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Giovannucci, Edward

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Giovannucci

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Edward

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Giovannucci, Edward
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    Optimal dietary patterns for prevention of chronic disease
    (Springer Science and Business Media LLC, 2023-03) Giovannucci, Edward L; Wang, Peilu; Song, Mingyang; Eliassen, A; Wang, Molin; Fung, Teresa; Clinton, Steven K.; Rimm, Eric; Hu, Frank; Willet, Walter C.; Tabung, Fred; Giovannucci, Edward
    Multiple dietary patterns have been associated with different diseases; however, their comparability to improve overall health is yet to be determined. In 205,852 healthcare professionals from three US cohorts followed for up to 32 years, we prospectively assessed two mechanism-based diets and six diets based on dietary recommendations in relation to major chronic disease, defined as a composite outcome of incident major cardiovascular disease, type 2 diabetes, and cancer. We demonstrated that adherence to a healthy diet was generally associated with a lower risk of major chronic disease (hazard ratio [HR] comparing the 90th to 10th percentile of dietary pattern scores: 0.58–0.80). Participants with low insulinemic (HR 0.58, 95% CI 0.57, 0.60), low inflammatory (HR 0.61, 95% CI 0.60, 0.63), or diabetes risk-reducing diet (HR 0.70, 95% CI 0.69, 0.72) had the largest risk reduction for incident major cardiovascular disease, type 2 diabetes, and cancer in composite and individually. Similar findings were observed across sex, and diverse ethnic groups. Our results suggest that dietary patterns that are associated with markers of hyperinsulinemia and inflammation and diabetes development may inform on future dietary guidelines for chronic disease prevention.
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    Genome-wide association study identifies multiple susceptibility loci for pancreatic cancer
    (2014) Wolpin, Brian M.; Rizzato, Cosmeri; Kraft, Phillip; Kooperberg, Charles; Petersen, Gloria M.; Wang, Zhaoming; Arslan, Alan A.; Beane-Freeman, Laura; Bracci, Paige M.; Buring, Julie; Canzian, Federico; Duell, Eric J.; Gallinger, Steven; Giles, Graham G.; Goodman, Gary E.; Goodman, Phyllis J.; Jacobs, Eric J.; Kamineni, Aruna; Klein, Alison P.; Kolonel, Laurence N.; Kulke, Matthew H.; Li, Donghui; Malats, Núria; Olson, Sara H.; Risch, Harvey A.; Sesso, Howard; Visvanathan, Kala; White, Emily; Zheng, Wei; Abnet, Christian C.; Albanes, Demetrius; Andreotti, Gabriella; Austin, Melissa A.; Barfield, Richard; Basso, Daniela; Berndt, Sonja I.; Boutron-Ruault, Marie-Christine; Brotzman, Michelle; Büchler, Markus W.; Bueno-de-Mesquita, H. Bas; Bugert, Peter; Burdette, Laurie; Campa, Daniele; Caporaso, Neil E.; Capurso, Gabriele; Chung, Charles; Cotterchio, Michelle; Costello, Eithne; Elena, Joanne; Funel, Niccola; Gaziano, John; Giese, Nathalia A.; Giovannucci, Edward; Goggins, Michael; Gorman, Megan J.; Gross, Myron; Haiman, Christopher A.; Hassan, Manal; Helzlsouer, Kathy J.; Henderson, Brian E.; Holly, Elizabeth A.; Hu, Nan; Hunter, David; Innocenti, Federico; Jenab, Mazda; Kaaks, Rudolf; Key, Timothy J.; Khaw, Kay-Tee; Klein, Eric A.; Kogevinas, Manolis; Krogh, Vittorio; Kupcinskas, Juozas; Kurtz, Robert C.; LaCroix, Andrea; Landi, Maria T.; Landi, Stefano; Le Marchand, Loic; Mambrini, Andrea; Mannisto, Satu; Milne, Roger L.; Nakamura, Yusuke; Oberg, Ann L.; Owzar, Kouros; Patel, Alpa V.; Peeters, Petra H. M.; Peters, Ulrike; Pezzilli, Raffaele; Piepoli, Ada; Porta, Miquel; Real, Francisco X.; Riboli, Elio; Rothman, Nathaniel; Scarpa, Aldo; Shu, Xiao-Ou; Silverman, Debra T.; Soucek, Pavel; Sund, Malin; Talar-Wojnarowska, Renata; Taylor, Philip R.; Theodoropoulos, George E.; Thornquist, Mark; Tjønneland, Anne; Tobias, Geoffrey S.; Trichopoulos, Dimitrios; Vodicka, Pavel; Wactawski-Wende, Jean; Wentzensen, Nicolas; Wu, Chen; Yu, Herbert; Yu, Kai; Zeleniuch-Jacquotte, Anne; Hoover, Robert; Hartge, Patricia; Fuchs, Charles; Chanock, Stephen J.; Stolzenberg-Solomon, Rachael S.; Amundadottir, Laufey T.
