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558 results on '"Joshu, Corinne E."'

152. Adiposity, metabolites, and colorectal cancer risk: Mendelian randomization study

Author

Bull, Caroline J., primary, Bell, Joshua A., additional, Murphy, Neil, additional, Sanderson, Eleanor, additional, Smith, George Davey, additional, Timpson, Nicholas J., additional, Banbury, Barbara L., additional, Albanes, Demetrius, additional, Berndt, Sonja I., additional, Bézieau, Stéphane, additional, Bishop, D Timothy T., additional, Brenner, Hermann, additional, Buchanan, Daniel D., additional, Burnett-Hartman, Andrea, additional, Casey, Graham, additional, Castellví-Bel, Sergi, additional, Chan, Andrew T., additional, Chang-Claude, Jenny, additional, Cross, Amanda J., additional, de la Chapelle, Albert, additional, Figueiredo, Jane C., additional, Gallinger, Steven J., additional, Gapstur, Sue M., additional, Giles, Graham G., additional, Gruber, Stephen B., additional, Gsur, Andrea, additional, Hampe, Jochen, additional, Hampel, Heather, additional, Harrison, Tabitha A., additional, Hoffmeister, Michael, additional, Hsu, Li, additional, Huang, Wen-Yi, additional, Huyghe, Jeroen R., additional, Jenkins, Mark A., additional, Joshu, Corinne E., additional, Keku, Temitope O., additional, Kühn, Tilman, additional, Kweon, Sun-Seog, additional, Le Marchand, Loic, additional, Li, Christopher I., additional, Li, Li, additional, Lindblom, Annika, additional, Martín, Vicente, additional, May, Anne M., additional, Milne, Roger L., additional, Moreno, Victor, additional, Newcomb, Polly A., additional, Offit, Kenneth, additional, Ogino, Shuji, additional, Phipps, Amanda I., additional, Platz, Elizabeth A., additional, Potter, John D., additional, Qu, Conghui, additional, Quirós, J. Ramón, additional, Rennert, Gad, additional, Riboli, Elio, additional, Sakoda, Lori C., additional, Schafmayer, Clemens, additional, Schoen, Robert E., additional, Slattery, Martha L., additional, Tangen, Catherine M., additional, Tsilidis, Kostas K., additional, Ulrich, Cornelia M., additional, van Duijnhoven, Franzel JB., additional, Van Guelpen, Bethany, additional, Visvanathan, Kala, additional, Vodicka, Pavel, additional, Vodickova, Ludmila, additional, Wang, Hansong, additional, White, Emily, additional, Wolk, Alicja, additional, Woods, Michael O., additional, Wu, Anna H., additional, Campbell, Peter T., additional, Zheng, Wei, additional, Peters, Ulrike, additional, Vincent, Emma E., additional, and Gunter, Marc J., additional

Published
2020
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153. Racial Difference in Prostate Cancer Cell Telomere Lengths in Men with Higher Grade Prostate Cancer: A Clue to the Racial Disparity in Prostate Cancer Outcomes

Author

Heaphy, Christopher M., primary, Joshu, Corinne E., additional, Barber, John R., additional, Davis, Christine, additional, Zarinshenas, Reza, additional, De Marzo, Angelo M., additional, Lotan, Tamara L., additional, Sfanos, Karen S., additional, Meeker, Alan K., additional, and Platz, Elizabeth A., additional

Published
2020
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157. Trends in breast cancer incidence rates by race/ethnicity: Patterns by stage, socioeconomic position, and geography in the United States, 1999‐2017.

Author

Kaur, Maneet, Joshu, Corinne E., Visvanathan, Kala, and Connor, Avonne E.

Subjects
*BREAST cancer, *ETHNICITY, *POVERTY areas, *GEOGRAPHY, *CANCER-related mortality
Abstract

Background: The incidence rate of breast cancer has been increasing over time across race/ethnicity in the United States. It is unclear whether these trends differ among stage, poverty, and geography subgroups. Methods: Using data from the North American Association of Central Cancer Registries, this study estimated trends in age‐adjusted breast cancer incidence rates among women aged 50 to 84 years from 1999 to 2017 by race/ethnicity (non‐Hispanic Black, non‐Hispanic White, and Hispanic) and across subgroups (stage, county‐level poverty, county urban/rural status, and geographic region [West, Midwest, South, and Northeast]). Results: From 2004 to 2017, breast cancer incidence rates increased across race/ethnicity and subgroups, with the greatest average annual percent increases observed for non‐Hispanic Black women, overall (0.9%) and those living in lower poverty areas (0.8%), rural areas (1.2%), and all regions except the West (0.8%‐1.0%). Stronger increases among non‐Hispanic Black women were observed for local‐stage disease and for some subgroups of distant‐stage disease. Non‐Hispanic Black women had the smallest decrease in regional‐stage disease across most subgroups. Similarly, Hispanic women had the strongest increases in some subgroups, including areas with higher poverty (0.6%‐1.2%) and in the West (0.8%), for local‐ and distant‐stage disease. Conclusions: These trends highlight concerns for an increasing burden of breast cancer among subpopulations, with some already experiencing disparate breast cancer mortality rates, and they highlight the need for targeted breast cancer prevention and efforts to reduce mortality disparities in areas with increasing incidence. From 1999 to 2017, the incidence rate of breast cancer by race/ethnicity among women aged 50 to 84 years increased in certain socioeconomic‐position and geography subgroups, with greater increases overall and for local‐stage cancer and smaller declines for regional‐stage cancer among non‐Hispanic Black and Hispanic women. [ABSTRACT FROM AUTHOR]

Published
2022
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158. P2X4 purinergic receptors offer a therapeutic target for aggressive prostate cancer.

