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981 results on '"Haile, Robert W."'

162. Agreement in alcohol consumption levels as measured by two different questionnaires

Author

Witte, John S. and Haile, Robert W.

Subjects
Personality questionnaires -- Evaluation, Drinking of alcoholic beverages -- Research, Health, Psychology and mental health
Abstract

Objective: We evaluated the agreement in reported alcohol consumption between a standard food frequency questionnaire (FFQ) and a risk factor questionnaire (RFQ) developed for a genetic epidemiologic study of breast cancer. Method: The FFQ measured intake of alcoholic beverages by asking which of nine levels were consumed during a single time period. In contrast, the RFQ used open-ended questions to measure intake of alcoholic beverages during numerous time periods. Subjects (N = 765) completed both questionnaires at home. Results: Mean daily alcohol consumption levels were consistently higher in the FFQ than in the RFQ; for example, the mean alcohol consumption for all subjects was 7.0 g/day in the FFQ versus 5.3 g/day in the RFQ. Moreover, the RFQ overestimated the number of nondrinkers relative to the FFQ. Nonetheless, the Spearman correlation coefficients between daily alcohol consumption levels as measured by the two questionnaires were relatively high: total alcohol, r = 0.72; beer, r = 0.69: wine, r = 0.69; and distilled spirits, r :0.54. Conclusions: The reasonable agreement between these questionnaires supports the validity of historical alcohol consumption levels measured by the RFQ. (J. Stud. Alcohol 57: 406-409, 1996), The risk factor questionnaire (RFQ) is better than the food frequency questionnaire (FFQ) for measuring alcohol consumption, although both RFQ and FFQ give similar results. The Spearman coefficients of daily alcohol consumption measured by RFQ and FFQ are high. RFQ overestimates the number of nondrinkers while FFQ gives higher values of mean daily alcohol consumption. Both methods are more applicable for determining the alcohol consumption of younger educated individuals than older, less-educated individuals., SINCE ALCOHOL CONSUMPTION increases risk of numerous chronic diseases (Darnton-Hill, 1989) a valid measure of alcohol intake is crucial for accurate epidemiologic assessment of that risk. Common approaches to measuring [...]

Published
1996

163. Mortality associated with low plasma concentration of beta carotene and the effect of oral supplementation

Author

Greenberg, E. Robert, Baron, John A., Karagas, Margaret R., Stukel, Therese A., Nierenberg, David W., Stevens, Marguerite M., Mandel, Jack S., and Haile, Robert W.

Subjects
Beta carotene -- Health aspects, Mortality -- Health aspects
Abstract

Beta carotene supplementation may not reduce mortality from cardiovascular disease or other causes, though high beta carotene levels before supplementation may be associated with reduced risk of death. Some research has suggested that beta carotene may reduce the risk of coronary heart disease and cancer, though these findings are controversial. For a median of 4.3 years, 1,188 men and 532 women took either 50 milligrams a day of beta carotene or a placebo. During a median follow-up of 8.2 years, 285 of the participants died. In comparison to the people with the lowest beta carotene blood levels before supplementation, the people with the highest levels had approximately half the risk of death from cardiovascular disease or all causes. However, mortality rates among people who received placebos and among those who received beta carotene supplements were similar.

Published
1996

164. Discovery of common and rare genetic risk variants for colorectal cancer

Author

Huyghe, Jeroen R., Bien, Stephanie A., Harrison, Tabitha A., Kang, Hyun Min, Chen, Sai, Schmit, Stephanie L., Conti, David V., Qu, Conghui, Jeon, Jihyoun, Edlund, Christopher K., Greenside, Peyton, Wainberg, Michael, Schumacher, Fredrick R., Smith, Joshua D., Levine, David M., Nelson, Sarah C., Sinnott-Armstrong, Nasa A., Albanes, Demetrius, Alonso, M. Henar, Anderson, Kristin, Arnau-Collell, Coral, Arndt, Volker, Bamia, Christina, Banbury, Barbara L., Baron, John A., Berndt, Sonja I., Bezieau, Stephane, Bishop, D. Timothy, Boehm, Juergen, Boeing, Heiner, Brenner, Hermann, Brezina, Stefanie, Buch, Stephan, Buchanan, Daniel D., Burnett-Hartman, Andrea, Butterbach, Katja, Caan, Bette J., Campbell, Peter T., Carlson, Christopher S., Castellvi-Bel, Sergi, Chan, Andrew T., Chang-Claude, Jenny, Chanock, Stephen J., Chirlaque, Maria-Dolores, Cho, Sang Hee, Connolly, Charles M., Cross, Amanda J., Cuk, Katarina, Curtis, Keith R., de la Chapelle, Albert, Doheny, Kimberly F., Duggan, David, Easton, Douglas F., Elias, Sjoerd G., Elliott, Faye, English, Dallas R., Feskens, Edith J. M., Figueiredo, Jane C., Fischer, Rocky, FitzGerald, Liesel M., Forman, David, Gala, Manish, Gallinger, Steven, Gauderman, W. James, Giles, Graham G., Gillanders, Elizabeth, Gong, Jian, Goodman, Phyllis J., Grady, William M., Grove, John S., Gsur, Andrea, Gunter, Marc J., Haile, Robert W., Hampe, Jochen, Hampel, Heather, Harlid, Sophia, Hayes, Richard B., Hofer, Philipp, Hoffmeister, Michael, Hopper, John L., Hsu, Wan-Ling, Huang, Wen-Yi, Hudson, Thomas J., Hunter, David J., Ibanez-Sanz, Gemma, Idos, Gregory E., Ingersoll, Roxann, Jackson, Rebecca D., Jacobs, Eric J., Jenkins, Mark A., Joshi, Amit D., Joshu, Corinne E., Keku, Temitope O., Key, Timothy J., Kim, Hyeong Rok, Kobayashi, Emiko, Kolonel, Laurence N., Kooperberg, Charles, Kuehn, Tilman, Kury, Sebastien, Kweon, Sun-Seog, Larsson, Susanna C., Laurie, Cecelia A., Le Marchand, Loic, Leal, Suzanne M., Lee, Soo Chin, Lejbkowicz, Flavio, Lemire, Mathieu, Li, Christopher I., Li, Li, Lieb, Wolfgang, Lin, Yi, Lindblom, Annika, Lindor, Noralane M., Ling, Hua, Louie, Tin L., Mannisto, Satu, Markowitz, Sanford D., Martin, Vicente, Masala, Giovanna, McNeil, Caroline E., Melas, Marilena, Milne, Roger L., Moreno, Lorena, Murphy, Neil, Myte, Robin, Naccarati, Alessio, Newcomb, Polly A., Offit, Kenneth, Ogino, Shuji, Onland-Moret, N. Charlotte, Pardini, Barbara, Parfrey, Patrick S., Pearlman, Rachel, Perduca, Vittorio, Pharoah, Paul D. P., Pinchev, Mila, Platz, Elizabeth A., Prentice, Ross L., Pugh, Elizabeth, Raskin, Leon, Rennert, Gad, Rennert, Hedy S., Riboli, Elio, Rodriguez-Barranco, Miguel, Romm, Jane, Sakoda, Lori C., Schafmayer, Clemens, Schoen, Robert E., Seminara, Daniela, Shah, Mitul, Shelford, Tameka, Shin, Min-Ho, Shulman, Katerina, Sieri, Sabina, Slattery, Martha L., Southey, Melissa C., Stadler, Zsofia K., Stegmaier, Christa, Su, Yu-Ru, Tangen, Catherine M., Thibodeau, Stephen N., Thomas, Duncan C., Thomas, Sushma S., Toland, Amanda E., Trichopoulou, Antonia, Ulrich, Cornelia M., Van den Berg, David J., van Duijnhoven, Franzel J. B., Van Guelpen, Bethany, van Kranen, Henk, Vijai, Joseph, Visvanathan, Kala, Vodicka, Pavel, Vodickova, Ludmila, Vymetalkova, Veronika, Weigl, Korbinian, Weinstein, Stephanie J., White, Emily, Win, Aung Ko, Wolf, C. Roland, Wolk, Alicja, Woods, Michael O., Wu, Anna H., Zaidi, Syed H., Zanke, Brent W., Zhang, Qing, Zheng, Wei, Scacheri, Peter C., Potter, John D., Bassik, Michael C., Kundaje, Anshul, Casey, Graham, Moreno, Victor, Abecasis, Goncalo R., Nickerson, Deborah A., Gruber, Stephen B., Hsu, Li, Peters, Ulrike, Huyghe, Jeroen R., Bien, Stephanie A., Harrison, Tabitha A., Kang, Hyun Min, Chen, Sai, Schmit, Stephanie L., Conti, David V., Qu, Conghui, Jeon, Jihyoun, Edlund, Christopher K., Greenside, Peyton, Wainberg, Michael, Schumacher, Fredrick R., Smith, Joshua D., Levine, David M., Nelson, Sarah C., Sinnott-Armstrong, Nasa A., Albanes, Demetrius, Alonso, M. Henar, Anderson, Kristin, Arnau-Collell, Coral, Arndt, Volker, Bamia, Christina, Banbury, Barbara L., Baron, John A., Berndt, Sonja I., Bezieau, Stephane, Bishop, D. Timothy, Boehm, Juergen, Boeing, Heiner, Brenner, Hermann, Brezina, Stefanie, Buch, Stephan, Buchanan, Daniel D., Burnett-Hartman, Andrea, Butterbach, Katja, Caan, Bette J., Campbell, Peter T., Carlson, Christopher S., Castellvi-Bel, Sergi, Chan, Andrew T., Chang-Claude, Jenny, Chanock, Stephen J., Chirlaque, Maria-Dolores, Cho, Sang Hee, Connolly, Charles M., Cross, Amanda J., Cuk, Katarina, Curtis, Keith R., de la Chapelle, Albert, Doheny, Kimberly F., Duggan, David, Easton, Douglas F., Elias, Sjoerd G., Elliott, Faye, English, Dallas R., Feskens, Edith J. M., Figueiredo, Jane C., Fischer, Rocky, FitzGerald, Liesel M., Forman, David, Gala, Manish, Gallinger, Steven, Gauderman, W. James, Giles, Graham G., Gillanders, Elizabeth, Gong, Jian, Goodman, Phyllis J., Grady, William M., Grove, John S., Gsur, Andrea, Gunter, Marc J., Haile, Robert W., Hampe, Jochen, Hampel, Heather, Harlid, Sophia, Hayes, Richard B., Hofer, Philipp, Hoffmeister, Michael, Hopper, John L., Hsu, Wan-Ling, Huang, Wen-Yi, Hudson, Thomas J., Hunter, David J., Ibanez-Sanz, Gemma, Idos, Gregory E., Ingersoll, Roxann, Jackson, Rebecca D., Jacobs, Eric J., Jenkins, Mark A., Joshi, Amit D., Joshu, Corinne E., Keku, Temitope O., Key, Timothy J., Kim, Hyeong Rok, Kobayashi, Emiko, Kolonel, Laurence N., Kooperberg, Charles, Kuehn, Tilman, Kury, Sebastien, Kweon, Sun-Seog, Larsson, Susanna C., Laurie, Cecelia A., Le Marchand, Loic, Leal, Suzanne M., Lee, Soo Chin, Lejbkowicz, Flavio, Lemire, Mathieu, Li, Christopher I., Li, Li, Lieb, Wolfgang, Lin, Yi, Lindblom, Annika, Lindor, Noralane M., Ling, Hua, Louie, Tin L., Mannisto, Satu, Markowitz, Sanford D., Martin, Vicente, Masala, Giovanna, McNeil, Caroline E., Melas, Marilena, Milne, Roger L., Moreno, Lorena, Murphy, Neil, Myte, Robin, Naccarati, Alessio, Newcomb, Polly A., Offit, Kenneth, Ogino, Shuji, Onland-Moret, N. Charlotte, Pardini, Barbara, Parfrey, Patrick S., Pearlman, Rachel, Perduca, Vittorio, Pharoah, Paul D. P., Pinchev, Mila, Platz, Elizabeth A., Prentice, Ross L., Pugh, Elizabeth, Raskin, Leon, Rennert, Gad, Rennert, Hedy S., Riboli, Elio, Rodriguez-Barranco, Miguel, Romm, Jane, Sakoda, Lori C., Schafmayer, Clemens, Schoen, Robert E., Seminara, Daniela, Shah, Mitul, Shelford, Tameka, Shin, Min-Ho, Shulman, Katerina, Sieri, Sabina, Slattery, Martha L., Southey, Melissa C., Stadler, Zsofia K., Stegmaier, Christa, Su, Yu-Ru, Tangen, Catherine M., Thibodeau, Stephen N., Thomas, Duncan C., Thomas, Sushma S., Toland, Amanda E., Trichopoulou, Antonia, Ulrich, Cornelia M., Van den Berg, David J., van Duijnhoven, Franzel J. B., Van Guelpen, Bethany, van Kranen, Henk, Vijai, Joseph, Visvanathan, Kala, Vodicka, Pavel, Vodickova, Ludmila, Vymetalkova, Veronika, Weigl, Korbinian, Weinstein, Stephanie J., White, Emily, Win, Aung Ko, Wolf, C. Roland, Wolk, Alicja, Woods, Michael O., Wu, Anna H., Zaidi, Syed H., Zanke, Brent W., Zhang, Qing, Zheng, Wei, Scacheri, Peter C., Potter, John D., Bassik, Michael C., Kundaje, Anshul, Casey, Graham, Moreno, Victor, Abecasis, Goncalo R., Nickerson, Deborah A., Gruber, Stephen B., Hsu, Li, and Peters, Ulrike