    We performed a multistage genome-wide association study (GWAS) including 7,683 individuals with pancreatic cancer and 14,397 controls of European descent. Four new loci reached genome-wide significance: rs6971499 at 7q32.3 (LINC-PINT; per-allele odds ratio [OR] = 0.79; 95% confidence interval [CI] = 0.74–0.84; P = 3.0×10−12), rs7190458 at 16q23.1 (BCAR1/CTRB1/CTRB2; OR = 1.46; 95% CI = 1.30–1.65; P = 1.1×10−10), rs9581943 at 13q12.2 (PDX1; OR = 1.15; 95% CI = 1.10–1.20; P = 2.4×10−9), and rs16986825 at 22q12.1 (ZNRF3; OR = 1.18; 95% CI = 1.12–1.25; P = 1.2×10−8). An independent signal was identified in exon 2 of TERT at the established region 5p15.33 (rs2736098; OR = 0.80; 95% CI = 0.76–0.85; P = 9.8×10−14). We also identified a locus at 8q24.21 (rs1561927; P = 1.3×10−7) that approached genome-wide significance located 455 kb telomeric of PVT1. Our study has identified multiple new susceptibility alleles for pancreatic cancer worthy of follow-up studies.
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    Association between Body Mass Index and Prognosis of Colorectal Cancer: A Meta-Analysis of Prospective Cohort Studies
    (Public Library of Science, 2015) Lee, Junga; Meyerhardt, Jeffrey; Giovannucci, Edward; Jeon, Justin Y.
    Studies have reported conflicting results on the association between body mass index (BMI) and prognosis of colorectal cancer. Therefore, we have conducted a meta-analysis of prospective studies, which examined the association of pre- and post-diagnostic BMI with colorectal cancer-specific mortality and all-cause mortality in patients with colorectal cancer. We searched Medline and EMBASE database published between 1970 and September 2014. A total of 508 articles were identified, of which 16 prospective cohort studies were included for the current meta-analysis. The analysis included 58,917 patients who were followed up over a period ranging from 4.9 to 20 years (median: 9.9 years). We found that being underweight before cancer diagnosis was associated with increased all-cause mortality (Relative risk [RR]: 1.63, 95% CI: 1.18–2.23, p < 0.01) and being obese (BMI ≥ 30 kg/m2) before cancer diagnosis was associated with increased colorectal cancer-specific mortality (RR: 1.22, 95% CI: 1.003–1.35, p < 0.01) and all-cause mortality (RR: 1.25, 95% CI: 1.14–1.36, p < 0.01). On the other hand, being underweight (RR: 1.33, 95% CI: 1.20–1.47, p < 0.01), obese (RR: 1.08, 95% CI: 1.03–1.3, p < 0.01), and class II/III obese (BMI ≥ 35 kg/m2; RR: 1.13, 95% CI: 1.04–1.23, p < 0.01) after diagnosis were associated with significantly increased all-cause mortality. Being obese prior to diagnosis of colorectal cancer was associated with increased colorectal cancer-specific mortality and all-cause mortality, whereas being obese after diagnosis was associated with increased all-cause mortality. The associations with being underweight may reflect reverse causation. Maintaining a healthy body weight should be discussed with colorectal cancer survivors.