Author

Maynard, Janielle P, Lu, Jiayun, Vidal, Igor, Hicks, Jessica, Mummert, Luke, Ali, Tamirat, Kempski, Ryan, Carter, Ayanna M., Sosa, Rebecca Y, Peiffer, Lauren B, Joshu, Corinne E, Lotan, Tamara L, De Marzo, Angelo M., and Sfanos, Karen S

Subjects
PURINERGIC receptors, PROSTATE cancer, RADICAL prostatectomy, CELL migration, EPITHELIAL cells, PROTEIN expression
Abstract

Prostate cancer (PCa) remains a leading cause of cancer‐related deaths in American men and treatment options for metastatic PCa are limited. There is a critical need to identify new mechanisms that contribute to PCa progression, that distinguish benign from lethal disease, and that have potential for therapeutic targeting. P2X4 belongs to the P2 purinergic receptor family that is commonly upregulated in cancer and is associated with poorer outcomes. We observed P2X4 protein expression primarily in epithelial cells of the prostate, a subset of CD66+ neutrophils, and most CD68+ macrophages. Our analysis of tissue microarrays representing 491 PCa cases demonstrated significantly elevated P2X4 expression in cancer‐ compared with benign‐tissue spots, in prostatic intraepithelial neoplasia, and in PCa with ERG positivity or with PTEN loss. High‐level P2X4 expression in benign tissues was likewise associated with the development of metastasis after radical prostatectomy. Treatment with the P2X4‐specific agonist cytidine 5′‐triphosphate (CTP) increased Transwell migration and invasion of PC3, DU145, and CWR22Rv1 PCa cells. The P2X4 antagonist 5‐(3‐bromophenyl)‐1,3‐dihydro‐2H‐benzofuro[3,2‐e]‐1,4‐diazepin‐2‐one (5‐BDBD) resulted in a dose‐dependent decrease in viability of PC3, DU145, LNCaP, CWR22Rv1, TRAMP‐C2, Myc‐CaP, BMPC1, and BMPC2 cells and decreased DU145 cell migration and invasion. Knockdown of P2X4 attenuated growth, migration, and invasion of PCa cells. Finally, knockdown of P2X4 in Myc‐CaP cells resulted in significantly attenuated subcutaneous allograft growth in FVB/NJ mice. Collectively, these data strongly support a role for the P2X4 purinergic receptor in PCa aggressiveness and identify P2X4 as a candidate for therapeutic targeting. © 2021 The Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Published
2022
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159. Life expectancy estimates based on comorbidities and frailty to inform preventive care.

Author

Schoenborn, Nancy L., Blackford, Amanda L., Joshu, Corinne E., Boyd, Cynthia M., and Varadhan, Ravi

Subjects
FEE for service (Medical fees), SURVIVAL, FRAIL elderly, CONFIDENCE intervals, LIFE expectancy, AGE distribution, RETROSPECTIVE studies, PREVENTIVE health services, SEX distribution, DESCRIPTIVE statistics, ODDS ratio, COMORBIDITY, LONGITUDINAL method, MEDICARE, PROPORTIONAL hazards models
Abstract

Background: Long‐term prognostication is important to inform preventive care in older adults. Existing prediction indices incorporate age and comorbidities. Frailty is another important factor in prognostication. In this project, we aimed at developing life expectancy estimates that incorporate both comorbidities and frailty. Methods: In this retrospective cohort study, we used data from a 5% sample of Medicare beneficiaries with and without history of cancer from Surveillance, Epidemiology, and End Results (SEER) cancer registry areas. We included adults aged 66–95 years who were continuously enrolled in fee‐for‐service Medicare for ≥1 year from 1998 to 2014. Participants were followed for survival until 12/31/2015, death, or disenrollment. Comorbidity (none, low/medium, high) and frailty categories (low, high) were defined using established methods for claims. We estimated 5‐ and 10‐year survival probabilities and median life expectancies by age, sex, comorbidities, and frailty. Results: The study included 479,646 individuals (4,128,316 person‐years), of whom most were women (58.7%). Frailty scores varied widely among participants in the same comorbidity category. In Cox models, both comorbidities and frailty were independent predictors of mortality. Individuals with high comorbidities (HR, 3.24; 95% CI, 3.20–3.28) and low/medium comorbidities (HR, 1.36; 95% CI, 1.34–1.39) had higher risks of death than those with no comorbidities. Compared to low frailty, high frailty was associated with higher risk of death (HR, 1.55; 95% CI, 1.52–1.58). Frailty affected life expectancy estimates in ways relevant to preventive care (i.e., distinguishing <10‐year versus >10‐year life expectancy) in multiple subgroups. Conclusion: Incorporating both comorbidities and frailty may be important in estimating long‐term life expectancies of older adults. Our life expectancy tables can aid clinicians' prognostication and inform simulation models and population health management. [ABSTRACT FROM AUTHOR]

Published
2022
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161. 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

162. A Collaborative Analysis of Individual Participant Data from 19 Prospective Studies Assesses Circulating Vitamin D and Prostate Cancer Risk

