional, and Bellocco, Rino, additional
- Published
- 2016
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43. Depression in amyotrophic lateral sclerosis
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Roos, Elin, primary, Mariosa, Daniela, additional, Ingre, Caroline, additional, Lundholm, Cecilia, additional, Wirdefeldt, Karin, additional, Roos, Per M., additional, and Fang, Fang, additional
- Published
- 2016
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44. A prospective cohort study of the combined effects of physical activity and anthropometric measures on the risk of post-menopausal breast cancer
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Bellocco, Rino, primary, Marrone, Gaetano, additional, Ye, Weimin, additional, Nyrén, Olof, additional, Adami, Hans-Olov, additional, Mariosa, Daniela, additional, and Lagerros, Ylva Trolle, additional
- Published
- 2015
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45. Dose–Response Relationship of Total and Leisure Time Physical Activity to Risk of Heart Failure
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Andersen, Kasper, primary, Mariosa, Daniela, additional, Adami, Hans-Olov, additional, Held, Claes, additional, Ingelsson, Erik, additional, Lagerros, Ylva Trolle, additional, Nyrén, Olof, additional, Ye, Weimin, additional, Bellocco, Rino, additional, and Sundström, Johan, additional
- Published
- 2014
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46. VARIAZIONI SPAZIALI DEI CASI DI MALFORMAZIONE CONGENITA IN EMILIA ROMAGNA: PRIMI RISULTATI DI UNO STUDIO CONDOTTO NELL’AMBITO DEL PROGETTO EUROPEO HIWATE
- Author
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Righi, Elena, Bechtold, PETRA ELISABETH, Mariosa, Daniela, Giacobazzi, Pierluigi, Mastroianni, Katia, Calzolari, E, Rivieri, F, Astolfi, G, Lauriola, P, Borgoni, R, Fantuzzi, Guglielmina, Tortrici, D, and Aggazzotti, Gabriella
- Subjects
analisi spaziale ,malformazioni congenite ,Emilia-Romagna - Published
- 2009
47. Cohort Profile: The Swedish National March Cohort.
- Author
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Lagerros, Ylva Trolle, Hantikainen, Essi, Mariosa, Daniela, Weimin Ye, Adami, Hans-Olov, Grotta, Alessandra, Ghilotti, Francesca, Bellocco, Rino, Trolle Lagerros, Ylva, and Ye, Weimin
- Subjects
COLON (Anatomy) ,LARGE intestine ,PROSTATE cancer ,DIAGNOSIS ,SWEDISH national character ,CANCER prevention - Published
- 2017
- Full Text
- View/download PDF
48. Chlorate and Chlorite Exposure Through Drinking Water During Pregnancy and the Risk of Congenital Anomalies
- Author
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Righi, Elena, primary, Bechtold, Petra, additional, Mariosa, Daniela, additional, Mastroianni, Katia, additional, Giacobazzi, Pierluigi, additional, Predieri, Guerrino, additional, Calzolari, Elisa, additional, Astolfi, Gianni, additional, Lauriola, Paolo, additional, Tortorici, Danila, additional, Fantuzzi, Gugliemina, additional, and Aggazzotti, Gabriella, additional
- Published
- 2011
- Full Text
- View/download PDF
49. A Case-control Study on Congenital Anomalies and Trihalomethanes Exposure in Emilia Romagna (Northern Italy)
- Author
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Righi, Elena, primary, Bechtold, Petra, additional, Mariosa, Daniela, additional, Mastrorianni, Katia, additional, Giacobazzi, Pierluigi, additional, Predieri, Guerrino, additional, Calzolari, Elisa, additional, Astolfi, Gianni, additional, Lauriola, Paolo, additional, Tortorici, Danila, additional, Fantuzzi, Gugliemina, additional, and Aggazzotti, Gabriella, additional
- Published
- 2011
- Full Text
- View/download PDF
50. The influence of obesity-related factors in the etiology of renal cell carcinoma-A mendelian randomization study
- Author
