tbuckley/cabot-search huggingface dataset:
Neurocognitive, Psychosocial, and Quality of Life Outcomes in Adult Survivors of Childhood Non-Hodgkin Lymphoma in the St. Jude Lifetime (SJLIFE) Cohort
Authors: Matthew J. Ehrhardt, Daniel A. Mulrooney, Chenghong Li, John T. Sandlund, Tara M. Brinkman, I-Chan Huang, DeoKumar Srivastava, Kirsten K. Ness, Leslie L. Robison, Melissa M. Hudson, Kevin R. Krull
Journal: Blood (2015)
The Balance Between Access and Quality in Transcatheter Valve Therapies
Authors: Patrick T. O’Gara
Journal: JAMA Cardiology (2017)

Sahil Khera, MD, MPH; Dhaval Kolte, MD, PhD; Tanush Gupta, MD; Andrew Goldsweig, MD; Poonam Velagapudi, MD, MS; Ankur Kalra, MD; Gilbert H. L. Tang, MD, MSc, MBA; Wilbert S. Aronow, MD; Gregg C. Fonarow, MD; Deepak L. Bhatt, MD, MPH; Herbert D. Aronow, MD, MPH; Neal S. Kleiman, MD; Michael Reardon, MD; Paul C. Gordon, MD; Barry Sharaf, MD; J. Dawn Abbott, MD
Functional role of CCL5/RANTES for hepatocellular carcinoma progression during chronic liver disease
Authors: A. Mohs, N. Kuttkat, J. Reißing, H.W. Zimmermann, R. Sonntag, S.A. Youssef, A. de Bruin, F.J. Cubero, C. Trautwein
Journal: Journal of Hepatology (2017)
Abstract A31: A novel 3D osteoblastic niche assay is useful to study the characteristics of bone metastatic cancers
Authors: Seunghwan Lim, Tej Pareek, Rasmi Palassery, John Letterio
Journal: Cancer Research (2016)

Abstract (Background) Many patients with metastatic cancer (i.e. Prostate, breast, lung, kidney, and melanoma) struggle with skeletal metastases which is frequently causing cancer-related death. Thus, there is an imminent demand for a better understanding of how bone-homing cancers communicate and physically interact with the bone microenvironment. It is known that cancer-stromal cell interaction in bone marrow is a pivotal step in determining bone metastasis and tumor behavior and is seen in the events of competition with HSC for the osteoblastic niche, entering dormant status, and enhanced tumor growth. However, the lack of biologically relevant assay platforms has hampered interrogation of the mechanism of cancer-bone interaction as well as the development of bone-targeted anti-metastatic drugs. (Methods) Here, we present a novel method that can measure the bone-homing ability of cancers by co-culturing 3D osteoblastic niche (3D-ObN) spheroids derived from human mesenchymal stem cells along with reporter cell lines carrying hypoxia response element (HRE)-regulated reporter genes (pGF-HRE4-GFP/SecNLuc). First, the migration ability of metastatic cancers into the 3D-ObN was examined by analyses of O.C.T. frozen section images using confocal microscopy. Next, the metastatic ability of highly metastatic cancers were compared to normal epithelial cells and assessed by using either fluorescent microscopy (IncuCyte) or a luminometer. (Results) The HRE-driven reporter was activated in a 3D-ObN spheroid-specific manner in response to the nature of the hypoxia gradient within the spheroid. While the 3D-ObN provided signals that suppressed cancer cell proliferation, highly metastatic cancer cells displayed higher homing ability in the 3D-ObN assay relative to the normal epithelial cells. Prostate cancer cells expressing putative cancer stem cell markers (CD44/CD133high) showed higher homing ability compared to CD44/CD133low populations. (Conclusion) This assay platform is the first of its kind through the fact that it mimics cancer-osteoblastic niche interactions and allows for quantification of the ability of cancer cells including cancer stem-like cells to invade and anchor in osteoblastic niche. Furthermore, this assay system can be readily amended to an efficient and effective high throughput screening system useful for identifying molecules potentially preventive to critical process of bone metastases. Citation Format: Seunghwan Lim, Tej Pareek, Rasmi Palassery, John Letterio. A novel 3D osteoblastic niche assay is useful to study the characteristics of bone metastatic cancers. [abstract]. In: Proceedings of the AACR Special Conference on Tumor Metastasis; 2015 Nov 30-Dec 3; Austin, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(7 Suppl):Abstract nr A31.