Author

Epi Kanker Team 1, Cancer, JC onderzoeksprogramma Kanker, MS MDL 1, Travis, Ruth C, Perez-Cornago, Aurora, Appleby, Paul N, Albanes, Demetrius, Joshu, Corinne E, Lutsey, Pamela L, Mondul, Alison M, Platz, Elizabeth A, Weinstein, Stephanie J, Layne, Tracy M, Helzlsouer, Kathy J, Visvanathan, Kala, Palli, Domenico, Peeters, Petra H, Bueno-de-Mesquita, Bas, Trichopoulou, Antonia, Gunter, Marc J, Tsilidis, Konstantinos K, Sánchez, Maria-Jose, Olsen, Anja, Brenner, Hermann, Schöttker, Ben, Perna, Laura, Holleczek, Bernd, Knekt, Paul, Rissanen, Harri, Yeap, Bu B, Flicker, Leon, Almeida, Osvaldo P, Wong, Yuen Yee Elizabeth, Chan, June M, Giovannucci, Edward L, Stampfer, Meir J, Ursin, Giske, Gislefoss, Randi E, Bjørge, Tone, Meyer, Haakon E, Blomhoff, Rune, Tsugane, Shoichiro, Sawada, Norie, English, Dallas R, Eyles, Darryl W, Heath, Alicia K, Williamson, Elizabeth J, Manjer, Jonas, Malm, Johan, Almquist, Martin, Marchand, Loic Le, Haiman, Christopher A, Wilkens, Lynne R, Schenk, Jeannette M, Tangen, Cathy M, Black, Amanda, Cook, Michael B, Huang, Wen-Yi, Ziegler, Regina G, Martin, Richard M, Hamdy, Freddie C, Donovan, Jenny L, Neal, David E, Touvier, Mathilde, Hercberg, Serge, Galan, Pilar, Deschasaux, Mélanie, Key, Timothy J, Allen, Naomi E, Epi Kanker Team 1, Cancer, JC onderzoeksprogramma Kanker, MS MDL 1, Travis, Ruth C, Perez-Cornago, Aurora, Appleby, Paul N, Albanes, Demetrius, Joshu, Corinne E, Lutsey, Pamela L, Mondul, Alison M, Platz, Elizabeth A, Weinstein, Stephanie J, Layne, Tracy M, Helzlsouer, Kathy J, Visvanathan, Kala, Palli, Domenico, Peeters, Petra H, Bueno-de-Mesquita, Bas, Trichopoulou, Antonia, Gunter, Marc J, Tsilidis, Konstantinos K, Sánchez, Maria-Jose, Olsen, Anja, Brenner, Hermann, Schöttker, Ben, Perna, Laura, Holleczek, Bernd, Knekt, Paul, Rissanen, Harri, Yeap, Bu B, Flicker, Leon, Almeida, Osvaldo P, Wong, Yuen Yee Elizabeth, Chan, June M, Giovannucci, Edward L, Stampfer, Meir J, Ursin, Giske, Gislefoss, Randi E, Bjørge, Tone, Meyer, Haakon E, Blomhoff, Rune, Tsugane, Shoichiro, Sawada, Norie, English, Dallas R, Eyles, Darryl W, Heath, Alicia K, Williamson, Elizabeth J, Manjer, Jonas, Malm, Johan, Almquist, Martin, Marchand, Loic Le, Haiman, Christopher A, Wilkens, Lynne R, Schenk, Jeannette M, Tangen, Cathy M, Black, Amanda, Cook, Michael B, Huang, Wen-Yi, Ziegler, Regina G, Martin, Richard M, Hamdy, Freddie C, Donovan, Jenny L, Neal, David E, Touvier, Mathilde, Hercberg, Serge, Galan, Pilar, Deschasaux, Mélanie, Key, Timothy J, and Allen, Naomi E

Published
2019

163. Racial differences in maternal and umbilical cord blood leukocyte telomere length and their correlations

Author

Weber, Kari A, Heaphy, Christopher M, Joshu, Corinne E, Lu, Jiayun, Rohrmann, Sabine, Bienstock, Jessica L, Agurs-Collins, Tanya, Meeker, Alan K, Platz, Elizabeth A, University of Zurich, and Platz, Elizabeth A

Subjects
610 Medicine & health, 2730 Oncology, 1306 Cancer Research, 10060 Epidemiology, Biostatistics and Prevention Institute (EBPI)
Published
2018
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166. Cancer Survivorship and Subclinical Myocardial Damage

Author

Florido, Roberta, primary, Lee, Alexandra K, primary, McEvoy, John W, primary, Hoogeveen, Ron C, primary, Koton, Silvia, primary, Vitolins, Mara Z, primary, Shenoy, Chetan, primary, Russell, Stuart D, primary, Blumenthal, Roger S, primary, Ndumele, Chiadi E, primary, Ballantyne, Christie M, primary, Joshu, Corinne E, primary, Platz, Elizabeth A, primary, and Selvin, Elizabeth, primary

Published
2019
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171. A Collaborative Analysis of Individual Participant Data from 19 Prospective Studies Assesses Circulating Vitamin D and Prostate Cancer Risk

Author

Travis, Ruth C., primary, Perez-Cornago, Aurora, additional, Appleby, Paul N., additional, Albanes, Demetrius, additional, Joshu, Corinne E., additional, Lutsey, Pamela L., additional, Mondul, Alison M., additional, Platz, Elizabeth A., additional, Weinstein, Stephanie J., additional, Layne, Tracy M., additional, Helzlsouer, Kathy J., additional, Visvanathan, Kala, additional, Palli, Domenico, additional, Peeters, Petra H., additional, Bueno-de-Mesquita, Bas, additional, Trichopoulou, Antonia, additional, Gunter, Marc J., additional, Tsilidis, Konstantinos K., additional, Sánchez, Maria-Jose, additional, Olsen, Anja, additional, Brenner, Hermann, additional, Schöttker, Ben, additional, Perna, Laura, additional, Holleczek, Bernd, additional, Knekt, Paul, additional, Rissanen, Harri, additional, Yeap, Bu B., additional, Flicker, Leon, additional, Almeida, Osvaldo P., additional, Wong, Yuen Yee Elizabeth, additional, Chan, June M., additional, Giovannucci, Edward L., additional, Stampfer, Meir J., additional, Ursin, Giske, additional, Gislefoss, Randi E., additional, Bjørge, Tone, additional, Meyer, Haakon E., additional, Blomhoff, Rune, additional, Tsugane, Shoichiro, additional, Sawada, Norie, additional, English, Dallas R., additional, Eyles, Darryl W., additional, Heath, Alicia K., additional, Williamson, Elizabeth J., additional, Manjer, Jonas, additional, Malm, Johan, additional, Almquist, Martin, additional, Marchand, Loic Le, additional, Haiman, Christopher A., additional, Wilkens, Lynne R., additional, Schenk, Jeannette M., additional, Tangen, Cathy M., additional, Black, Amanda, additional, Cook, Michael B., additional, Huang, Wen-Yi, additional, Ziegler, Regina G., additional, Martin, Richard M., additional, Hamdy, Freddie C., additional, Donovan, Jenny L., additional, Neal, David E., additional, Touvier, Mathilde, additional, Hercberg, Serge, additional, Galan, Pilar, additional, Deschasaux, Mélanie, additional, Key, Timothy J., additional, and Allen, Naomi E., additional

Published
2019
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172. Recommended Definitions of Aggressive Prostate Cancer for Etiologic Epidemiologic Research.