Abstract

To further dissect the genetic architecture of colorectal cancer (CRC), we performed whole-genome sequencing of 1,439 cases and 720 controls, imputed discovered sequence variants and Haplotype Reference Consortium panel variants into genome-wide association study data, and tested for association in 34,869 cases and 29,051 controls. Findings were followed up in an additional 23,262 cases and 38,296 controls. We discovered a strongly protective 0.3% frequency variant signal at CHD1. In a combined meta-analysis of 125,478 individuals, we identified 40 new independent signals at P < 5 x 10(-8), bringing the number of known independent signals for CRC to similar to 100. New signals implicate lower-frequency variants, Kruppel-like factors, Hedgehog signaling, Hippo-YAP signaling, long noncoding RNAs and somatic drivers, and support a role for immune function. Heritability analyses suggest that CRC risk is highly polygenic, and larger, more comprehensive studies enabling rare variant analysis will improve understanding of biology underlying this risk and influence personalized screening strategies and drug development.

Published
2019
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165. Methylated SEPTIN9 plasma test for colorectal cancer detection may be applicable to Lynch syndrome.

Author

Hitchins, Megan P, Hitchins, Megan P, Vogelaar, Ingrid P, Brennan, Kevin, Haraldsdottir, Sigurdis, Zhou, Nianmin, Martin, Brock, Alvarez, Rocio, Yuan, Xiaopu, Kim, Sungjin, Guindi, Maha, Hendifar, Andrew E, Kalady, Matthew F, DeVecchio, Jennifer, Church, James M, de la Chapelle, Albert, Hampel, Heather, Pearlman, Rachel, Christensen, Maria, Snyder, Carrie, Lanspa, Stephen J, Haile, Robert W, Lynch, Henry T, Hitchins, Megan P, Hitchins, Megan P, Vogelaar, Ingrid P, Brennan, Kevin, Haraldsdottir, Sigurdis, Zhou, Nianmin, Martin, Brock, Alvarez, Rocio, Yuan, Xiaopu, Kim, Sungjin, Guindi, Maha, Hendifar, Andrew E, Kalady, Matthew F, DeVecchio, Jennifer, Church, James M, de la Chapelle, Albert, Hampel, Heather, Pearlman, Rachel, Christensen, Maria, Snyder, Carrie, Lanspa, Stephen J, Haile, Robert W, and Lynch, Henry T

Abstract

ObjectiveThe plasma-based methylated SEPTIN9 (mSEPT9) is a colorectal cancer (CRC) screening test for adults aged 50-75 years who are at average risk for CRC and have refused colonoscopy or faecal-based screening tests. The applicability of mSEPT9 for high-risk persons with Lynch syndrome (LS), the most common hereditary CRC condition, has not been assessed. This study sought preliminary evidence for the utility of mSEPT9 for CRC detection in LS.DesignFirstly, SEPT9 methylation was measured in LS-associated CRC, advanced adenoma, and subject-matched normal colorectal mucosa tissues by pyrosequencing. Secondly, to detect mSEPT9 as circulating tumor DNA, the plasma-based mSEPT9 test was retrospectively evaluated in LS subjects using the Epi proColon 2.0 CE assay adapted for 1mL plasma using the "1/1 algorithm". LS case groups included 20 peri-surgical cases with acolonoscopy-based diagnosis of CRC (stages I-IV), 13 post-surgical metastatic CRC, and 17 pre-diagnosis cases. The control group comprised 31 cancer-free LS subjects.ResultsDifferential hypermethylation was found in 97.3% (36/37) of primary CRC and 90.0% (18/20) of advanced adenomas, showing LS-associated neoplasia frequently produce the mSEPT9 biomarker. Sensitivity of plasma mSEPT9 to detect CRC was 70.0% (95% CI, 48%-88%)in cases with a colonoscopy-based CRC diagnosis and 92.3% (95% CI, 64%-100%) inpost-surgical metastatic cases. In pre-diagnosis cases, plasma mSEPT9 was detected within two months prior to colonoscopy-based CRC diagnosis in 3/5 cases. Specificity in controls was 100% (95% CI 89%-100%).ConclusionThese preliminary findings suggest mSEPT9 may demonstrate similar diagnostic performance characteristics in LS as in the average-risk population, warranting a well-powered prospective case-control study.