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Johansson, Mattias, Carreras-Torres, Robert, Scelo, Ghislaine, Purdue, Mark P, Mariosa, Daniela, Muller, David C, Timpson, Nicolas J, Haycock, Philip C, Brown, Kevin M, Wang, Zhaoming, Ye, Yuanqing, Hofmann, Jonathan N, Foll, Matthieu, Gaborieau, Valerie, Machiela, Mitchell J, Colli, Leandro M, Li, Peng, Garnier, Jean-Guillaume, Blanche, Helene, Boland, Anne, Burdette, Laurie, Prokhortchouk, Egor, Skryabin, Konstantin G, Yeager, Meredith, Radojevic-Skodric, Sanja, Ognjanovic, Simona, Foretova, Lenka, Holcatova, Ivana, Janout, Vladimir, Mates, Dana, Mukeriya, Anush, Rascu, Stefan, Zaridze, David, Bencko, Vladimir, Cybulski, Cezary, Fabianova, Eleonora, Jinga, Viorel, Lissowska, Jolanta, Lubinski, Jan, Navratilova, Marie, Rudnai, Peter, Benhamou, Simone, Cancel-Tassin, Geraldine, Cussenot, Olivier, Weiderpass, Elisabete, Ljungberg, Börje, Tumkur Sitaram, Raviprakash, Häggström, Christel, Bruinsma, Fiona, Jordan, Susan J, Severi, Gianluca, Winship, Ingrid, Hveem, Kristian, Vatten, Lars J, Fletcher, Tony, Larsson, Susanna C, Wolk, Alicja, Banks, Rosamonde E, Selby, Peter J, Easton, Douglas F, Andreotti, Gabriella, Beane Freeman, Laura E, Koutros, Stella, Männistö, Satu, Weinstein, Stephanie, Clark, Peter E, Edwards, Todd L, Lipworth, Loren, Gapstur, Susan M, Stevens, Victoria L, Carol, Hallie, Freedman, Matthew L, Pomerantz, Mark M, Cho, Eunyoung, Wilson, Kathryn M, Gaziano, J Michael, Sesso, Howard D, Freedman, Neal D, Parker, Alexander S, Eckel-Passow, Jeanette E, Huang, Wen-Yi, Kahnoski, Richard J, Lane, Brian R, Noyes, Sabrina L, Petillo, David, Teh, Bin Tean, Peters, Ulrike, White, Emily, Anderson, Garnet L, Johnson, Lisa, Luo, Juhua, Buring, Julie, Lee, I-Min, Chow, Wong-Ho, Moore, Lee E, Eisen, Timothy, Henrion, Marc, Larkin, James, Barman, Poulami, Leibovich, Bradley C, Choueiri, Toni K, Lathrop, G Mark, Deleuze, Jean-Francois, Gunter, Marc, McKay, James D, Wu, Xifeng, Houlston, Richard S, Chanock, Stephen J, Relton, Caroline, Richards, J Brent, Martin, Richard M, Davey Smith, George, and Brennan, Paul
- Subjects
2. Zero hunger ,Blood Glucose ,Genetic Markers ,Male ,Blood Pressure ,Mendelian Randomization Analysis ,urologic and male genital diseases ,Lipids ,Kidney Neoplasms ,Body Mass Index ,Diabetes Mellitus, Type 2 ,Risk Factors ,Humans ,Insulin ,Female ,Obesity ,Carcinoma, Renal Cell ,Genome-Wide Association Study - Abstract
BACKGROUND: Several obesity-related factors have been associated with renal cell carcinoma (RCC), but it is unclear which individual factors directly influence risk. We addressed this question using genetic markers as proxies for putative risk factors and evaluated their relation to RCC risk in a mendelian randomization (MR) framework. This methodology limits bias due to confounding and is not affected by reverse causation. METHODS AND FINDINGS: Genetic markers associated with obesity measures, blood pressure, lipids, type 2 diabetes, insulin, and glucose were initially identified as instrumental variables, and their association with RCC risk was subsequently evaluated in a genome-wide association study (GWAS) of 10,784 RCC patients and 20,406 control participants in a 2-sample MR framework. The effect on RCC risk was estimated by calculating odds ratios (ORSD) for a standard deviation (SD) increment in each risk factor. The MR analysis indicated that higher body mass index increases the risk of RCC (ORSD: 1.56, 95% confidence interval [CI] 1.44-1.70), with comparable results for waist-to-hip ratio (ORSD: 1.63, 95% CI 1.40-1.90) and body fat percentage (ORSD: 1.66, 95% CI 1.44-1.90). This analysis further indicated that higher fasting insulin (ORSD: 1.82, 95% CI 1.30-2.55) and diastolic blood pressure (DBP; ORSD: 1.28, 95% CI 1.11-1.47), but not systolic blood pressure (ORSD: 0.98, 95% CI 0.84-1.14), increase the risk for RCC. No association with RCC risk was seen for lipids, overall type 2 diabetes, or fasting glucose. CONCLUSIONS: This study provides novel evidence for an etiological role of insulin in RCC, as well as confirmatory evidence that obesity and DBP influence RCC risk.
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