Author

Hurwitz, Lauren M, Agalliu, Ilir, Albanes, Demetrius, Barry, Kathryn Hughes, Berndt, Sonja I, Cai, Qiuyin, Chen, Chu, Cheng, Iona, Genkinger, Jeanine M, Giles, Graham G, Huang, Jiaqi, Joshu, Corinne E, Key, Tim J, Knutsen, Synnove, Koutros, Stella, Langseth, Hilde, Li, Sherly X, MacInnis, Robert J, Markt, Sarah C, and Penney, Kathryn L

Subjects
PROSTATE cancer, CANCER diagnosis, PROSTATE-specific antigen, ETIOLOGY of cancer, GLEASON grading system, RESEARCH, PREDICTIVE tests, RESEARCH methodology, PROSTATE, EVALUATION research, TUMOR classification, COMPARATIVE studies, RESEARCH funding, PROSTATE tumors, TUMOR grading
Abstract

Background: In the era of widespread prostate-specific antigen testing, it is important to focus etiologic research on the outcome of aggressive prostate cancer, but studies have defined this outcome differently. We aimed to develop an evidence-based consensus definition of aggressive prostate cancer using clinical features at diagnosis for etiologic epidemiologic research.Methods: Among prostate cancer cases diagnosed in 2007 in the National Cancer Institute's Surveillance, Epidemiology, and End Results-18 database with follow-up through 2017, we compared the performance of categorizations of aggressive prostate cancer in discriminating fatal prostate cancer within 10 years of diagnosis, placing the most emphasis on sensitivity and positive predictive value (PPV).Results: In our case population (n = 55 900), 3073 men died of prostate cancer within 10 years. Among 12 definitions that included TNM staging and Gleason score, sensitivities ranged from 0.64 to 0.89 and PPVs ranged from 0.09 to 0.23. We propose defining aggressive prostate cancer as diagnosis of category T4 or N1 or M1 or Gleason score of 8 or greater prostate cancer, because this definition had one of the higher PPVs (0.23, 95% confidence interval = 0.22 to 0.24) and reasonable sensitivity (0.66, 95% confidence interval = 0.64 to 0.67) for prostate cancer death within 10 years. Results were similar across sensitivity analyses.Conclusions: We recommend that etiologic epidemiologic studies of prostate cancer report results for this definition of aggressive prostate cancer. We also recommend that studies separately report results for advanced category (T4 or N1 or M1), high-grade (Gleason score ≥8), and fatal prostate cancer. Use of this comprehensive set of endpoints will facilitate comparison of results from different studies and help elucidate prostate cancer etiology. [ABSTRACT FROM AUTHOR]

Published
2021
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173. Prediagnostic Obesity and Physical Inactivity Are Associated with Shorter Telomere Length in Prostate Stromal Cells.

Author

Joshu, Corinne E, Joshu, Corinne E, Peskoe, Sarah B, Heaphy, Christopher M, Kenfield, Stacey A, Van Blarigan, Erin L, Mucci, Lorelei A, Giovannucci, Edward L, Stampfer, Meir J, Yoon, GhilSuk, Lee, Thomas K, Hicks, Jessica L, De Marzo, Angelo M, Meeker, Alan K, Platz, Elizabeth A, Joshu, Corinne E, Joshu, Corinne E, Peskoe, Sarah B, Heaphy, Christopher M, Kenfield, Stacey A, Van Blarigan, Erin L, Mucci, Lorelei A, Giovannucci, Edward L, Stampfer, Meir J, Yoon, GhilSuk, Lee, Thomas K, Hicks, Jessica L, De Marzo, Angelo M, Meeker, Alan K, and Platz, Elizabeth A

Abstract

Obesity and inactivity have been associated with advanced-stage prostate cancer, and poor prostate cancer outcomes, though the underlying mechanism(s) is unknown. To determine whether telomere shortening, which has been associated with lethal prostate cancer, may be a potential underlying mechanism, we prospectively evaluated the association between measures of adiposity, physical activity, and telomere length in 596 participants in the Health Professionals Follow-up Study, who were surgically treated for prostate cancer. Using tissue microarrays, we measured telomere length in cancer and benign cells using a telomere-specific FISH assay. Adiposity and activity were assessed via questionnaire within 2 years of diagnosis. Adjusting for age, pathologic stage, and grade, the median and SD of the per cell telomere signals were determined for each man for stromal cells and cancer cells by adiposity and activity categories. Overweight/obese men (54%) were similar to normal weight men on most factors, but had higher Gleason sum and lower activity levels. Overweight/obese men had 7.4% shorter telomeres in stromal cells than normal weight men (P = 0.06). The least active men had shorter telomeres in stromal cells than more active men (Ptrend = 0.002). Men who were overweight/obese and the least active had the shortest telomeres in stromal cells (20.7% shorter; P = 0.0005) compared with normal weight men who were the most active. Cancer cell telomere length and telomere length variability did not differ by measures of adiposity or activity. Telomere shortening in prostate cells may be one mechanism through which lifestyle influences prostate cancer risk and outcomes.

Published
2015

174. A comparison of cancer stage at diagnosis and treatment initiation between enrollees in an urban HIV clinic and SEER.

Author

Calkins, Keri L., Chander, Geetanjali, Joshu, Corinne E., Visvanathan, Kala, Fojo, Anthony T., Lesko, Catherine R., Moore, Richard D., and Lau, Bryan

Subjects
TUMOR classification, CANCER diagnosis, HIV, HIV status, CANCER treatment
Abstract

Purpose: A comparison of stage at cancer diagnosis and cancer treatment rates between people with HIV (PWH) and the general US population is needed to identify any disparities by HIV status.Methods: We compared 236 PWH in clinical care diagnosed with cancer from 1997 to 2014 to a sample from NCI's Surveillance, Epidemiology and End Results (SEER) Program, presumed to be HIV negative. We performed G-computation using random forest methods to estimate stage and treatment percent differences (PD) by HIV. We conducted sensitivity analyses among non-AIDS-defining cancers (NADC), by sex and by CD4 ≤ 200 or > 200 cells/mm3.Results: PWH were less likely to be diagnosed at localized stage (PD = - 16%; 95% CI - 21, - 11) and more likely to be diagnosed at regional stage (PD = 14%; 95% CI 8, 19) than those in SEER. Cancer treatment rates were 13% lower among PWH as compared to SEER (95% CI - 18, - 8). The difference in percent receiving cancer treatment was more pronounced for those with lower CD4 at cancer diagnosis (PD -15%; 95% CI - 27, - 6). Lower treatment rates were observed among NADC, males, and women with CD4 ≤ 200.Conclusion: Cancer care for PWH could be improved by diagnosis at earlier stages and increasing rates of cancer treatment. [ABSTRACT FROM AUTHOR]

Published
2020
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175. High Extratumoral Mast Cell Counts Are Associated with a Higher Risk of Adverse Prostate Cancer Outcomes.