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    Height, height-related SNPs, and risk of non-melanoma skin cancer
    (Nature Publishing Group, 2016) Li, Xin; Liang, Liming; Feng, Yen-Chen Anne; De Vivo, Immaculata; Giovannucci, Edward; Tang, Jean Y; Han, Jiali
    Background: Adult height has been associated with risk of several site-specific cancers, including melanoma. However, less attention has been given to non-melanoma skin cancer (NMSC). Methods: We prospectively examined the risk of squamous cell carcinoma (SCC) and basal cell carcinoma (BCC) in relation to adult height in the Nurses' Health Study (NHS, n=117 863) and the Health Professionals Follow-up Study (HPFS, n=51 111). We also investigated the relationships between height-related genetic markers and risk of BCC and SCC in the genetic data sets of the NHS and HPFS (3898 BCC cases, and 8530 BCC controls; 527 SCC cases, and 8962 SCC controls). Results: After controlling for potential confounding factors, the hazard ratios were 1.09 (95% CI: 1.02, 1.15) and 1.10 (95% CI: 1.07, 1.13) for the associations between every 10 cm increase in height and risk of SCC and BCC respectively. None of the 687 height-related single-nucleotide polymorphisms (SNPs) was significantly associated with the risk of SCC or BCC, nor were the genetic scores combining independent height-related loci. Conclusions: Our data from two large cohorts provide further evidence that height is associated with an increased risk of NMSC. More studies on height-related genetic loci and early-life exposures may help clarify the underlying mechanisms.
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    Fine-mapping of prostate cancer susceptibility loci in a large meta-analysis identifies candidate causal variants
    (Nature Publishing Group UK, 2018) Dadaev, Tokhir; Saunders, Edward J.; Newcombe, Paul J.; Anokian, Ezequiel; Leongamornlert, Daniel A.; Brook, Mark N.; Cieza-Borrella, Clara; Mijuskovic, Martina; Wakerell, Sarah; Olama, Ali Amin Al; Schumacher, Fredrick R.; Berndt, Sonja I.; Benlloch, Sara; Ahmed, Mahbubl; Goh, Chee; Sheng, Xin; Zhang, Zhuo; Muir, Kenneth; Govindasami, Koveela; Lophatananon, Artitaya; Stevens, Victoria L.; Gapstur, Susan M.; Carter, Brian D.; Tangen, Catherine M.; Goodman, Phyllis; Thompson, Ian M.; Batra, Jyotsna; Chambers, Suzanne; Moya, Leire; Clements, Judith; Horvath, Lisa; Tilley, Wayne; Risbridger, Gail; Gronberg, Henrik; Aly, Markus; Nordström, Tobias; Pharoah, Paul; Pashayan, Nora; Schleutker, Johanna; Tammela, Teuvo L. J.; Sipeky, Csilla; Auvinen, Anssi; Albanes, Demetrius; Weinstein, Stephanie; Wolk, Alicja; Hakansson, Niclas; West, Catharine; Dunning, Alison M.; Burnet, Neil; Mucci, Lorelei; Giovannucci, Edward; Andriole, Gerald; Cussenot, Olivier; Cancel-Tassin, Géraldine; Koutros, Stella; Freeman, Laura E. Beane; Sorensen, Karina Dalsgaard; Orntoft, Torben Falck; Borre, Michael; Maehle, Lovise; Grindedal, Eli Marie; Neal, David E.; Donovan, Jenny L.; Hamdy, Freddie C.; Martin, Richard M.; Travis, Ruth C.; Key, Tim J.; Hamilton, Robert J.; Fleshner, Neil E.; Finelli, Antonio; Ingles, Sue Ann; Stern, Mariana