M480, a novel non-bile acid FXR agonist, shows improvement across multiple parameters in a diet-induced obese mouse model with biopsy-confirmed NASH
Authors: B. Wagner, D. Brigham, K.-J. Lee, A. Ortiz, N. Lu, K. Douglas, S. Govek, M. Feigh, S. Veidal, N. Vrang, K. Song, N. Smith, H. Dedman, A. Milik
Journal: Journal of Hepatology (2017)
Efficacy and safety of Simeprevir-containing hepatitis C therapy in patients on opiate substitution therapy
Authors: J. Dillon, S. Mauss, C. Nalpas, C. Bicer, M. Schlag, I. Lonjon-Domanec, W. Jessner, M. Beumont-Mauviel, R. Kalmeijer
Journal: Journal of Hepatology (2017)
Different Pediatric Survival After Cardiac Arrest
Authors: Camila Olarte Parra, Linda Nyanchoka, Els Goetghebeur
Journal: JAMA Pediatrics (2017)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Pediatrics HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Pediatrics journal
The selective FXR agonist EYP001 is well tolerated in healthy subjects and has additive anti-HBV effect with nucleoside analogues in HepaRG cells
Authors: S. Joly, M. Porcherot, P. Radreau, J. Vonderscher, P. André, E. Meldrum, G. Arold, J. Van de Wetering de Rooij, C. Staner, C. Laveille, P. Scalfaro
Journal: Journal of Hepatology (2017)
Impact of NASH, gender, fasting glucose and body mass index on the liver fibrosis transition rate (FTR) in metabolic liver disease (MLD)
Authors: T. Poynard, O. Deckmyn, V. Peta, M. Munteanu, R. Pais, Y. Ngo, F. Drane, C. Housset, V. Ratziu
Journal: Journal of Hepatology (2017)
The impact of initial cerebrospinal fluid (CSF) findings on outcome among patients with NCI standard (SR) and high-risk (HR) B-lymphoblastic leukemia (ALL): A report from the Children’s Oncology Group (COG) Studies AALL0331 and AALL0232.
Authors: Naomi Joan Winick, Meenakshi Devidas, Kelly W. Maloney, Eric Larsen, Leonard A. Mattano, Michael J. Borowitz, Andrew J Carroll, Julie M Gastier-Foster, Nyla A. Heerema, Cheryl L. Willman, Brent L. Wood, Mignon L. Loh, Elizabeth A. Raetz, Stephen Hunger, William L. Carroll
Journal: Journal of Clinical Oncology (2014)

10016 Background: To determine the prognostic significance of variable numbers of white cells (WBC), blasts and/or red cells (RBC) in diagnostic CSF samples of ALL patients, COG protocols, AALL0331 (SR)/AALL0232 (HR) incorporated a uniform CSF and risk group classification schema for all newly diagnosed patients. Methods: Patients, 1-31 years, were enrolled on the classification protocol, AALL03B1. CSF status was designated as: CNS1-no blasts; CNS2a- < 5 WBC + blasts + < 10 RBC/ml; CNS2b-< 5 WBC + blasts + > 10 RBC/ml; CNS2c- > 5 WBC + blasts, with excess WBC proportional to RBC; CNS3a- > 5 WBC + blasts + < 10 RBC/ml; CNS3b - > 5 WBC + blasts + > 10 RBC/ml, with excess WBC not proportional to RBC; CNS3c- clinical signs of CNS leukemia (e.g. cranial nerve deficits, hypothalamic disease). Only CNS1 patients could be allocated to the SR-low risk arm. CNS2 status did not impact therapy but CNS3 patients received augmented therapy and 1800 cGY cranial radiation. Results: In multivariate analysis that includes age and WBC at diagnosis and Day 29 MRD < 0.1%, the presence of CSF blasts, regardless of the number of CSF WBC or RBC is