Author

Sullivan, Heidi Hempel, Heaphy, Christopher M., Kulac, Ibrahim, Cuka, Nathan, Jiayun Lu, Barber, John R., De Marzo, Angelo M., Lotan, Tamara L., Joshu, Corinne E., and Sfanos, Karen S.

Abstract

Background: Given our previous findings that low intratumoral and high extratumoral mast cell numbers are associated with higher risk of biochemical recurrence after radical prostatectomy, we now assessed this relationship with race and the development of metastases. Methods: We stained for mast cell tryptase via IHC and fluorescent immunolabeling in 885 men across multiple tissue microarray sets designed to assess biomarkers in association with race and prostate cancer outcomes (median follow-up, 7.0 years). Results: Intratumoral and extratumoral mast cell counts were significantly lower in tissues from African-American compared with European-American men, but not within strata of cancer grade. There was no association between mast cell counts and ERG positivity, PTEN loss, or TP53 missense mutation. Higher minimum extratumoral mast cells were associated with an increased risk of biochemical recurrence [comparing highest with lowest tertiles: HR, 1.61; 95% confidence interval (CI), 1.12-2.29; P trend = 0.01]; this pattern was similar among European-American and African-American men and by grade of disease. There was no significant association between minimum intratumoral mast cell count and biochemical recurrence, overall or within strata of race and grade. Finally, high minimum number of extratumoral mast cells was associated with prostate cancer metastases (comparing highest with lowest tertiles: HR, 2.12; 95% CI, 1.24-3.63; P trend = 0.01). Conclusions: High extratumoral mast cell numbers are associated with biochemical recurrence and the development of metastases after radical prostatectomy. Impact: Higher numbers of benign tissue mast cells are associated with a higher risk of adverse outcomes after radical prostatectomy, including metastatic prostate cancer. [ABSTRACT FROM AUTHOR]

Published
2020
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176. 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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180. Abstract 5248: Adherence to the WCRF/AICR cancer prevention guidelines and colorectal cancer incidence and mortality in the biracial cohort–the Atherosclerosis Risk in Communities (ARIC) study

Author

Lintelmann, Anna K., primary, Onyeaghala, Guillaume, additional, Joshu, Corinne E., additional, Lutsey, Pamela L., additional, Folsom, Aaron R., additional, Robien, Kimberly, additional, Platz, Elizabeth A., additional, and Prizment, Anna E., additional

Published
2018
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181. Circulating Vitamin D and Colorectal Cancer Risk: An International Pooling Project of 17 Cohorts

Author

McCullough, Marjorie L, primary, Zoltick, Emilie S, additional, Weinstein, Stephanie J, additional, Fedirko, Veronika, additional, Wang, Molin, additional, Cook, Nancy R, additional, Eliassen, A Heather, additional, Zeleniuch-Jacquotte, Anne, additional, Agnoli, Claudia, additional, Albanes, Demetrius, additional, Barnett, Matthew J, additional, Buring, Julie E, additional, Campbell, Peter T, additional, Clendenen, Tess V, additional, Freedman, Neal D, additional, Gapstur, Susan M, additional, Giovannucci, Edward L, additional, Goodman, Gary G, additional, Haiman, Christopher A, additional, Ho, Gloria Y F, additional, Horst, Ronald L, additional, Hou, Tao, additional, Huang, Wen-Yi, additional, Jenab, Mazda, additional, Jones, Michael E, additional, Joshu, Corinne E, additional, Krogh, Vittorio, additional, Lee, I-Min, additional, Lee, Jung Eun, additional, Männistö, Satu, additional, Le Marchand, Loic, additional, Mondul, Alison M, additional, Neuhouser, Marian L, additional, Platz, Elizabeth A, additional, Purdue, Mark P, additional, Riboli, Elio, additional, Robsahm, Trude Eid, additional, Rohan, Thomas E, additional, Sasazuki, Shizuka, additional, Schoemaker, Minouk J, additional, Sieri, Sabina, additional, Stampfer, Meir J, additional, Swerdlow, Anthony J, additional, Thomson, Cynthia A, additional, Tretli, Steinar, additional, Tsugane, Schoichiro, additional, Ursin, Giske, additional, Visvanathan, Kala, additional, White, Kami K, additional, Wu, Kana, additional, Yaun, Shiaw-Shyuan, additional, Zhang, Xuehong, additional, Willett, Walter C, additional, Gail, Mitchel H, additional, Ziegler, Regina G, additional, and Smith-Warner, Stephanie A, additional

Published
2018
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183. A unique telomere DNA expansion phenotype in human retinal rod photoreceptors associated with aging and disease

Author

Bell, W. Robert, primary, Meeker, Alan K., additional, Rizzo, Anthony, additional, Rajpara, Sumit, additional, Rosenthal, Ian M., additional, Flores Bellver, Miguel, additional, Aparicio Domingo, Silvia, additional, Zhong, Xiufeng, additional, Barber, John R., additional, Joshu, Corinne E., additional, Canto‐Soler, M. Valeria, additional, Eberhart, Charles G., additional, and Heaphy, Christopher M., additional

Published
2018
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185. Enhancing the Infrastructure of the Atherosclerosis Risk in Communities (ARIC) Study for Cancer Epidemiology Research: ARIC Cancer

Author

Joshu, Corinne E., primary, Barber, John R., additional, Coresh, Josef, additional, Couper, David J., additional, Mosley, Thomas H., additional, Vitolins, Mara Z., additional, Butler, Kenneth R., additional, Nelson, Heather H., additional, Prizment, Anna E., additional, Selvin, Elizabeth, additional, Tooze, Janet A., additional, Visvanathan, Kala, additional, Folsom, Aaron R., additional, and Platz, Elizabeth A., additional

Published
2018
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187. Association of tumor-infiltrating T-cell density with molecular subtype, racial ancestry and clinical outcomes in prostate cancer

Author

Kaur, Harsimar B., primary, Guedes, Liana B., additional, Lu, Jiayun, additional, Maldonado, Laneisha, additional, Reitz, Logan, additional, Barber, John R., additional, De Marzo, Angelo M., additional, Tosoian, Jeffrey J., additional, Tomlins, Scott A., additional, Schaeffer, Edward M., additional, Joshu, Corinne E., additional, Sfanos, Karen S., additional, and Lotan, Tamara L., additional

Published
2018
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188. A Prospective Study of Chronic Inflammation in Benign Prostate Tissue and Risk of Prostate Cancer: Linked PCPT and SELECT Cohorts.