Published
2019

166. Discovery of common and rare genetic risk variants for colorectal cancer

Author

Epi Kanker Team A, Cancer, JC onderzoeksprogramma Kanker, CMM Groep Burgering, Cardiovasculaire Epi Team 3, Brain, Circulatory Health, JC onderzoeksprogramma Cardiovasculaire Epidemiologie, Huyghe, Jeroen R., Bien, Stephanie A., Harrison, Tabitha A., Kang, Hyun Min, Chen, Sai, Schmit, Stephanie L., Conti, David V., Qu, Conghui, Jeon, Jihyoun, Edlund, Christopher K., Greenside, Peyton, Wainberg, Michael, Schumacher, Fredrick R., Smith, Joshua D., Levine, David M., Nelson, Sarah C., Sinnott-Armstrong, Nasa A., Albanes, Demetrius, Alonso, M. Henar, Anderson, Kristin, Arnau-Collell, Coral, Arndt, Volker, Bamia, Christina, Banbury, Barbara L., Baron, John A., Berndt, Sonja I., Bézieau, Stéphane, Bishop, D. Timothy, Boehm, Juergen, Boeing, Heiner, Brenner, Hermann, Brezina, Stefanie, Buch, Stephan, Buchanan, Daniel D., Burnett-Hartman, Andrea, Butterbach, Katja, Caan, Bette J., Campbell, Peter T., Carlson, Christopher S., Castellví-Bel, Sergi, Chan, Andrew T., Chang-Claude, Jenny, Chanock, Stephen J., Chirlaque, Maria Dolores, Cho, Sang Hee, Connolly, Charles M., Cross, Amanda J., Cuk, Katarina, Curtis, Keith R., de la Chapelle, Albert, Doheny, Kimberly F., Duggan, David, Easton, Douglas F., Elias, Sjoerd G., Elliott, Faye, English, Dallas R., Feskens, Edith J.M., Figueiredo, Jane C., Fischer, Rocky, FitzGerald, Liesel M., Forman, David, Gala, Manish, Gallinger, Steven, Gauderman, W. James, Giles, Graham G., Gillanders, Elizabeth, Gong, Jian, Goodman, Phyllis J., Grady, William M., Grove, John S., Gsur, Andrea, Gunter, Marc J., Haile, Robert W., Hampe, Jochen, Hampel, Heather, Harlid, Sophia, Hayes, Richard B., Hofer, Philipp, Hoffmeister, Michael, Hopper, John L., Hsu, Wan Ling, Huang, Wen Yi, Hudson, Thomas J., Hunter, David J., Ibañez-Sanz, Gemma, Idos, Gregory E., Ingersoll, Roxann, Jackson, Rebecca D., Jacobs, Eric J., Jenkins, Mark A., Joshi, Amit D., Joshu, Corinne E., Keku, Temitope O., Key, Timothy J., Kim, Hyeong Rok, Kobayashi, Emiko, Kolonel, Laurence N., Kooperberg, Charles, Kühn, Tilman, Küry, Sébastien, Kweon, Sun Seog, Larsson, Susanna C., Laurie, Cecelia A., Le Marchand, Loic, Leal, Suzanne M., Lee, Soo Chin, Lejbkowicz, Flavio, Lemire, Mathieu, Li, Christopher I., Li, Li, Lieb, Wolfgang, Lin, Yi, Lindblom, Annika, Lindor, Noralane M., Ling, Hua, Louie, Tin L., Männistö, Satu, Markowitz, Sanford D., Martín, Vicente, Masala, Giovanna, McNeil, Caroline E., Melas, Marilena, Milne, Roger L., Moreno, Lorena, Murphy, Neil, Myte, Robin, Naccarati, Alessio, Newcomb, Polly A., Offit, Kenneth, Ogino, Shuji, Onland-Moret, N. Charlotte, Pardini, Barbara, Parfrey, Patrick S., Pearlman, Rachel, Perduca, Vittorio, Pharoah, Paul D.P., Pinchev, Mila, Platz, Elizabeth A., Prentice, Ross L., Pugh, Elizabeth, Raskin, Leon, Rennert, Gad, Rennert, Hedy S., Riboli, Elio, Rodríguez-Barranco, Miguel, Romm, Jane, Sakoda, Lori C., Schafmayer, Clemens, Schoen, Robert E., Seminara, Daniela, Shah, Mitul, Shelford, Tameka, Shin, Min Ho, Shulman, Katerina, Sieri, Sabina, Slattery, Martha L., Southey, Melissa C., Stadler, Zsofia K., Stegmaier, Christa, Su, Yu Ru, Tangen, Catherine M., Thibodeau, Stephen N., Thomas, Duncan C., Thomas, Sushma S., Toland, Amanda E., Trichopoulou, Antonia, Ulrich, Cornelia M., Van Den Berg, David J., van Duijnhoven, Franzel J.B., Van Guelpen, Bethany, van Kranen, Henk, Vijai, Joseph, Visvanathan, Kala, Vodicka, Pavel, Vodickova, Ludmila, Vymetalkova, Veronika, Weigl, Korbinian, Weinstein, Stephanie J., White, Emily, Win, Aung Ko, Wolf, C. Roland, Wolk, Alicja, Woods, Michael O., Wu, Anna H., Zaidi, Syed H., Zanke, Brent W., Zhang, Qing, Zheng, Wei, Scacheri, Peter C., Potter, John D., Bassik, Michael C., Kundaje, Anshul, Casey, Graham, Moreno, Victor, Abecasis, Goncalo R., Nickerson, Deborah A., Gruber, Stephen B., Hsu, Li, Peters, Ulrike, Epi Kanker Team A, Cancer, JC onderzoeksprogramma Kanker, CMM Groep Burgering, Cardiovasculaire Epi Team 3, Brain, Circulatory Health, JC onderzoeksprogramma Cardiovasculaire Epidemiologie, Huyghe, Jeroen R., Bien, Stephanie A., Harrison, Tabitha A., Kang, Hyun Min, Chen, Sai, Schmit, Stephanie L., Conti, David V., Qu, Conghui, Jeon, Jihyoun, Edlund, Christopher K., Greenside, Peyton, Wainberg, Michael, Schumacher, Fredrick R., Smith, Joshua D., Levine, David M., Nelson, Sarah C., Sinnott-Armstrong, Nasa A., Albanes, Demetrius, Alonso, M. Henar, Anderson, Kristin, Arnau-Collell, Coral, Arndt, Volker, Bamia, Christina, Banbury, Barbara L., Baron, John A., Berndt, Sonja I., Bézieau, Stéphane, Bishop, D. Timothy, Boehm, Juergen, Boeing, Heiner, Brenner, Hermann, Brezina, Stefanie, Buch, Stephan, Buchanan, Daniel D., Burnett-Hartman, Andrea, Butterbach, Katja, Caan, Bette J., Campbell, Peter T., Carlson, Christopher S., Castellví-Bel, Sergi, Chan, Andrew T., Chang-Claude, Jenny, Chanock, Stephen J., Chirlaque, Maria Dolores, Cho, Sang Hee, Connolly, Charles M., Cross, Amanda J., Cuk, Katarina, Curtis, Keith R., de la Chapelle, Albert, Doheny, Kimberly F., Duggan, David, Easton, Douglas F., Elias, Sjoerd G., Elliott, Faye, English, Dallas R., Feskens, Edith J.M., Figueiredo, Jane C., Fischer, Rocky, FitzGerald, Liesel M., Forman, David, Gala, Manish, Gallinger, Steven, Gauderman, W. James, Giles, Graham G., Gillanders, Elizabeth, Gong, Jian, Goodman, Phyllis J., Grady, William M., Grove, John S., Gsur, Andrea, Gunter, Marc J., Haile, Robert W., Hampe, Jochen, Hampel, Heather, Harlid, Sophia, Hayes, Richard B., Hofer, Philipp, Hoffmeister, Michael, Hopper, John L., Hsu, Wan Ling, Huang, Wen Yi, Hudson, Thomas J., Hunter, David J., Ibañez-Sanz, Gemma, Idos, Gregory E., Ingersoll, Roxann, Jackson, Rebecca D., Jacobs, Eric J., Jenkins, Mark A., Joshi, Amit D., Joshu, Corinne E., Keku, Temitope O., Key, Timothy J., Kim, Hyeong Rok, Kobayashi, Emiko, Kolonel, Laurence N., Kooperberg, Charles, Kühn, Tilman, Küry, Sébastien, Kweon, Sun Seog, Larsson, Susanna C., Laurie, Cecelia A., Le Marchand, Loic, Leal, Suzanne M., Lee, Soo Chin, Lejbkowicz, Flavio, Lemire, Mathieu, Li, Christopher I., Li, Li, Lieb, Wolfgang, Lin, Yi, Lindblom, Annika, Lindor, Noralane M., Ling, Hua, Louie, Tin L., Männistö, Satu, Markowitz, Sanford D., Martín, Vicente, Masala, Giovanna, McNeil, Caroline E., Melas, Marilena, Milne, Roger L., Moreno, Lorena, Murphy, Neil, Myte, Robin, Naccarati, Alessio, Newcomb, Polly A., Offit, Kenneth, Ogino, Shuji, Onland-Moret, N. Charlotte, Pardini, Barbara, Parfrey, Patrick S., Pearlman, Rachel, Perduca, Vittorio, Pharoah, Paul D.P., Pinchev, Mila, Platz, Elizabeth A., Prentice, Ross L., Pugh, Elizabeth, Raskin, Leon, Rennert, Gad, Rennert, Hedy S., Riboli, Elio, Rodríguez-Barranco, Miguel, Romm, Jane, Sakoda, Lori C., Schafmayer, Clemens, Schoen, Robert E., Seminara, Daniela, Shah, Mitul, Shelford, Tameka, Shin, Min Ho, Shulman, Katerina, Sieri, Sabina, Slattery, Martha L., Southey, Melissa C., Stadler, Zsofia K., Stegmaier, Christa, Su, Yu Ru, Tangen, Catherine M., Thibodeau, Stephen N., Thomas, Duncan C., Thomas, Sushma S., Toland, Amanda E., Trichopoulou, Antonia, Ulrich, Cornelia M., Van Den Berg, David J., van Duijnhoven, Franzel J.B., Van Guelpen, Bethany, van Kranen, Henk, Vijai, Joseph, Visvanathan, Kala, Vodicka, Pavel, Vodickova, Ludmila, Vymetalkova, Veronika, Weigl, Korbinian, Weinstein, Stephanie J., White, Emily, Win, Aung Ko, Wolf, C. Roland, Wolk, Alicja, Woods, Michael O., Wu, Anna H., Zaidi, Syed H., Zanke, Brent W., Zhang, Qing, Zheng, Wei, Scacheri, Peter C., Potter, John D., Bassik, Michael C., Kundaje, Anshul, Casey, Graham, Moreno, Victor, Abecasis, Goncalo R., Nickerson, Deborah A., Gruber, Stephen B., Hsu, Li, and Peters, Ulrike

Published
2019

169. A clinical trial of antioxidant vitamins to prevent colorectal adenoma

Author

Greenberg, E. Robert, Baron, John A., Tosteson, Tor D., Freeman, Daniel H., Jr., Beck, Gerald J., Bond, John H., Colacchio, Thomas A., Coller, John A., Frankl, Harold D., Haile, Robert W., Mandel, Jack S., Nierenberg, David W., Rothstein, Richard, Snover, Dale C., Stevens, Marguerite M., Summers, Robert W., and van Stolk, Rosalind U.

Subjects
Adenoma -- Prevention, Colorectal cancer -- Prevention, Beta carotene -- Evaluation, Vitamin A -- Evaluation, Vitamin D -- Evaluation
Abstract

It appears that taking supplemental beta carotene and vitamins A and D does not help prevent colorectal adenoma. Colorectal adenoma is a precursor of cancer of the bowels, which is less common in people with diets that include antioxidant vitamin-rich foods such as vegetables and fish. Different combinations of a placebo, beta carotene, and vitamins A and D were given to 751 people who had previously had an adenoma removed. After four years, plasma levels of beta carotene had risen in the group receiving beta carotene supplements, and vitamin C and D levels rose in the groups receiving those vitamins. The incidences of colorectal adenoma were similar in all groups, suggesting that beta carotene and vitamins A and D do not provide added protection against cancer.

Published
1994

171. Body mass index, weight change, and risk of second primary breast cancer in the <scp>WECARE</scp> study: influence of estrogen receptor status of the first breast cancer

Author

Brooks, Jennifer D., John, Esther M., Mellemkjær, Lene, Lynch, Charles F., Knight, Julia A., Malone, Kathleen E., Reiner, Anne S., Bernstein, Leslie, Liang, Xiaolin, Shore, Roy E., Stovall, Marilyn, Bernstein, Jonine L., Capanu, Marinela, Orlow, Irene, Robson, Mark, Woods, Meghan, Boice, John D., Brooks, Jennifer, Concannon, Patrick, Conti, Dave V., Duggan, David, Elena, Joanne W., Haile, Robert W., Olsen, Jørgen H., Seminara, Daniela, Stram, Daniel O., Tischkowitz, Marc, and Thomas, Duncan C.