C.; Rosenstein, Barry; Kerns, Sarah; Ostrer, Harry; Lu, Yong-Jie; Zhang, Hong-Wei; Feng, Ninghan; Mao, Xueying; Guo, Xin; Wang, Guomin; Sun, Zan; Giles, Graham G.; Southey, Melissa C.; MacInnis, Robert J.; FitzGerald, Liesel M.; Kibel, Adam S.; Drake, Bettina F.; Vega, Ana; Gómez-Caamaño, Antonio; Fachal, Laura; Szulkin, Robert; Eklund, Martin; Kogevinas, Manolis; Llorca, Javier; Castaño-Vinyals, Gemma; Penney, Kathryn; Stampfer, Meir; Park, Jong Y.; Sellers, Thomas A.; Lin, Hui-Yi; Stanford, Janet L.; Cybulski, Cezary; Wokolorczyk, Dominika; Lubinski, Jan; Ostrander, Elaine A.; Geybels, Milan S.; Nordestgaard, Børge G.; Nielsen, Sune F.; Weisher, Maren; Bisbjerg, Rasmus; Røder, Martin Andreas; Iversen, Peter; Brenner, Hermann; Cuk, Katarina; Holleczek, Bernd; Maier, Christiane; Luedeke, Manuel; Schnoeller, Thomas; Kim, Jeri; Logothetis, Christopher J.; John, Esther M.; Teixeira, Manuel R.; Paulo, Paula; Cardoso, Marta; Neuhausen, Susan L.; Steele, Linda; Ding, Yuan Chun; De Ruyck, Kim; De Meerleer, Gert; Ost, Piet; Razack, Azad; Lim, Jasmine; Teo, Soo-Hwang; Lin, Daniel W.; Newcomb, Lisa F.; Lessel, Davor; Gamulin, Marija; Kulis, Tomislav; Kaneva, Radka; Usmani, Nawaid; Slavov, Chavdar; Mitev, Vanio; Parliament, Matthew; Singhal, Sandeep; Claessens, Frank; Joniau, Steven; Van den Broeck, Thomas; Larkin, Samantha; Townsend, Paul A.; Aukim-Hastie, Claire; Gago-Dominguez, Manuela; Castelao, Jose Esteban; Martinez, Maria Elena; Roobol, Monique J.; Jenster, Guido; van Schaik, Ron H. N.; Menegaux, Florence; Truong, Thérèse; Koudou, Yves Akoli; Xu, Jianfeng; Khaw, Kay-Tee; Cannon-Albright, Lisa; Pandha, Hardev; Michael, Agnieszka; Kierzek, Andrzej; Thibodeau, Stephen N.; McDonnell, Shannon K.; Schaid, Daniel J.; Lindstrom, Sara; Turman, Constance; Ma, Jing; Hunter, David; Riboli, Elio; Siddiq, Afshan; Canzian, Federico; Kolonel, Laurence N.; Le Marchand, Loic; Hoover, Robert N.; Machiela, Mitchell J.; Kraft, Phillip; Cook, Margaret; Thwaites, Alison; Guy, Michelle; Whitmore, Ian; Morgan, Angela; Fisher, Cyril; Hazel, Steve; Livni, Naomi; Spurdle, Amanda; Srinivasan, Srilakshmi; Kedda, Mary-Anne; Aitken, Joanne; Gardiner, Robert; Hayes, Vanessa; Butler, Lisa; Taylor, Renea; Yeadon, Trina; Eckert, Allison; Saunders, Pamela; Haynes, Anne-Maree; Papargiris, Melissa; Kujala, Paula; Talala, Kirsi; Murtola, Teemu; Taari, Kimmo; Dearnaley, David; Barnett, Gill; Bentzen, Søren; Elliott, Rebecca; Ranu, Hardeep; Hicks, Belynda; Vogt, Aurelie; Hutchinson, Amy; Cox, Angela; Davis, Michael; Brown, Paul; George, Anne; Marsden, Gemma; Lane, Athene; Lewis, Sarah J.; Berry, Clare; Kulkarni, Girish S.; Toi, Ants; Evans, Andrew; Zlotta, Alexandre R.; van der Kwast, Theodorus H.; Imai, Takashi; Saito, Shiro; Marzec, Jacek; Cao, Guangwen; Lin, Ji; Ling, Jin; Li, Meiling; Zhao, Shan-Chao; Ren, Guoping; Yu, Yongwei; Wu, Yudong; Wu, Ji; Zhou, Bo; Zhang, Yangling; Li, Jie; He, Weiyang; Guo, Jianming; Pedersen, John; Hopper, John L.; Milne, Roger; Klim, Aleksandra; Carballo, Ana; Lobato-Busto, Ramón; Peleteiro, Paula; Calvo, Patricia; Aguado, Miguel; Ruiz-Dominguez, José Manuel; Cecchini, Lluís; Mengual, Lourdes; Alcaraz, Antonio; Bustamante, Mariona; Gracia-Lavedan, Esther; Dierssen-Sotos, Trinidad; Gomez-Acebo, Ines; Pow-Sang, Julio; Park, Hyun; Zachariah, Babu; Kluzniak, Wojciech; Kolb, Suzanne; Klarskov, Peter; Stegmaier, Christa; Vogel, Walther; Herkommer, Kathleen; Bohnert, Philipp; Maia, Sofia; Silva, Maria