Author

Platz, Elizabeth A, Platz, Elizabeth A, Kulac, Ibrahim, Barber, John R, Drake, Charles G, Joshu, Corinne E, Nelson, William G, Lucia, M Scott, Klein, Eric A, Lippman, Scott M, Parnes, Howard L, Thompson, Ian M, Goodman, Phyllis J, Tangen, Catherine M, De Marzo, Angelo M, Platz, Elizabeth A, Platz, Elizabeth A, Kulac, Ibrahim, Barber, John R, Drake, Charles G, Joshu, Corinne E, Nelson, William G, Lucia, M Scott, Klein, Eric A, Lippman, Scott M, Parnes, Howard L, Thompson, Ian M, Goodman, Phyllis J, Tangen, Catherine M, and De Marzo, Angelo M

Abstract

Background: We leveraged two trials to test the hypothesis of an inflammation-prostate cancer link prospectively in men without indication for biopsy.Methods: Prostate Cancer Prevention Trial (PCPT) participants who had an end-of-study biopsy performed per protocol that was negative for cancer and who subsequently enrolled in the Selenium and Vitamin E Cancer Prevention Trial (SELECT) were eligible. We selected all 100 cases and sampled 200 frequency-matched controls and used PCPT end-of-study biopsies as "baseline." Five men with PSA > 4 ng/mL at end-of-study biopsy were excluded. Tissue was located for 92 cases and 193 controls. We visually assessed inflammation in benign tissue. We estimated ORs and 95% confidence intervals (CI) using logistic regression adjusting for age and race.Results: Mean time between biopsy and diagnosis was 5.9 years. In men previously in the PCPT placebo arm, 78.1% of cases (N = 41) and 68.2% of controls (N = 85) had at least one baseline biopsy core (∼5 evaluated per man) with inflammation. The odds of prostate cancer (N = 41 cases) appeared to increase with increasing mean percentage of tissue area with inflammation, a trend that was statistically significant for Gleason sum <4+3 disease (N = 31 cases; vs. 0%, >0-<1.8% OR = 1.70, 1.8-<5.0% OR = 2.39, ≥5% OR = 3.31, Ptrend = 0.047). In men previously in the finasteride arm, prevalence of inflammation did not differ between cases (76.5%; N = 51) and controls (75.0%; N = 108).Conclusions: Benign tissue inflammation was positively associated with prostate cancer.Impact: This first prospective study of men without biopsy indication supports the hypothesis that inflammation influences prostate cancer development. Cancer Epidemiol Biomarkers Prev; 26(10); 1549-57. ©2017 AACR.

Published
2017

189. Racial/ethnic differences in the associations of overall and central body fatness with circulating hormones and metabolic factors in US Men

Author

Lopez, David S, Rohrmann, Sabine, Peskoe, Sarah B, Joshu, Corinne E, Tsilidis, Konstantinos K, Selvin, Elizabeth, Dobs, Adrian S, Kanarek, Norma, Canfield, Steven, Nelson, William G, Platz, Elizabeth A, Lopez, David S, Rohrmann, Sabine, Peskoe, Sarah B, Joshu, Corinne E, Tsilidis, Konstantinos K, Selvin, Elizabeth, Dobs, Adrian S, Kanarek, Norma, Canfield, Steven, Nelson, William G, and Platz, Elizabeth A

Abstract

BACKGROUND: Racial/ethnic disparities in the associations of body fatness with hormones and metabolic factors remain poorly understood. Therefore, we evaluated whether the associations of overall and central body fatness with circulating sex steroid hormones and metabolic factors differ by race/ethnicity. METHODS: Data from 1,243 non-Hispanic white (NHW), non-Hispanic black (NHB) and Mexican-American (MA) adult men in the third national health and nutrition examination survey (NHANES III) were analyzed. Waist circumference (central body fatness) was measured during the physical examination. Percent body fat (overall body fatness) was calculated from bioelectrical impedance. Associations were estimated by using weighted linear regression models to adjust the two measures of body fatness for each other. RESULTS. Waist circumference, but not percent body fat was inversely associated with total testosterone and SHBG in all three racial/ethnic groups after their mutual adjustment (all P < 0.0001). Percent body fat (P = 0.02), but not waist circumference was positively associated with total estradiol in NHB men; no association was present in NHW and MA men (P-interaction = 0.04). Waist circumference, but not body fat was strongly positively associated with fasting insulin (all P < 0.0001) and inversely associated with HDL cholesterol (all P ≤ 0.003) in all three racial/ethnic groups. Both percent body fat and waist circumference were positively associated with leptin (all P < 0.0001) in all three racial/ethnic groups. CONCLUSIONS. There was no strong evidence in the associations of sex hormones and metabolic factors with body fatness in different racial/ethnic groups. These findings should be further explored in prospective studies to determine their relevance in racial/ethnic disparities of chronic diseases.