Subjects
Adult, Risk, Cancer Research, medicine.medical_specialty, Population, Estrogen receptor, Breast Neoplasms, lcsh:RC254-282, Body Mass Index, Young Adult, 03 medical and health sciences, 0302 clinical medicine, Breast cancer, medicine, Humans, Radiology, Nuclear Medicine and imaging, 030212 general & internal medicine, education, Estrogen Receptor Status, Original Research, Aged, Neoplasm Staging, 2. Zero hunger, Gynecology, education.field_of_study, business.industry, Obstetrics, Body Weight, Weight change, Cancer, Neoplasms, Second Primary, Middle Aged, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, medicine.disease, 3. Good health, Receptors, Estrogen, Oncology, Case-Control Studies, Population Surveillance, 030220 oncology & carcinogenesis, contralateral breast cancer, Female, medicine.symptom, business, Cancer Prevention, Body mass index, Weight gain, estrogen receptor, SEER Program
Abstract

Studies examining the relationship between body mass index (BMI) and risk of contralateral breast cancer (CBC) have reported mixed findings. We previously showed that obese postmenopausal women with estrogen receptor (ER)‐negative breast cancer have a fivefold higher risk of CBC compared with normal weight women. In the current analysis, we reexamined this relationship in the expanded Women's Environmental Cancer and Radiation Epidemiology (WECARE) Study, focusing on the impact of menopausal status and ER status of the first breast cancer. The WECARE Study is a population‐based case–control study of young women with CBC (cases, N = 1386) and with unilateral breast cancer (controls, N = 2045). Rate ratios (RR) and 95% confidence intervals (CI) were calculated to assess the relationship between BMI and risk of CBC stratified by menopausal and ER status. Positive associations with obesity and weight gain were limited to women who became postmenopausal following their first primary breast cancer. Among those with an ER‐negative first breast cancer, obesity (vs. normal weight) at first diagnosis was associated with an increased risk of CBC (RR = 1.9, 95% CI: 1.02, 3.4). Also, weight gain of ≥10 kg after first diagnosis was associated with an almost twofold increased risk of CBC (RR = 1.9, 95% CI: 0.99, 3.8). These results suggest that women with an ER‐negative first primary cancer who are obese at first primary diagnosis or who experience a large weight gain afterward may benefit from heightened surveillance. Future studies are needed to address the impact of weight loss interventions on risk of CBC.

Published
2016

173. Folic acid supplementation and risk of colorectal neoplasia during long-term follow-up of a randomized clinical trial

Author

Passarelli, Michael N, primary, Barry, Elizabeth L, additional, Rees, Judy R, additional, Mott, Leila A, additional, Zhang, Dongyu, additional, Ahnen, Dennis J, additional, Bresalier, Robert S, additional, Haile, Robert W, additional, McKeown-Eyssen, Gail, additional, Snover, Dale C, additional, Cole, Bernard F, additional, and Baron, John A, additional

Published
2019
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174. Association of a Pathway-Specific Genetic Risk Score With Risk of Radiation-Associated Contralateral Breast Cancer

Author

Watt, Gordon P., primary, Reiner, Anne S., additional, Smith, Susan A., additional, Stram, Daniel O., additional, Capanu, Marinela, additional, Malone, Kathleen E., additional, Lynch, Charles F., additional, John, Esther M., additional, Knight, Julia A., additional, Mellemkjær, Lene, additional, Bernstein, Leslie, additional, Brooks, Jennifer D., additional, Woods, Meghan, additional, Liang, Xiaolin, additional, Haile, Robert W., additional, Riaz, Nadeem, additional, Conti, David V., additional, Robson, Mark, additional, Duggan, David, additional, Boice, John D., additional, Shore, Roy E., additional, Tischkowitz, Marc, additional, Orlow, Irene, additional, Thomas, Duncan C., additional, Concannon, Patrick, additional, and Bernstein, Jonine L., additional

Published
2019
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175. Type 2 diabetes mellitus, blood cholesterol, triglyceride and colorectal cancer risk in Lynch syndrome

Author

Dashti, S. Ghazaleh, primary, Li, Wing Yan, additional, Buchanan, Daniel D., additional, Clendenning, Mark, additional, Rosty, Christophe, additional, Winship, Ingrid M., additional, Macrae, Finlay A., additional, Giles, Graham G., additional, Hardikar, Sheetal, additional, Hua, Xinwei, additional, Thibodeau, Stephen N., additional, Figueiredo, Jane C., additional, Casey, Graham, additional, Haile, Robert W., additional, Gallinger, Steven, additional, Le Marchand, Loïc, additional, Newcomb, Polly A., additional, Potter, John D., additional, Lindor, Noralane M., additional, Hopper, John L., additional, Jenkins, Mark A., additional, and Win, Aung Ko, additional

Published
2019
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176. DNA repair and cancer in colon and rectum: Novel players in genetic susceptibility

Author

Pardini, Barbara, primary, Corrado, Alda, additional, Paolicchi, Elisa, additional, Cugliari, Giovanni, additional, Berndt, Sonja I., additional, Bezieau, Stephane, additional, Bien, Stephanie A., additional, Brenner, Hermann, additional, Caan, Bette J., additional, Campbell, Peter T., additional, Casey, Graham, additional, Chan, Andrew T., additional, Chang‐Claude, Jenny, additional, Cotterchio, Michelle, additional, Gala, Manish, additional, Gallinger, Steven J., additional, Haile, Robert W., additional, Harrison, Tabitha A., additional, Hayes, Richard B., additional, Hoffmeister, Michael, additional, Hopper, John L., additional, Hsu, Li, additional, Huyghe, Jeroen, additional, Jenkins, Mark A., additional, Le Marchand, Loic, additional, Lin, Yi, additional, Lindor, Noralane M., additional, Nan, Hongmei, additional, Newcomb, Polly A., additional, Ogino, Shuji, additional, Potter, John D., additional, Schoen, Robert E., additional, Slattery, Martha L., additional, White, Emily, additional, Vodickova, Ludmila, additional, Vymetalkova, Veronika, additional, Vodicka, Pavel, additional, Gemignani, Federica, additional, Peters, Ulrike, additional, Naccarati, Alessio, additional, and Landi, Stefano, additional

Published
2019
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177. Ability of known susceptibility SNPs to predict colorectal cancer risk for persons with and without a family history

Author

Jenkins, Mark A., primary, Win, Aung K., additional, Dowty, James G., additional, MacInnis, Robert J., additional, Makalic, Enes, additional, Schmidt, Daniel F., additional, Dite, Gillian S., additional, Kapuscinski, Mirosl, additional, Clendenning, Mark, additional, Rosty, Christophe, additional, Winship, Ingrid M., additional, Emery, Jon D., additional, Saya, Sibel, additional, Macrae, Finlay A., additional, Ahnen, Dennis J., additional, Duggan, David, additional, Figueiredo, Jane C., additional, Lindor, Noralane M., additional, Haile, Robert W., additional, Potter, John D., additional, Cotterchio, Michelle, additional, Gallinger, Steven, additional, Newcomb, Polly A., additional, Buchanan, Daniel D., additional, Casey, Graham, additional, and Hopper, John L., additional

Published
2019
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178. Methylated SEPTIN9 plasma test for colorectal cancer detection may be applicable to Lynch syndrome

Author

Hitchins, Megan P, primary, Vogelaar, Ingrid P, additional, Brennan, Kevin, additional, Haraldsdottir, Sigurdis, additional, Zhou, Nianmin, additional, Martin, Brock, additional, Alvarez, Rocio, additional, Yuan, Xiaopu, additional, Kim, Sungjin, additional, Guindi, Maha, additional, Hendifar, Andrew E, additional, Kalady, Matthew F, additional, DeVecchio, Jennifer, additional, Church, James M, additional, de la Chapelle, Albert, additional, Hampel, Heather, additional, Pearlman, Rachel, additional, Christensen, Maria, additional, Snyder, Carrie, additional, Lanspa, Stephen J, additional, Haile, Robert W, additional, and Lynch, Henry T, additional

Published
2019
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179. Discovery of common and rare genetic risk variants for colorectal cancer

