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  • Author: David C Chang x
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Ryan K Orosco, Timon Hussain, Julia E Noel, David C Chang, Chrysoula Dosiou, Erik Mittra, Vasu Divi and Lisa A Orloff

Radioactive iodine (RAI) is a key component in the treatment of differentiated thyroid cancer. RAI has been recommended more selectively in recent years as guidelines evolve to reflect risks and utility in certain patient subsets. In this study we sought to evaluate the survival impact of radioactive iodine in specific thyroid cancer subgroups. Nationwide retrospective cohort study of patients using the National Cancer Database (NCDB) from 2004 to 2012 and Surveillance, Epidemiology, and End Results (SEER) database from 1992 to 2009 examining patients with differentiated thyroid cancer treated with or without RAI. Primary outcomes included all-cause mortality (NCDB and SEER), and cancer-specific mortality (SEER). Cox multivariate survival analyses were applied to each dataset, and in 135 patient subgroups based on clinical and non-clinical parameters. A total of 199,371 NCDB and 77,187 SEER patients were identified. RAI was associated with improved all-cause mortality (NCDB: RAI hazard ratio (HR) 0.55, P < 0.001; SEER: HR 0.64, P < 0.001); and cancer-specific mortality (SEER: HR 0.82, P = 0.029). Iodine therapy showed varied efficacy within each subgroup. Patients with high-risk disease experienced the greatest benefit in all-cause mortality, followed by intermediate-risk, then low-risk subgroups. Regarding cancer-specific mortality, radioactive iodine therapy was protective in high-risk patients, but did not achieve statistical significance in most intermediate-risk subgroups. Low-risk T1a subgroups demonstrated an increased likelihood of cancer-specific mortality with iodine therapy. The efficacy of RAI in patients with differentiated thyroid cancer varies by disease severity. A negative cancer-specific survival association was identified in patients with T1a disease. These findings warrant further evaluation with prospective studies.

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Catherine M Olsen, Christina M Nagle, David C Whiteman, Roberta Ness, Celeste Leigh Pearce, Malcolm C Pike, Mary Anne Rossing, Kathryn L Terry, Anna H Wu, The Australian Cancer Study (Ovarian Cancer), Australian Ovarian Cancer Study Group, Harvey A Risch, Herbert Yu, Jennifer A Doherty, Jenny Chang-Claude, Rebecca Hein, Stefan Nickels, Shan Wang-Gohrke, Marc T Goodman, Michael E Carney, Rayna K Matsuno, Galina Lurie, Kirsten Moysich, Susanne K Kjaer, Allan Jensen, Estrid Hogdall, Ellen L Goode, Brooke L Fridley, Robert A Vierkant, Melissa C Larson, Joellen Schildkraut, Cathrine Hoyo, Patricia Moorman, Rachel P Weber, Daniel W Cramer, Allison F Vitonis, Elisa V Bandera, Sara H Olson, Lorna Rodriguez-Rodriguez, Melony King, Louise A Brinton, Hannah Yang, Montserrat Garcia-Closas, Jolanta Lissowska, Hoda Anton-Culver, Argyrios Ziogas, Simon A Gayther, Susan J Ramus, Usha Menon, Aleksandra Gentry-Maharaj and Penelope M Webb

Whilst previous studies have reported that higher BMI increases a woman's risk of developing ovarian cancer, associations for the different histological subtypes have not been well defined. As the prevalence of obesity has increased dramatically, and classification of ovarian histology has improved in the last decade, we sought to examine the association in a pooled analysis of recent studies participating in the Ovarian Cancer Association Consortium. We evaluated the association between BMI (recent, maximum and in young adulthood) and ovarian cancer risk using original data from 15 case–control studies (13 548 cases and 17 913 controls). We combined study-specific adjusted odds ratios (ORs) using a random-effects model. We further examined the associations by histological subtype, menopausal status and post-menopausal hormone use. High BMI (all time-points) was associated with increased risk. This was most pronounced for borderline serous (recent BMI: pooled OR=1.24 per 5 kg/m2; 95% CI 1.18–1.30), invasive endometrioid (1.17; 1.11–1.23) and invasive mucinous (1.19; 1.06–1.32) tumours. There was no association with serous invasive cancer overall (0.98; 0.94–1.02), but increased risks for low-grade serous invasive tumours (1.13, 1.03–1.25) and in pre-menopausal women (1.11; 1.04–1.18). Among post-menopausal women, the associations did not differ between hormone replacement therapy users and non-users. Whilst obesity appears to increase risk of the less common histological subtypes of ovarian cancer, it does not increase risk of high-grade invasive serous cancers, and reducing BMI is therefore unlikely to prevent the majority of ovarian cancer deaths. Other modifiable factors must be identified to control this disease.