P.; De Langhe, Sofie; Thierens, Hubert; Tan, Meng H.; Ong, Aik T.; Kastelan, Zeljko; Popov, Elenko; Kachakova, Darina; Mitkova, Atanaska; Vlahova, Aleksandrina; Dikov, Tihomir; Christova, Svetlana; Carracedo, Angel; Bangma, Christopher; Schroder, F. H.; Cenee, Sylvie; Tretarre, Brigitte; Rebillard, Xavier; Mulot, Claire; Sanchez, Marie; Adolfsson, Jan; Stattin, Par; Johansson, Jan-Erik; Cavalli-Bjoerkman, Carin; Karlsson, Ami; Broms, Michael; Wu, Huihai; Tillmans, Lori; Riska, Shaun; Freedman, Matthew; Wiklund, Fredrik; Chanock, Stephen; Henderson, Brian E.; Easton, Douglas F.; Haiman, Christopher A.; Eeles, Rosalind A.; Conti, David V.; Kote-Jarai, Zsofia
    Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling.
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    Grain Intake and Clinical Outcome in Stage III Colon Cancer: Results From CALGB 89803 (Alliance)
    (Oxford University Press, 2018) Brown, Justin C; Zhang, Sui; Niedzwiecki, Donna; Saltz, Leonard B; Mayer, Robert J; Mowat, Rex B; Whittom, Renaud; Hantel, Alexander; Benson, Al; Atienza, Daniel; Messino, Michael; Kindler, Hedy; Venook, Alan; Ogino, Shuji; Li, Yanping; Zhang, Xuehong; Ng, Kimmie; Willett, Walter; Giovannucci, Edward; Fuchs, Charles S; Meyerhardt, Jeffrey A
    Abstract Background: Energy balance–related risk factors for colon cancer recurrence and mortality—type II diabetes, hyperinsulinemia, inflammation, and visceral obesity—are positively correlated with consumption of refined grains and negatively correlated with consumption of whole grains. We examined the relationship between the consumption of refined and whole grains with cancer recurrence and mortality in a cohort of patients with colon cancer. Methods: We conducted a prospective observational study of 1024 patients with stage III colon cancer who participated in a randomized trial of postoperative chemotherapy. Patients reported consumption of refined and whole grains using a food frequency questionnaire during and six months after chemotherapy. The primary outcome was disease-free survival (DFS). Multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox regression models. All P values are two-sided. Results: During a median follow-up of 7.3 years, 394 patients experienced a DFS event. The hazard ratio for DFS was 1.56 (95% CI = 1.09 to 2.24) for patients consuming three or more servings per day of refined grains compared with patients consuming less than one serving per day (Ptrend = .005). The hazard ratio for DFS was 0.89 (95% CI = 0.66 to 1.20) for patients consuming three or more servings per day of whole grains compared with patients consuming less than one serving per day (Ptrend = .54). The hazard ratio for DFS of substituting one serving per day of refined grain with one serving per day of whole grain was 0.87 (95% CI = 0.79 to 0.96, P = .007). Conclusions: The choice of grain consumed may be associated with cancer recurrence and mortality. Future studies are necessary to confirm our findings and to inform the design of randomized trials.