Author

Huyghe, Jeroen R., primary, Bien, Stephanie A., additional, Harrison, Tabitha A., additional, Kang, Hyun Min, additional, Chen, Sai, additional, Schmit, Stephanie L., additional, Conti, David V., additional, Qu, Conghui, additional, Jeon, Jihyoun, additional, Edlund, Christopher K., additional, Greenside, Peyton, additional, Wainberg, Michael, additional, Schumacher, Fredrick R., additional, Smith, Joshua D., additional, Levine, David M., additional, Nelson, Sarah C., additional, Sinnott-Armstrong, Nasa A., additional, Albanes, Demetrius, additional, Alonso, M. Henar, additional, Anderson, Kristin, additional, Arnau-Collell, Coral, additional, Arndt, Volker, additional, Bamia, Christina, additional, Banbury, Barbara L., additional, Baron, John A., additional, Berndt, Sonja I., additional, Bézieau, Stéphane, additional, Bishop, D. Timothy, additional, Boehm, Juergen, additional, Boeing, Heiner, additional, Brenner, Hermann, additional, Brezina, Stefanie, additional, Buch, Stephan, additional, Buchanan, Daniel D., additional, Burnett-Hartman, Andrea, additional, Butterbach, Katja, additional, Caan, Bette J., additional, Campbell, Peter T., additional, Carlson, Christopher S., additional, Castellví-Bel, Sergi, additional, Chan, Andrew T., additional, Chang-Claude, Jenny, additional, Chanock, Stephen J., additional, Chirlaque, Maria-Dolores, additional, Cho, Sang Hee, additional, Connolly, Charles M., additional, Cross, Amanda J., additional, Cuk, Katarina, additional, Curtis, Keith R., additional, de la Chapelle, Albert, additional, Doheny, Kimberly F., additional, Duggan, David, additional, Easton, Douglas F., additional, Elias, Sjoerd G., additional, Elliott, Faye, additional, English, Dallas R., additional, Feskens, Edith J. M., additional, Figueiredo, Jane C., additional, Fischer, Rocky, additional, FitzGerald, Liesel M., additional, Forman, David, additional, Gala, Manish, additional, Gallinger, Steven, additional, Gauderman, W. James, additional, Giles, Graham G., additional, Gillanders, Elizabeth, additional, Gong, Jian, additional, Goodman, Phyllis J., additional, Grady, William M., additional, Grove, John S., additional, Gsur, Andrea, additional, Gunter, Marc J., additional, Haile, Robert W., additional, Hampe, Jochen, additional, Hampel, Heather, additional, Harlid, Sophia, additional, Hayes, Richard B., additional, Hofer, Philipp, additional, Hoffmeister, Michael, additional, Hopper, John L., additional, Hsu, Wan-Ling, additional, Huang, Wen-Yi, additional, Hudson, Thomas J., additional, Hunter, David J., additional, Ibañez-Sanz, Gemma, additional, Idos, Gregory E., additional, Ingersoll, Roxann, additional, Jackson, Rebecca D., additional, Jacobs, Eric J., additional, Jenkins, Mark A., additional, Joshi, Amit D., additional, Joshu, Corinne E., additional, Keku, Temitope O., additional, Key, Timothy J., additional, Kim, Hyeong Rok, additional, Kobayashi, Emiko, additional, Kolonel, Laurence N., additional, Kooperberg, Charles, additional, Kühn, Tilman, additional, Küry, Sébastien, additional, Kweon, Sun-Seog, additional, Larsson, Susanna C., additional, Laurie, Cecelia A., additional, Le Marchand, Loic, additional, Leal, Suzanne M., additional, Lee, Soo Chin, additional, Lejbkowicz, Flavio, additional, Lemire, Mathieu, additional, Li, Christopher I., additional, Li, Li, additional, Lieb, Wolfgang, additional, Lin, Yi, additional, Lindblom, Annika, additional, Lindor, Noralane M., additional, Ling, Hua, additional, Louie, Tin L., additional, Männistö, Satu, additional, Markowitz, Sanford D., additional, Martín, Vicente, additional, Masala, Giovanna, additional, McNeil, Caroline E., additional, Melas, Marilena, additional, Milne, Roger L., additional, Moreno, Lorena, additional, Murphy, Neil, additional, Myte, Robin, additional, Naccarati, Alessio, additional, Newcomb, Polly A., additional, Offit, Kenneth, additional, Ogino, Shuji, additional, Onland-Moret, N. Charlotte, additional, Pardini, Barbara, additional, Parfrey, Patrick S., additional, Pearlman, Rachel, additional, Perduca, Vittorio, additional, Pharoah, Paul D. P., additional, Pinchev, Mila, additional, Platz, Elizabeth A., additional, Prentice, Ross L., additional, Pugh, Elizabeth, additional, Raskin, Leon, additional, Rennert, Gad, additional, Rennert, Hedy S., additional, Riboli, Elio, additional, Rodríguez-Barranco, Miguel, additional, Romm, Jane, additional, Sakoda, Lori C., additional, Schafmayer, Clemens, additional, Schoen, Robert E., additional, Seminara, Daniela, additional, Shah, Mitul, additional, Shelford, Tameka, additional, Shin, Min-Ho, additional, Shulman, Katerina, additional, Sieri, Sabina, additional, Slattery, Martha L., additional, Southey, Melissa C., additional, Stadler, Zsofia K., additional, Stegmaier, Christa, additional, Su, Yu-Ru, additional, Tangen, Catherine M., additional, Thibodeau, Stephen N., additional, Thomas, Duncan C., additional, Thomas, Sushma S., additional, Toland, Amanda E., additional, Trichopoulou, Antonia, additional, Ulrich, Cornelia M., additional, Van Den Berg, David J., additional, van Duijnhoven, Franzel J. B., additional, Van Guelpen, Bethany, additional, van Kranen, Henk, additional, Vijai, Joseph, additional, Visvanathan, Kala, additional, Vodicka, Pavel, additional, Vodickova, Ludmila, additional, Vymetalkova, Veronika, additional, Weigl, Korbinian, additional, Weinstein, Stephanie J., additional, White, Emily, additional, Win, Aung Ko, additional, Wolf, C. Roland, additional, Wolk, Alicja, additional, Woods, Michael O., additional, Wu, Anna H., additional, Zaidi, Syed H., additional, Zanke, Brent W., additional, Zhang, Qing, additional, Zheng, Wei, additional, Scacheri, Peter C., additional, Potter, John D., additional, Bassik, Michael C., additional, Kundaje, Anshul, additional, Casey, Graham, additional, Moreno, Victor, additional, Abecasis, Goncalo R., additional, Nickerson, Deborah A., additional, Gruber, Stephen B., additional, Hsu, Li, additional, and Peters, Ulrike, additional

Published
2018
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181. Study design: Evaluating gene–environment interactions in the etiology of breast cancer – the WECARE study

Author

Bernstein, Jonine L, Langholz, Bryan, Haile, Robert W, Bernstein, Leslie, Thomas, Duncan C, Stovall, Marilyn, Malone, Kathleen E, Lynch, Charles F, Olsen, Jørgen H, Anton-Culver, Hoda, Shore, Roy E, Boice, Jr, John D, Berkowitz, Gertrud S, Gatti, Richard A, Teitelbaum, Susan L, Smith, Susan A, Rosenstein, Barry S, Børresen-Dale, Anne-Lise, Concannon, Patrick, and Thompson, W Douglas

Published
2004
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182. Folate intake, alcohol consumption, cigarette smoking, and risk of colorectal adenomas

Author

Baron, John A., Sandler, Robert S., Haile, Robert W., Mandel, Jack S., Mott, Leila A., and Greenberg, E. Robert

Subjects
Colorectal cancer -- Risk factors, Folic acid -- Health aspects, Drinking of alcoholic beverages -- Health aspects, Health
Abstract

Background: Recent evidence suggests that folic acid (and derivatives) could contribute to the protective effect of fruits and vegetables against the risk of large-bowel cancer. Other evidence indicates that alcohol drinking and cigarette smoking may impair the biologic actions of folate. We used data from an adenoma prevention trial to investigate the occurrence of colorectal adenomas (possible precursors of colorectal cancer) in association with folate intake, alcohol consumption, and cigarette smoking. Methods: Patients with at least one recent large-bowel adenoma were followed with colonoscopy 1 year and 4 years after their qualifying colon examinations. Adenomas detected after the year 1 examination were used as end points. A food-frequency questionnaire was administered at study entry and at study completion; nutrient intake at study entry was used in this analysis. All statistical tests were two-sided. Results: After adjustment for caloric intake, dietary folate had a significant protective association with the risk of recurrence of large-bowel adenoma (P for trend = .04). However, this inverse association was attenuated by further adjustment for intake of dietary fiber and fat. Use of folate supplements was not associated with a reduction in risk. Alcohol intake (seven or more drinks/week) was associated with increased risk (odds ratio = 2.04; 95% confidence interval = 1.28-3.26). Cigarette smoking, even smoking for long duration, was not related to adenoma recurrence. Conclusions: These data provide only modest support for previous findings suggesting beneficial effects of folate on colorectal adenoma risk. We rind no evidence that cigarette smoking increases risk. These findings do suggest a substantial increase in risk with alcohol consumption. [J Natl Cancer Inst 1998;90:57-62]

Published
1998

183. Association of prostate cancer risk with genetic polymorphisms in vitamin D receptor and androgen receptor

Author

Ingles, Sue Ann, Ross, Ronald K., Yu, Mimi C., Irvine, Ryan A., La Pera, Giuseppe, Haile, Robert W., and Coetzee, Gerhard A.

Subjects
Prostate cancer -- Risk factors, Disease susceptibility -- Models, Vitamin D metabolism -- Physiological aspects, Health
Abstract

Background: Prostate cancer is an increasingly common disease for which there are few well-established risk factors. Family history data suggest a genetic component, however, the majority of prostate cancer cases cannot be explained by a single-gene model. Prostate cell division is influenced by two steroid hormones, testosterone and vitamin D, the action of each being mediated by its respective receptor. The genes for the two receptors are candidates in a multigenic model for prostate cancer susceptibility. Purpose: We examined genetic polymorphisms in two steroid receptors, the androgen receptor (AR) and the vitamin D receptor (VDR), in a case-control pilot study of prostate cancer. Methods: Fifty-seven non-Hispanic white case patients with prostate cancer and 169 non-Hispanic white control subjects were genotyped for a previously described microsatellite (CAG repeats) in the AR gene and for a newly discovered poly-A microsatellite in the 3'-untranslated region (3'UTR) of the VDR gene. To compare genotypes with respect to prostate cancer risk, we estimated odds ratios (ORs) by using logistic regression. ORs were also estimated separately for advanced and localized cases of disease. All P values resulted from two-sided tests. Results: Both the AR and the VDR polymorphisms were associated, individually and after mutual adjustment, with prostate cancer. Adjusted ORs (95% confidence intervals [CIs]) for prostate cancer were 2.10 (95% CI = 1.11-3.99) for individuals carrying an AR CAG allele with fewer than 20 repeats versus an allele with 20 or more repeats and 4.61 (95 CI = 1.34-15.82) for individuals carrying at least one long ([A.sub.18] to [A.sub.22]) VDR poly-A allele versus two short ([A.sub.14] to [A.sub.17]) poly-A alleles. For both the AR and VDR genes, the at-risk genotypes were more strongly associated with advanced disease than with localized disease. Conclusions: In this pilot study, genetic variation in both the VDR and the AR genes was associated with prostate cancer, and both genes appear to preferentially confer risk for advanced disease. These two genetic risk factors, if confirmed, are among the strongest risk factors yet identified for prostate cancer. Implications: These results are consistent with a multigenic model of prostate cancer susceptibility. On the basis of the joint effect of several genetic loci, one might ultimately be able to construct a risk profile to predict advanced disease, so that men whose disease is unlikely to progress to an advanced stage can possibly be spared aggressive treatment. [J Natl Cancer Inst 1997;89:166-70]

Published
1997

184. Continued Increase in Melanoma Incidence across all Socioeconomic Status Groups in California, 1998-2012

Author

Clarke, Christina A, McKinley, Meg, Hurley, Susan, Haile, Robert W, Glaser, Sally L, Keegan, Theresa HM, and Swetter, Susan M

Subjects
Adult, Male, Skin Neoplasms, Incidence, Dermatology & Venereal Diseases, European Continental Ancestry Group, Clinical Sciences, Oncology and Carcinogenesis, Ethnic Groups, Middle Aged, Risk Assessment, Health Services Accessibility, California, Asian Americans, Socioeconomic Factors, Humans, Female, Registries, Hispanic Americans, Melanoma, Needs Assessment, Early Detection of Cancer, SEER Program, Retrospective Studies, Aged
Abstract

Melanoma incidence has been increasing in light-skinned populations worldwide, but the reasons for the increase have been controversial. Our prior assessment in California non-Hispanic whites showed substantial increases in invasive melanoma incidence for tumors of all thicknesses in all neighborhoods categorized by socioeconomic status (SES) between 1988-1992 and 1998-2002. To understand whether these trends continued, we updated our assessment to include the diagnosis period 2008-2012 and more accurate pathologic stage at diagnosis. We used the California Cancer Registry to calculate age-adjusted incidence rates for over 58,000 newly diagnosed melanomas. Incidence rates not only continued to rise over the 10-year period from 1998-2002 and 2008-2012 but also showed significant increases in almost all groups defined jointly by tumor thickness or stage at diagnosis and a small area (census tract) SES measure. The largest relative rate increases were seen for regional, distant, and ulcerated disease, especially among males living in the lowest SES neighborhoods. Considering tumor thickness and stage as proxies for time to screening detection and neighborhood SES as a proxy for health care access, we interpret this pattern to indicate continued, true increases in melanoma occurrence as opposed to a thin tumor phenomenon simply driven by improved access to care.