Published
2017

190. Current or recent smoking is associated with more variable telomere length in prostate stromal cells and prostate cancer cells

Author

Joshu, Corinne E., primary, Peskoe, Sarah B, additional, Heaphy, Christopher M., additional, Kenfield, Stacey A., additional, Mucci, Lorelei A., additional, Giovannucci, Edward L., additional, Stampfer, Meir J., additional, Yoon, Ghilsuk, additional, Lee, Thomas K., additional, Hicks, Jessica L., additional, De Marzo, Angelo M., additional, Meeker, Alan K., additional, and Platz, Elizabeth A., additional

Published
2017
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191. A Prospective Study of Chronic Inflammation in Benign Prostate Tissue and Risk of Prostate Cancer: Linked PCPT and SELECT Cohorts

Author

Platz, Elizabeth A., primary, Kulac, Ibrahim, additional, Barber, John R., additional, Drake, Charles G., additional, Joshu, Corinne E., additional, Nelson, William G., additional, Lucia, M. Scott, additional, Klein, Eric A., additional, Lippman, Scott M., additional, Parnes, Howard L., additional, Thompson, Ian M., additional, Goodman, Phyllis J., additional, Tangen, Catherine M., additional, and De Marzo, Angelo M., additional

Published
2017
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194. Racial/Ethnic Differences in the Associations of Overall and Central Body Fatness with Circulating Hormones and Metabolic Factors in US Men

Author

Lopez, David S., primary, Rohrmann, Sabine, additional, Peskoe, Sarah B., additional, Joshu, Corinne E., additional, Tsilidis, Konstantinos K., additional, Selvin, Elizabeth, additional, Dobs, Adrian S., additional, Kanarek, Norma, additional, Canfield, Steven, additional, Nelson, William G., additional, and Platz, Elizabeth A., additional

Published
2017
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195. Prostate stromal cell telomere shortening is associated with risk of prostate cancer in the placebo arm of the Prostate Cancer Prevention Trial

Author

Heaphy, Christopher M, Gaonkar, Gaurav, Peskoe, Sarah B, Joshu, Corinne E, De Marzo, Angelo M, Lucia, M Scott, Goodman, Phyllis J, Lippman, Scott M, Thompson, Ian M, Platz, Elizabeth A, and Meeker, Alan K

Subjects
Male, Urologic Diseases, Aging, Biopsy, Clinical Trials and Supportive Activities, Clinical Sciences, Oncology and Carcinogenesis, Paediatrics and Reproductive Medicine, 5-alpha Reductase Inhibitors, Risk Factors, Clinical Research, Chromosomal Instability, stroma, Genetics, Humans, tumor microenvironment, 2.1 Biological and endogenous factors, Oncology & Carcinogenesis, Aetiology, Telomere Shortening, Cancer, Prevention, Prostate Cancer, Finasteride, Prostate, Prostatic Neoplasms, Telomere Homeostasis, Middle Aged, Telomere, Disease Progression, Stromal Cells
Abstract

BackgroundTelomeres are repetitive nucleoproteins that help maintain chromosomal stability by inhibiting exonucleolytic degradation, prohibiting inappropriate homologous recombination, and preventing chromosomal fusions by suppressing double-strand break signals. We recently observed that men treated for clinically localized prostate cancer with shorter telomeres in their cancer-associated stromal cells, in combination with greater variation in cancer cell telomere lengths, were significantly more likely to progress to distant metastases, and die from their disease. Here, we hypothesized that shorter stromal cell telomere length would be associated with prostate cancer risk at time of biopsy.MethodsTelomere-specific fluorescence in situ hybridization (FISH) analysis was performed in normal-appearing stromal, basal epithelial, and luminal epithelial cells in biopsies from men randomized to the placebo arm of the Prostate Cancer Prevention Trial. Prostate cancer cases (N = 32) were either detected on a biopsy performed for cause or at the end of the study per trial protocol, and controls (N = 50), defined as negative for cancer on an end-of-study biopsy performed per trial protocol (e.g., irrespective of indication), were sampled. Logistic regression was used to estimate the association between mean telomere length of the particular cell populations, cell-to-cell telomere length variability, and risk of prostate cancer.ResultsMen with short stromal cell telomere lengths (below median) had 2.66 (95% CI 1.04-3.06; P = 0.04) times the odds of prostate cancer compared with men who had longer lengths (at or above median). Conversely, we did not observe statistically significant associations for short telomere lengths in normal-appearing basal (OR = 2.15, 95% CI 0.86-5.39; P= 0 .10) or luminal (OR = 1.15, 95% CI 0.47-2.80; P = 0.77) cells.ConclusionsThese findings suggest that telomere shortening in normal stromal cells is associated with prostate cancer risk. It is essential to extend and validate these findings, while also identifying the cellular milieu that comprises the subset of cells with short telomeres within the prostate tumor microenvironment.

Published
2015

196. Circulating total testosterone and PSA concentrations in a nationally representative sample of men without a diagnosis of prostate cancer

Author

Peskoe, Sarah B, Joshu, Corinne E, Rohrmann, Sabine, McGlynn, Katherine A, Nyante, Sarah J, Bradwin, Gary, Dobs, Adrian S, Kanarek, Norma, Nelson, William G, Platz, Elizabeth A, University of Zurich, and Platz, Elizabeth A

Subjects
2748 Urology, 610 Medicine & health, 2730 Oncology, 10060 Epidemiology, Biostatistics and Prevention Institute (EBPI)
Published
2015
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197. Association between greater leg length and increased incidence of colorectal cancer: the atherosclerosis risk in communities (ARIC) study.

Author

Onyeaghala, Guillaume, Lutsey, Pamela L., Demerath, Ellen W., Folsom, Aaron R., Joshu, Corinne E., Platz, Elizabeth A., and Prizment, Anna E.

Subjects
COLORECTAL cancer, LEG, PRECOCIOUS puberty, ATHEROSCLEROSIS, RECTAL cancer, LEG length inequality, COMMUNITIES, COLON tumors, LONGITUDINAL method, RECTUM tumors, RESEARCH funding, STATURE, DISEASE incidence
Abstract

Purpose: Previous studies have reported that taller people have an increased risk of colorectal cancer (CRC). We examined the association of two height components-leg length and sitting height-with CRC risk in 14,532 individuals aged 45-64 years in the Atherosclerosis Risk in Communities study.Methods: Anthropometrics were measured at baseline (1987-1989). Incident CRC cases (n = 382) were ascertained from 1987 to 2012. Cox proportional hazards regression was used to estimate multivariable-adjusted hazard ratios for CRC and colon cancer across quintiles of sex-specific leg length and sitting height.Results: The highest (versus the lowest) quintile of leg length was associated with a 36% greater CRC risk (p-trend = 0.04), and 51% greater colon cancer risk (p-trend = 0.01). For the top four quintiles combined, risk was increased by 34% for CRC and by 45% for colon cancer versus the lowest quintile. Total height and sitting height were not significantly associated with CRC or colon cancer risk. A small number of cases (n = 57) limited our ability to conduct subgroup analyses for rectal cancer.Conclusions: A positive association of leg length with CRC and colon cancer risk suggests that biological mechanisms leading to greater leg length during puberty may explain the association between taller height and CRC. [ABSTRACT FROM AUTHOR]

Published
2019
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198. Dietary choline and betaine intakes and risk of total and lethal prostate cancer in the Atherosclerosis Risk in Communities (ARIC) Study.