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    Association between Vitamin D Genetic Risk Score and Cancer Risk in a Large Cohort of U.S. Women
    (MDPI, 2018) Chandler, Paulette; Tobias, Deirdre; Wang, Lu; Smith-Warner, Stephanie; Chasman, Daniel; Rose, Lynda; Giovannucci, Edward; Buring, Julie; Ridker, Paul; Cook, Nancy; Manson, JoAnn; Sesso, Howard
    Some observational studies suggest an inverse association between circulating 25-hydroxyvitamin D (25OHD) and cancer incidence and mortality. We conducted a Mendelian randomization analysis of the relationship between a vitamin D genetic risk score (GRS, range 0–10), comprised of five single nucleotide polymorphisms (SNPs) of vitamin D status in the DHCR7, CYP2R1 and GC genes and cancer risk among women. Analysis was performed in the Women’s Genome Health Study (WGHS), including 23,294 women of European ancestry who were cancer-free at baseline and followed for 20 years for incident cancer. In a subgroup of 1782 WGHS participants with 25OHD measures at baseline, the GRS was associated with circulating 25OHD mean (SD) = 67.8 (26.1) nmol/L, 56.9 (18.7) nmol/L in the lowest versus 73.2 (27.9) nmol/L in the highest quintile of the GRS (p trend < 0.0001 across quintiles). However, in age-adjusted Cox proportional hazards models, higher GRS (reflecting higher 25OHD levels) was not associated (cases; Hazard Ratio (HR) (95% Confidence Interval (CI)), p-value) with incident total cancer: (n = 3985; 1.01 (1.00–1.03), p = 0.17), breast (n = 1560; 1.02 (0.99–1.05), p = 0.21), colorectal (n = 329; 1.06 (1.00–1.13), p = 0.07), lung (n = 330; 1.00 (0.94–1.06), p = 0.89) or total cancer death (n = 770; 1.00 (0.96–1.04), p = 0.90). Results were similar in fully-adjusted models. A GRS for higher circulating 25OHD was not associated with cancer incidence or mortality.
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    Fusobacterium nucleatum in Colorectal Carcinoma Tissue According to Tumor Location
    (Nature Publishing Group, 2016) Mima, Kosuke; Cao, Yin; Chan, Andrew; Qian, Zhi Rong; Nowak, Jonathan; Masugi, Yohei; Shi, Yan; Song, Mingyang; da Silva, Annacarolina; Gu, Mancang; Li, Wanwan; Hamada, Tsuyoshi; Kosumi, Keisuke; Hanyuda, Akiko; Liu, Li; Kostic, Aleksandar; Giannakis, Marios; Bullman, Susan; Brennan, Caitlin; Milner, Danny; Baba, Hideo; Garraway, Levi; Meyerhardt, Jeffrey; Garrett, Wendy; Huttenhower, Curtis; Meyerson, Matthew; Giovannucci, Edward; Fuchs, Charles; Nakashima, Reiko; Ogino, Shuji
    Objectives: Evidence suggests a possible role of Fusobacterium nucleatum in colorectal carcinogenesis, especially in right-sided proximal colorectum. Considering a change in bowel contents and microbiome from proximal to distal colorectal segments, we hypothesized that the proportion of colorectal carcinoma enriched with F. nucleatum might gradually increase along the bowel subsites from rectum to cecum. Methods: A retrospective, cross-sectional analysis was conducted on 1,102 colon and rectal carcinomas in molecular pathological epidemiology databases of the Nurses’ Health Study and the Health Professionals Follow-up Study. We measured the amount of F. nucleatum DNA in colorectal tumor tissue using a quantitative PCR assay and equally dichotomized F. nucleatum-positive cases (high vs. low). We used multivariable logistic regression analysis to examine the relationship of a bowel subsite variable (rectum, rectosigmoid junction, sigmoid colon, descending colon, splenic flexure, transverse colon, hepatic flexure, ascending colon, and cecum) with the amount of F. nucleatum. Results: The proportion of F. nucleatum-high colorectal cancers gradually increased from rectal cancers (2.5% 4/157) to cecal cancers (11% 19/178), with a statistically significant linear trend along all subsites (P<0.0001) and little evidence of non-linearity. The proportion of F. nucleatum-low cancers was higher in rectal, ascending colon, and cecal cancers than in cancers of middle segments. Conclusions: The proportion of F. nucleatum-high colorectal cancers gradually increases from rectum to cecum. Our data support the colorectal continuum model that reflects pathogenic influences of the gut microbiota on neoplastic and immune cells and challenges the prevailing two-colon (proximal vs. distal) dichotomy paradigm.