Published
2017

185. Hormone receptor status of a first primary breast cancer predicts contralateral breast cancer risk in the WECARE study population

Author

Reiner, Anne S, Lynch, Charles F, Sisti, Julia S, John, Esther M, Brooks, Jennifer D, Bernstein, Leslie, Knight, Julia A, Hsu, Li, Concannon, Patrick, Mellemkjær, Lene, Tischkowitz, Marc, Haile, Robert W, Shen, Ronglai, Malone, Kathleen E, Woods, Meghan, Liang, Xiaolin, Morrow, Monica, Bernstein, Jonine L, and Apollo - University of Cambridge Repository

Subjects
skin and connective tissue diseases
Abstract

Background Previous population-based studies have described first primary breast cancer tumor characteristics and their association with contralateral breast cancer (CBC) risk. However, information on influential covariates such as treatment, family history of breast cancer, and BRCA1/2 mutation carrier status was not available. In a large, population-based, case-control study, we evaluated whether tumor characteristics of the first primary breast cancer are associated with risk of developing second primary asynchronous CBC, overall and in subgroups of interest, including among BRCA1/2 mutation non-carriers, women who are not treated with tamoxifen, and women without a breast cancer family history. Methods The Women’s Environmental Cancer and Radiation Epidemiology Study is a population-based case-control study of 1521 CBC cases and 2212 individually-matched controls with unilateral breast cancer. Detailed information about breast cancer risk factors, treatment for and characteristics of first tumors, including estrogen receptor (ER) and progesterone receptor (PR) status, was obtained by telephone interview and medical record abstraction. Multivariable risk ratios (RRs) and 95% confidence intervals (CIs) were estimated in conditional logistic regression models, adjusting for demographics, treatment, and personal medical and family history. A subset of women was screened for BRCA1/2 mutations. Results Lobular histology of the first tumor was associated with a 30% increase in CBC risk (95% CI 1.0–1.6). Compared to women with ER+/PR+ first tumors, those with ER-/PR- tumors had increased risk of CBC (RR = 1.4, 95% CI 1.1–1.7). Notably, women with ER-/PR- first tumors were more likely to develop CBC with the ER-/PR- phenotype (RR = 5.4, 95% CI 3.0–9.5), and risk remained elevated in multiple subgroups: BRCA1/2 mutation non-carriers, women younger than 45 years of age, women without a breast cancer family history, and women who were not treated with tamoxifen. Conclusions Having a hormone receptor negative first primary breast cancer is associated with increased risk of CBC. Women with ER-/PR- primary tumors were more likely to develop ER-/PR- CBC, even after excluding BRCA1/2 mutation carriers. Hormone receptor status, which is routinely evaluated in breast tumors, may be used clinically to determine treatment protocols and identify patients who may benefit from increased surveillance for CBC.

Published
2017

186. Exploratory Genome-Wide Interaction Analysis of Nonsteroidal Anti-inflammatory Drugs and Predicted Gene Expression on Colorectal Cancer Risk.

Author

Xiaoliang Wang, Yu-Ru Su, Petersen, Paneen S., Bien, Stephanie, Schmit, Stephanie L., Drew, David A., Albanes, Demetrius, Berndt, Sonja I., Brenner, Hermann, Campbell, Peter T., Casey, Graham, Chang-Claude, Jenny, Gallinger, Steven J., Gruber, Stephen B., Haile, Robert W., Harrison, Tabitha A., Hoffmeister, Michael, Jacobs, Eric J., Jenkins, Mark A., and Joshi, Amit D.

Abstract

Background: Regular use of nonsteroidal anti-inflammatory drugs (NSAID) is associated with lower risk of colorectal cancer. Genome-wide interaction analysis on single variants (G × E) has identified several SNPs that may interact with NSAIDs to confer colorectal cancer risk, but variations in gene expression levels may also modify the effect of NSAID use. Therefore, we tested interactions between NSAID use and predicted gene expression levels in relation to colorectal cancer risk. Methods: Genetically predicted gene expressions were tested for interaction with NSAID use on colorectal cancer risk among 19,258 colorectal cancer cases and 18,597 controls from 21 observational studies. A Mixed Score Test for Interactions (MiSTi) approach was used to jointly assess G × E effects which are modeled via fixed interaction effects of the weighted burden within each gene set (burden) and residual G × E effects (variance). A false discovery rate (FDR) at 0.2 was applied to correct for multiple testing. Results: Among the 4,840 genes tested, genetically predicted expression levels of four genes modified the effect of any NSAID use on colorectal cancer risk, including DPP10 (PG×E = 1.96 × 10-4), KRT16 (PG×E = 2.3 × 10-4), CD14 (PG×E = 9.38 × 10-4), and CYP27A1 (PG×E = 1.44 × 10-3). There was a significant interaction between expression level of RP11-89N17 and regular use of aspirin only on colorectal cancer risk (PG×E = 3.23 × 10-5). No interactions were observed between predicted gene expression and nonaspirin NSAID use at FDR < 0.2. Conclusions: By incorporating functional information, we discovered several novel genes that interacted with NSAID use. [ABSTRACT FROM AUTHOR]

Published
2020
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187. Potential impact of family history-based screening guidelines on the detection of early-onset colorectal cancer.

Author

Gupta, Samir, Bharti, Balambal, Ahnen, Dennis J., Buchanan, Daniel D., Cheng, Iona C., Cotterchio, Michelle, Figueiredo, Jane C., Gallinger, Steven J., Haile, Robert W., Jenkins, Mark A., Lindor, Noralane M., Macrae, Finlay A., Le Marchand, Loïc, Newcomb, Polly A., Thibodeau, Stephen N., Win, Aung Ko, and Martinez, Maria Elena

Subjects
COLORECTAL cancer, TASK forces, FAMILY history (Medicine), GUIDELINES, FAMILIES, AGE distribution, FAMILY health, EARLY detection of cancer, CASE-control method, RETROSPECTIVE studies, MEDICAL protocols, AGE factors in disease
Abstract

Background: Initiating screening at an earlier age based on cancer family history is one of the primary recommended strategies for the prevention and detection of early-onset colorectal cancer (EOCRC), but data supporting the effectiveness of this approach are limited. The authors assessed the performance of family history-based guidelines for identifying individuals with EOCRC.Methods: The authors conducted a population-based, case-control study of individuals aged 40 to 49 years with (2473 individuals) and without (772 individuals) incident CRC in the Colon Cancer Family Registry from 1998 through 2007. They estimated the sensitivity and specificity of family history-based criteria jointly recommended by the American Cancer Society, the US Multi-Society Task Force on CRC, and the American College of Radiology in 2008 for early screening, and the age at which each participant could have been recommended screening initiation if these criteria had been applied.Results: Family history-based early screening criteria were met by approximately 25% of cases (614 of 2473 cases) and 10% of controls (74 of 772 controls), with a sensitivity of 25% and a specificity of 90% for identifying EOCRC cases aged 40 to 49 years. Among 614 individuals meeting early screening criteria, 98.4% could have been recommended screening initiation at an age younger than the observed age of diagnosis.Conclusions: Of CRC cases aged 40 to 49 years, 1 in 4 met family history-based early screening criteria, and nearly all cases who met these criteria could have had CRC diagnosed earlier (or possibly even prevented) if earlier screening had been implemented as per family history-based guidelines. Additional strategies are needed to improve the detection and prevention of EOCRC for individuals not meeting family history criteria for early screening. [ABSTRACT FROM AUTHOR]

Published
2020
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189. DNA repair and cancer in colon and rectum: Novel players in genetic susceptibility.

Author

Pardini, Barbara, Corrado, Alda, Paolicchi, Elisa, Cugliari, Giovanni, Berndt, Sonja I., Bezieau, Stephane, Bien, Stephanie A., Brenner, Hermann, Caan, Bette J., Campbell, Peter T., Casey, Graham, Chan, Andrew T., Chang‐Claude, Jenny, Cotterchio, Michelle, Gala, Manish, Gallinger, Steven J., Haile, Robert W., Harrison, Tabitha A., Hayes, Richard B., and Hoffmeister, Michael

Subjects
DNA repair, DNA mismatch repair, COLON cancer, RECTAL cancer, SINGLE nucleotide polymorphisms, EPIDEMIOLOGY of cancer
Abstract

Interindividual differences in DNA repair systems may play a role in modulating the individual risk of developing colorectal cancer. To better ascertain the role of DNA repair gene polymorphisms on colon and rectal cancer risk individually, we evaluated 15,419 single nucleotide polymorphisms (SNPs) within 185 DNA repair genes using GWAS data from the Colon Cancer Family Registry (CCFR) and the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO), which included 8,178 colon cancer, 2,936 rectum cancer cases and 14,659 controls. Rs1800734 (in MLH1 gene) was associated with colon cancer risk (p‐value = 3.5 × 10−6) and rs2189517 (in RAD51B) with rectal cancer risk (p‐value = 5.7 × 10−6). The results had statistical significance close to the Bonferroni corrected p‐value of 5.8 × 10−6. Ninety‐four SNPs were significantly associated with colorectal cancer risk after Binomial Sequential Goodness of Fit (BSGoF) procedure and confirmed the relevance of DNA mismatch repair (MMR) and homologous recombination pathways for colon and rectum cancer, respectively. Defects in MMR genes are known to be crucial for familial form of colorectal cancer but our findings suggest that specific genetic variations in MLH1 are important also in the individual predisposition to sporadic colon cancer. Other SNPs associated with the risk of colon cancer (e.g., rs16906252 in MGMT) were found to affect mRNA expression levels in colon transverse and therefore working as possible cis‐eQTL suggesting possible mechanisms of carcinogenesis. What's new? DNA repair defects allow mutations to pile up, which can lead to cancer. These authors searched for single nucleotide polymorphisms (SNPs) in DNA repair pathways associated with sporadic colorectal cancer. So far, genome‐wide association studies (GWAS) have not detected many such SNPs, likely due to the small effect of each variant individually. Here, the authors combined data from two large colorectal cancer consortia, evaluating 15,419 SNPs in 185 DNA repair genes. They uncovered 2 SNPs in genes in the mismatch repair and homologous recombination pathways associated with increased colon cancer risk. Further investigation of these variants could lead to better personalized treatments. [ABSTRACT FROM AUTHOR]