Author

Han, Peijin, Bidulescu, Aurelian, Barber, John R., Zeisel, Steven H., Joshu, Corinne E., Prizment, Anna E., Vitolins, Mara Z., and Platz, Elizabeth A.

Abstract

Purpose: Two prior cohort studies suggested that choline, but not betaine intake, is associated with an increased risk of advanced prostate cancer (PCa). Given that evidence remains limited, we evaluated whether intakes of choline and derivative betaine are associated with total and lethal PCa risk and PCa death in men with PCa. Methods: We included 6,528 men (24.4% African American) without a cancer diagnosis at baseline (1987–1989) followed through 2012. Dietary intake was assessed using a food frequency questionnaire coupled with a nutrient database. We used Cox proportional hazards regression to estimate hazards ratios (HRs) and 95% confidence intervals (CIs) of total and lethal PCa risk overall and by race. Results: Choline intake was not associated with total (n = 811) or lethal (n = 95) PCa risk overall or by race. Betaine intake was inversely associated with lethal (tertile 3 vs 1, HR 0.59, 95% CI 0.35–1.00, p trend = 0.04), but not total PCa risk; patterns for lethal PCa were similar by race. Neither nutrient was associated with PCa death in men with PCa. Conclusions: Choline intake was not associated with total or lethal PCa or with PCa death in men with PCa. Betaine intake was inversely associated with lethal, but not total PCa risk or with PCa death in men with PCa. Our results do not support the hypothesis that higher choline intake increases lethal PCa risk, but do suggest that higher betaine intake may be associated with lower lethal PCa risk. Further investigation with a larger number of lethal cases is needed. [ABSTRACT FROM AUTHOR]

Published
2019
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199. A unique telomere DNA expansion phenotype in human retinal rod photoreceptors associated with aging and disease.

Author

Bell, W. Robert, Meeker, Alan K., Rizzo, Anthony, Rajpara, Sumit, Rosenthal, Ian M., Flores Bellver, Miguel, Aparicio Domingo, Silvia, Zhong, Xiufeng, Barber, John R., Joshu, Corinne E., Canto‐Soler, M. Valeria, Eberhart, Charles G., and Heaphy, Christopher M.

Subjects
RETINAL rod photoreceptor cells, TELOMERES, AGING, DIABETIC retinopathy, GLAUCOMA
Abstract

We have identified a discrete, focal telomere DNA expansion phenotype in the photoreceptor cell layer of normal, non‐neoplastic human retinas. This phenotype is similar to that observed in a subset of human cancers, including a large fraction of tumors of the central nervous system, which maintain their telomeres via the non‐telomerase‐mediated alternative lengthening of telomeres (ALT) mechanism. We observed that these large, ultra‐bright telomere DNA foci are restricted to the rod photoreceptors and are not observed in other cell types. Additionally, focus‐positive rod cells are dispersed homogeneously throughout the posterior retinal photoreceptor cell layer and appear to be human‐specific. We examined 108 normal human retinas obtained at autopsy from a wide range of ages. These large, ultra‐bright telomere DNA foci were not observed in infants before 6 months of age; however, the prevalence of focus‐positive rod cells dramatically increased throughout life. To investigate associations between this phenotype and retinal pathology, we assessed adult glaucoma (N = 29) and diabetic retinopathy (N = 38) cases. Focus‐positive rod cells were prominent in these diseases. When compared to the normal group, after adjusting for age, logistic regression modeling revealed significantly increased odds of falling in the high category of focus‐positive rod cells for glaucoma and diabetic retinopathy. In summary, we have identified a dramatic telomere alteration associated with aging and diseases affecting the retina. [ABSTRACT FROM AUTHOR]

Published
2019
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200. Body mass index at early adulthood, subsequent weight change and cancer incidence and mortality: Body mass index, weight change and cancer risk

Author

Platz, Elizabeth A., Prizment, Anna E., Joshu, Corinne E., Stevens, June, Han, Xuesong, Kucharska-Newton, Anna, Truesdale, Kimberly P., and Bradshaw, Patrick T.

Abstract

Obesity later in adulthood is associated with increased risks of many cancers. However, the effect of body fatness in early adulthood, and change in weight from early to later adulthood on cancer risk later in life is less clear. We used data from 13,901 people aged 45-64 in the Atherosclerosis Risk in Communities cohort who at baseline (1987-1989) self-reported their weight at the age of 25 and had weight and height measured. Incident cancers were identified through 2006 and cancer deaths were ascertained through 2009. Multivariable Cox proportional hazard models were used to relate body mass index (BMI) at age 25 and percent weight change from age 25 to baseline to cancer incidence and mortality. After adjusting for weight change from age 25 until baseline, a 5 kg/m2 increment in BMI at age 25 was associated with a greater risk of incidence of all cancers in women [hazard ratio (95% confidence interval): 1.10 (1.02-1.20)], but not in men. Associations with incident endometrial cancer were strong [1.83 (1.47-2.26)]. After adjusting for BMI at age 25, a 5% increment in weight from age 25 to baseline was associated with a greater risk of incident post-menopausal breast cancer [1.05 (1.02-1.07)] and endometrial cancer [1.09 (1.04-1.14)] in women and incident colorectal cancer [1.05 (1.00-1.10)] in men. Excess weight during young adulthood and weight gain from young to older adulthood may be independently associated with subsequent cancer risk. Excess weight and weight gain in early adulthood should be avoided.

Published
2014
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