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    Sugar-Sweetened Beverage Intake and Cancer Recurrence and Survival in CALGB 89803 (Alliance)
    (Public Library of Science, 2014) Fuchs, Michael A.; Sato, Kaori; Niedzwiecki, Donna; Ye, Xing; Saltz, Leonard B.; Mayer, Robert J.; Mowat, Rex B.; Whittom, Renaud; Hantel, Alexander; Benson, Al; Atienza, Daniel; Messino, Michael; Kindler, Hedy; Venook, Alan; Ogino, Shuji; Wu, Kana; Willett, Walter; Giovannucci, Edward; Meyerhardt, Jeffrey A.
    Background: In colon cancer patients, obesity, sedentary lifestyle, and high dietary glycemic load have been associated with increased risk of cancer recurrence. High sugar-sweetened beverage intake has been associated with obesity, diabetes, and cardio-metabolic diseases, but the influence on colon cancer survival is unknown. Methods: We assessed the association between sugar-sweetened beverage consumption on cancer recurrence and mortality in 1,011 stage III colon cancer patients who completed food frequency questionnaires as part of a U.S. National Cancer Institute-sponsored adjuvant chemotherapy trial. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated with Cox proportional hazard models. Results: Patients consuming ≥2 servings of sugar-sweetened beverages per day experienced an adjusted HR for disease recurrence or mortality of 1.67 (95% CI, 1.04–2.68), compared with those consuming <2 servings per month (Ptrend = 0.02). The association of sugar-sweetened beverages on cancer recurrence or mortality appeared greater among patients who were both overweight (body mass index ≥25 kg/m2) and less physically active (metabolic equivalent task-hours per week <18) (HR = 2.22; 95% CI, 1.29–3.81, Ptrend = 0.0025). Conclusion: Higher sugar-sweetened beverage intake was associated with a significantly increased risk of cancer recurrence and mortality in stage III colon cancer patients.
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    Simple Methods of Determining Confidence Intervals for Functions of Estimates in Published Results
    (Public Library of Science, 2014) Fitzmaurice, Garrett; Lipsitz, Stuart; Natarajan, Sundar; Gawande, Atul; Sinha, Debajyoti; Greenberg, Caprice; Giovannucci, Edward
    Often, the reader of a published paper is interested in a comparison of parameters that has not been presented. It is not possible to make inferences beyond point estimation since the standard error for the contrast of the estimated parameters depends upon the (unreported) correlation. This study explores approaches to obtain valid confidence intervals when the correlation is unknown. We illustrate three proposed approaches using data from the National Health Interview Survey. The three approaches include the Bonferroni method and the standard confidence interval assuming (most conservative) or (when the correlation is known to be non-negative). The Bonferroni approach is found to be the most conservative. For the difference in two estimated parameter, the standard confidence interval assuming yields a 95% confidence interval that is approximately 12.5% narrower than the Bonferroni confidence interval; when the correlation is known to be positive, the standard 95% confidence interval assuming is approximately 38% narrower than the Bonferroni. In summary, this article demonstrates simple methods to determine confidence intervals for unreported comparisons. We suggest use of the standard confidence interval assuming if no information is available or if the correlation is known to be non-negative.