Published
2020
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190. Physical activity and the risk of colorectal cancer in Lynch syndrome

Author

Dashti, S. Ghazaleh, primary, Win, Aung Ko, additional, Hardikar, Sheetal S., additional, Glombicki, Stephen E., additional, Mallenahalli, Sheila, additional, Thirumurthi, Selvi, additional, Peterson, Susan K., additional, You, Y. Nancy, additional, Buchanan, Daniel D., additional, Figueiredo, Jane C., additional, Campbell, Peter T., additional, Gallinger, Steven, additional, Newcomb, Polly A., additional, Potter, John D., additional, Lindor, Noralane M., additional, Le Marchand, Loic, additional, Haile, Robert W., additional, Hopper, John L., additional, Jenkins, Mark A., additional, Basen-Engquist, Karen M., additional, Lynch, Patrick M., additional, and Pande, Mala, additional

Published
2018
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191. Abstract 2965: Functionally informed genome-wide interaction analysis of nonsteroidal anti-inflammatory drugs on colorectal cancer risk

Author

Wang, Xiaoliang, primary, Su, Yu-Ru, additional, Chan, Andrew T., additional, Bien, Stephanie, additional, Bernt, Sonja I., additional, Brenner, Hermann, additional, Casey, Graham, additional, Chang-Claude, Jenny, additional, Gallinger, Steven J., additional, Haile, Robert W., additional, Harrison, Tabitha A., additional, Hoffmeister, Michael, additional, Jenkins, Mark A., additional, Joshi, Amit, additional, Lin, Yi, additional, Lindor, Noralane M., additional, Marchand, Loic Le, additional, Nan, Hongmei, additional, Newcomb, Polly A., additional, Potter, John D., additional, Slattery, Martha L., additional, Thibodeau, Steve N., additional, White, Emily, additional, Hsu, Li, additional, and Peters, Ulrike, additional

Published
2018
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192. Ability of known susceptibility SNPs to predict colorectal cancer risk for persons with and without a family history

Author

Jenkins, Mark A., primary, Win, Aung K., additional, Dowty, James G., additional, MacInnis, Robert J., additional, Makalic, Enes, additional, Schmidt, Daniel F., additional, Dite, Gillian S., additional, Kapuscinski, Miroslaw, additional, Clendenning, Mark, additional, Rosty, Christophe, additional, Winship, Ingrid M., additional, Emery, Jon D., additional, Saya, Sibel, additional, Macrae, Finlay A., additional, Ahnen, Dennis J., additional, Duggan, David, additional, Figueiredo, Jane C., additional, Lindor, Noralane M., additional, Haile, Robert W., additional, Potter, John D., additional, Cotterchio, Michelle, additional, Gallinger, Steven, additional, Newcomb, Polly A., additional, Buchanan, Daniel D., additional, Casey, Graham, additional, and Hopper, John L., additional

Published
2018
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194. Risk-reducing hysterectomy and bilateral salpingo-oophorectomy in female heterozygotes of pathogenic mismatch repair variants: a Prospective Lynch Syndrome Database report

Author

Dominguez-Valentin, Mev, Crosbie, Emma J., Engel, Christoph, Aretz, Stefan, Macrae, Finlay, Winship, Ingrid, Capella, Gabriel, Thomas, Huw, Nakken, Sigve, Hovig, Eivind, Nielsen, Maartje, Sijmons, Rolf H., Bertario, Lucio, Bonanni, Bernardo, Tibiletti, Maria Grazia, Cavestro, Giulia Martina, Mints, Miriam, Gluck, Nathan, Katz, Lior, Heinimann, Karl, Vaccaro, Carlos A., Green, Kate, Lalloo, Fiona, Hill, James, Schmiegel, Wolff, Vangala, Deepak, Perne, Claudia, Strauß, Hans-Georg, Tecklenburg, Johanna, Holinski-Feder, Elke, Steinke-Lange, Verena, Mecklin, Jukka-Pekka, Plazzer, John-Paul, Pineda, Marta, Navarro, Matilde, Vidal, Joan Brunet, Kariv, Revital, Rosner, Guy, Piñero, Tamara Alejandra, Gonzalez, María Laura, Kalfayan, Pablo, Ryan, Neil, ten Broeke, Sanne W., Jenkins, Mark A., Sunde, Lone, Bernstein, Inge, Burn, John, Greenblatt, Marc, de Vos tot Nederveen Cappel, Wouter H., Della Valle, Adriana, Lopez-Koestner, Francisco, Alvarez, Karin, Büttner, Reinhard, Görgens, Heike, Morak, Monika, Holzapfel, Stefanie, Hüneburg, Robert, von Knebel Doeberitz, Magnus, Loeffler, Markus, Rahner, Nils, Weitz, Jürgen, Pylvänäinen, Kirsi, Renkonen-Sinisalo, Laura, Lepistö, Anna, Auranen, Annika, Hopper, John L., Win, Aung Ko, Haile, Robert W., Lindor, Noralane M., Gallinger, Steven, Le Marchand, Loïc, Newcomb, Polly A., Figueiredo, Jane C., Thibodeau, Stephen N., Therkildsen, Christina, Okkels, Henrik, Ketabi, Zohreh, Denton, Oliver G., Rødland, Einar Andreas, Vasen, Hans, Neffa, Florencia, Esperon, Patricia, Tjandra, Douglas, Möslein, Gabriela, Sampson, Julian R., Evans, D. Gareth, Seppälä, Toni T., and Møller, Pål

Abstract

To determine impact of risk-reducing hysterectomy and bilateral salpingo-oophorectomy (BSO) on gynecological cancer incidence and death in heterozygotes of pathogenic MMR (path_MMR) variants.

Published
2021
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196. Meat intake, cooking-related mutagens and risk of colorectal adenoma in a sigmoidoscopy-based case-control study

Author

Gunter, Marc J., Probst-Hensch, Nicole M., Cortessis, Victoria K., Kulldorff, Martin, Haile, Robert W., Sinha, Rashmi, Gunter, Marc J., Probst-Hensch, Nicole M., Cortessis, Victoria K., Kulldorff, Martin, Haile, Robert W., and Sinha, Rashmi

Abstract

Reported habits of red meat consumption, particularly red meat that has been cooked to the degree termed ‘well-done', is a positive risk factor for colorectal cancer. Under high, pyrolytic temperatures, heterocyclic amines (HCA) and benzo[a]pyrene (BP) molecules can form inside and on the surface of red meat, respectively. These compounds are precursors that are metabolically converted to compounds known to act as mutagens and carcinogens in animal models, yet their role in human colorectal carcinogenesis remains to be clarified. We investigated whether intake of these compounds is associated with risk of colorectal adenoma in the context of a polyp-screening study conducted in Southern California. Using a database of individual HCAs and BP in meats of various types and subjected to specified methods and degrees of cooking, we estimated nanogram consumption of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine, 2-amino-3,4,8-trimethylimidazo[4,5-f] quinoxaline, 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline and benzo[a]pyrene (BP). We observed a 6% increased risk of large (>1 cm) adenoma per 10 ng/day consumption of BP [OR = 1.06 (95% CI, 1.00-1.12), P (trend) = 0.04]. A major source of BP is red meat exposed to a naked flame, as occurs during the barbecuing process. Consistent with this finding an incremental increase of 10 g of barbecued red meat per day was associated with a 29% increased risk of large adenoma [OR = 1.29 (95% CI, 1.02-1.63), P (trend) = 0.04]. Individuals in the top quintile of barbecued red meat intake were at increased risk of large adenoma [OR = 1.90 (95% CI, 1.04-3.45)], compared with never consuming barbecued red meat. The consumption of oven-broiled red meat was inversely related to adenoma risk compared with non-consumers [OR = 0.49 (95% CI, 0.28-0.85)]. We did not identify any association with consumption of individual HCAs and colorectal adenoma risk. These results support the hypothesis that BP contributes to colorectal carcinogenesis

Published
2017

197. Cross-cancer genome-wide analysis of lung, ovary, breast, prostate and colorectal cancer reveals novel pleiotropic associations

Author

Fehringer, Gordon, Kraft, Peter, Pharoah, Paul D, Eeles, Rosalind A, Chatterjee, Nilanjan, Schumacher, Fredrick R, Schildkraut, Joellen M, Lindstrom, Sara, Brennan, Paul, Bickeboller, Heike, Houlston, Richard S, Landi, Maria Teresa, Caporaso, Neil, Risch, Angela, Al Olama, Ali Amin, Berndt, Sonja I, Giovannucci, Edward L, Gronberg, Henrik, Kote-Jarai, Zsofia, Ma, Jing, Muir, Kenneth, Stampfer, Meir J, Stevens, Victoria L, Wiklund, Fredrik, Willett, Walter C, Goode, Ellen L, Permuth, Jennifer B, Risch, Harvey A, Reid, Brett M, Bezieau, Stephane, Brenner, Hermann, Chan, Andrew T, Chang-Claude, Jenny, Hudson, Thomas J, Kocarnik, Jonathan K, Newcomb, Polly A, Schoen, Robert E, Slattery, Martha L, White, Emily, Adank, Muriel A, Ahsan, Habibul, Aittomaki, Kristiina, Baglietto, Laura, Blomquist, Carl, Canzian, Federico, Czene, Kamila, dos-Santos-Silva, Isabel, Eliassen, A Heather, Figueroa, Jonine D, Flesch-Janys, Dieter, Fletcher, Olivia, Garcia-Closas, Montserrat, Gaudet, Mia M, Johnson, Nichola, Hall, Per, Hazra, Aditi, Hein, Rebecca, Hofman, Albert, Hopper, John L, Irwanto, Astrid, Johansson, Mattias, Kaaks, Rudolf, Kibriya, Muhammad G, Lichtner, Peter, Liu, Jianjun, Lund, Eiliv, Makalic, Enes, Meindl, Alfons, Muller-Myhsok, Bertram, Muranen, Taru A, Nevanlinna, Heli, Peeters, Petra H, Peto, Julian, Prentice, Ross L, Rahman, Nazneen, Sanchez, Maria Jose, Schmidt, Daniel F, Schmutzler, Rita K, Southey, Melissa C, Tamimi, Rulla, Travis, Ruth C, Turnbull, Clare, Uitterlinden, Andre G, Wang, Zhaoming, Whittemore, Alice S, Yang, Xiaohong R, Zheng, Wei, Buchanan, Daniel D, Casey, Graham, Conti, David V, Edlund, Christopher K, Gallinger, Steven, Haile, Robert W, Jenkins, Mark, Le Marchand, Loic, Li, Li, Lindor, Noralene M, Schmit, Stephanie L, Thibodeau, Stephen N, Woods, Michael O, Rafnar, Thorunn, Gudmundsson, Julius, Stacey, Simon N, Stefansson, Kari, Sulem, Patrick, Chen, Y Ann, Tyrer, Jonathan P, Christiani, David C, Wei, Yongyue, Shen, Hongbing, Hu, Zhibin, Shu, Xiao-Ou, Shiraishi, Kouya, Takahashi, Atsushi, Bosse, Yohan, Obeidat, Ma'en, Nickle, David, Timens, Wim, Freedman, Matthew L, Li, Qiyuan, Seminara, Daniela, Chanock, Stephen J, Gong, Jian, Peters, Ulrike, Gruber, Stephen B, Amos, Christopher I, Sellers, Thomas A, Easton, Douglas F, Hunter, David J, Haiman, Christopher A, Henderson, Brian E, Hung, Rayjean J, OCAC, Consortium, PRACTICAL, Res, Hereditary Breast Ovarian Canc, Transdisciplinary, Colorectal, Canc, African Amer Breast, Canc, African Ancestry Prostate, Medical Oncology, Epidemiology, Internal Medicine, Surgery, Guided Treatment in Optimal Selected Cancer Patients (GUTS), and Groningen Research Institute for Asthma and COPD (GRIAC)

Subjects
0301 basic medicine, Oncology, Male, medicine.medical_specialty, Cancer Research, Lung Neoplasms, SUSCEPTIBILITY LOCI, Genotype, IDENTIFIES 2, Colorectal cancer, Locus (genetics), Genome-wide association study, Breast Neoplasms, Article, 03 medical and health sciences, Prostate cancer, AFRICAN ANCESTRY, Breast cancer, SDG 3 - Good Health and Well-being, Internal medicine, medicine, Journal Article, AGGRESSIVE PROSTATE, Humans, GENETIC POLYMORPHISMS, Lung cancer, METAANALYSIS, Ovarian Neoplasms, business.industry, COMMON VARIANTS, Prostatic Neoplasms, CELL CARCINOMA, medicine.disease, RISK LOCI, 3. Good health, 030104 developmental biology, Expression quantitative trait loci, Adenocarcinoma, Female, business, Colorectal Neoplasms, GASTRIC-CANCER, Genome-Wide Association Study
Abstract

Identifying genetic variants with pleiotropic associations can uncover common pathways influencing multiple cancers. We took a two-stage approach to conduct genome-wide association studies for lung, ovary, breast, prostate, and colorectal cancer from the GAME-ON/GECCO Network (61,851 cases, 61,820 controls) to identify pleiotropic loci. Findings were replicated in independent association studies (55,789 cases, 330,490 controls). We identified a novel pleiotropic association at 1q22 involving breast and lung squamous cell carcinoma, with eQTL analysis showing an association with ADAM15/THBS3 gene expression in lung. We also identified a known breast cancer locus CASP8/ALS2CR12 associated with prostate cancer, a known cancer locus at CDKN2B-AS1 with different variants associated with lung adenocarcinoma and prostate cancer, and confirmed the associations of a breast BRCA2 locus with lung and serous ovarian cancer. This is the largest study to date examining pleiotropy across multiple cancer-associated loci, identifying common mechanisms of cancer development and progression. Cancer Res; 76(17); 5103–14. ©2016 AACR.

Published
2016

198. Clinicopathologic Risk Factor Distributions for MLH1 Promoter Region Methylation in CIMP-Positive Tumors

Author

Buchanan, Daniel D., Levine, A. Joan, Weisenberger, Daniel J., Haile, Robert W., Laird, Peter W., Rosty, Christophe, Ahnen, Dennis J., Newcomb, Polly A., Lindor, Noralane M., Cohen, Stacey A., Phipps, Amanda I., and Baron, John A.

Subjects
congenital, hereditary, and neonatal diseases and abnormalities, nutritional and metabolic diseases, neoplasms, digestive system diseases
Abstract

The CpG Island Methylator Phenotype (CIMP) is a major molecular pathway in colorectal cancer (CRC). Approximately 25% to 60% of CIMP tumors are microsatellite unstable (MSI-H) due to DNA hypermethylation of the MLH1 gene promoter. Our aim was to determine if the distributions of clinicopathologic factors in CIMP-positive tumors with MLH1 DNA methylation differed from those in CIMP-positive tumors without DNA methylation of MLH1.

Published
2016
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199. Risk of extracolonic cancers for people with biallelic and monoallelic mutations in MUTYH: Extracolonic cancer risks for people with biallelic and monoallelicMUTYHmutations

Author

Casey, Graham, Newcomb, Polly A., Kim, Hyeja, Cotterchio, Michelle, Macrae, Finlay A., Hopper, John L., Le Marchand, Loïc, Reece, Jeanette C., Clendenning, Mark, Cleary, Sean P., Rosty, Christophe, Jenkins, Mark A., Dowty, James G., Buchanan, Daniel D., Young, Joanne P., Winship, Ingrid M., Haile, Robert W., Win, Aung Ko, Baron, John A., Southey, Melissa C., Gallinger, Steven, Thibodeau, Stephen N., Tucker, Katherine M., Lindor, Noralane M., and Burnett, Terrilea

Abstract

Germline mutations in the DNA base excision repair gene MUTYH are known to increase a carrier’s risk of colorectal cancer. However, the risks of other (extracolonic) cancers for MUTYH mutation carriers are not well defined. We identified 266 probands (91% Caucasians) with a MUTYH mutation (41 biallelic and 225 monoallelic) from the Colon Cancer Family Registry. Mutation status, sex, age, and histories of cancer from their 1,903 first- and 3,255 second-degree relatives, were analysed using modified segregation analysis conditioned on the ascertainment criteria. Compared with incidences for the general population, hazard ratios (HRs) (95% confidence intervals [CIs]) for biallelic MUTYH mutation carriers were: urinary bladder cancer, 19(3.7–97); and ovarian cancer, 17(2.4–115). The HRs (95%CI) for monoallelic MUTYH mutation carriers were: gastric cancer, 9.3(6.7–13); hepatobiliary cancer, 4.5(2.7–7.5); endometrial cancer, 2.1(1.1–3.9); and breast cancer, 1.4(1.0–2.0). There was no evidence for an increased risk of cancers at the other sites examined (brain, pancreas, kidney or prostate). Based on the USA population incidences, the estimated cumulative risks (95%CI) to age 70 years for biallelic mutation carriers were: bladder cancer, 25%(5%–77%) for males and 8%(2%–33%) for females; and ovarian cancer, 14%(2%–65%). The cumulative risks (95%CI) for monoallelic mutation carriers were: gastric cancer, 5%(4%–7%) for males and 2.3%(1.7%–3.3%) for females; hepatobiliary cancer, 3%(2%–5%) for males and 1.4%(0.8%–2.3%) for females; endometrial cancer, 3%(2%–6%); and breast cancer 11%(8%–16%). These unbiased estimates of both relative and absolute risks of extracolonic cancers for people, mostly Caucasians, with MUTYH mutations will be important for their clinical management.

Published
2016
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200. Meta-analysis of genome-wide association studies identifies common susceptibility polymorphisms for colorectal and endometrial cancer near SH2B3 and TSHZ1

Author

Cheng, Timothy HT, Thompson, Deborah, Painter, Jodie, O’Mara, Tracy, Gorman, Maggie, Martin, Lynn, Palles, Claire, Jones, Angela, Buchanan, Daniel D., Ko Win, Aung, Hopper, John, Jenkins, Mark, Lindor, Noralane M., Newcomb, Polly A., Gallinger, Steve, Conti, David, Schumacher, Fred, Casey, Graham, Giles, Graham G, Pharoah, Paul, Peto, Julian, Cox, Angela, Swerdlow, Anthony, Couch, Fergus, Cunningham, Julie M, Goode, Ellen L, Winham, Stacey J, Lambrechts, Diether, Fasching, Peter, Burwinkel, Barbara, Brenner, Hermann, Brauch, Hiltrud, Chang-Claude, Jenny, Salvesen, Helga B., Kristensen, Vessela, Darabi, Hatef, Li, Jingmei, Liu, Tao, Lindblom, Annika, Hall, Per, de Polanco, Magdalena Echeverry, Sans, Monica, Carracedo, Angel, Castellvi-Bel, Sergi, Rojas-Martinez, Augusto, Aguiar Jnr, Samuel, Teixeira, Manuel R., Dunning, Alison M, Dennis, Joe, Otton, Geoffrey, Proietto, Tony, Holliday, Elizabeth, Attia, John, Ashton, Katie, Scott, Rodney J, McEvoy, Mark, Dowdy, Sean C, Fridley, Brooke L, Werner, Henrica MJ, Trovik, Jone, Njolstad, Tormund S, Tham, Emma, Mints, Miriam, Runnebaum, Ingo, Hillemanns, Peter, Dörk, Thilo, Amant, Frederic, Schrauwen, Stefanie, Hein, Alexander, Beckmann, Matthias W, Ekici, Arif, Czene, Kamila, Meindl, Alfons, Bolla, Manjeet K, Michailidou, Kyriaki, Tyrer, Jonathan P, Wang, Qin, Ahmed, Shahana, Healey, Catherine S, Shah, Mitul, Annibali, Daniela, Depreeuw, Jeroen, Al-Tassan, Nada A., Harris, Rebecca, Meyer, Brian F., Whiffin, Nicola, Hosking, Fay J, Kinnersley, Ben, Farrington, Susan M., Timofeeva, Maria, Tenesa, Albert, Campbell, Harry, Haile, Robert W., Hodgson, Shirley, Carvajal-Carmona, Luis, Cheadle, Jeremy P., Easton, Douglas, Dunlop, Malcolm, Houlston, Richard, Spurdle, Amanda, and Tomlinson, Ian

Subjects
ddc
Published
2015

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