an independent adverse predictor of outcome for NCI SR (all of whom received dexamethasone) and HR patients. The EFS difference reflects a significant difference in the incidence of CNS, not marrow relapse in CNS1vs CNS2/3 patients (see Table). Conclusion: Even low levels of CNS leukemia, regardless of the number of RBCs, are associated with a lower EFS/OS and an increase in the likelihood of CNS relapse. The use of dexamethasone in NCI SR patients did not negate the impact of CSF blasts. Further augmentation of CNS directed therapy is needed for patients with CNS2/3 disease. Clinical trial information: NCY00482352. Cohort CNS 1 CNS 2 a, b, c CNS 3 a, b, c p-value 5 yr EFS N 5 yr EFS N 5 yr EFS N Overall NCI SR/HR 85.3 ± .56% 7214 76 ± 2% 836 75.7 ± 5.2% 124 < 0.0001 NCI SR-AALL0331 89.9% ± .59% 4721 85 ± 2.3% 415 82 ± 7.1% 52 0.0003 NCI HR-AALL0232 76.5 ± 1.2% 2493 67.1± 3% 421 70.5 ± 7.2% 72 < 0.0001 Cumulative Incidence of Marrow relapse 6.3 ± .3% 7395 7.1 ± .9% 857 9.3 ± 2.9% 127 0.18 CNS relapse 2.9 ± .21% 7.8 ± 1% 5.9 ± 2.2% < 0.0001
Lenalidomide with Ipilimumab for Lymphoid Malignancies after Allogeneic or Autologous Stem Cell Transplantation (SCT)
Authors: Issa F. Khouri, Irina Fernandez Curbelo, Francesco Turturro, Denái R. Milton, Rang A Kim, Elias J. Jabbour, Roland L Bassett, Luis M Vence, Padmanee Sharma, Alison M Gulbis
Journal: Blood (2016)
Tamoxifen-associated hot flash severity and its correlation with endoxifen concentration.
Authors: Simon Daniel Baxter, Wendy A. Teft, Yun-Hee Choi, Eric Winquist, Richard B. Kim
Journal: Journal of Clinical Oncology (2014)

e20657 Background: Tamoxifen is the most widely used anti-estrogen therapy for the treatment and prevention of hormone receptor positive breast cancers. However, its use is limited in some patients due to adverse effects including significant hot flash symptoms. Tamoxifen undergoes hepatic bioactivation by CYP2D6 and CYP3A4 to form the active metabolite endoxifen considered to be major determinant of its therapeutic efficacy, but also postulated to contribute to tamoxifen-associated adverse effects. It remains unclear whether systemic exposure of endoxifen or polymorphisms in drug metabolizing enzymes are associated with the frequency and severity of hot flashes. Methods: 132 female breast cancer patients on tamoxifen were recruited to this study. Self-reported surveys were used to assess tamoxifen side effects experienced in the prior-one week period, and to calculate hot flash severity scores. Blood samples were obtained to determine tamoxifen and metabolite levels and CYP2D6 and CYP3A4 genotypes. Results: The majority of participants (77%) experienced hot flashes, with 11% experiencing severe or very severe symptoms. We observed an inverse correlation between endoxifen concentration and hot flash severity score following adjustment for age, BMI, and menopausal status in patients with non-zero scores (p < 0.001). CYP2D6 genotype was not significantly associated with hot flash scores in patients taking no known inhibitory medications. Interestingly, CYP3A4*22 carriers were more likely to have a zero score compared to wild-type patients (p < 0.01; odds ratio 8.87 (1.78-44.14)). Conclusions: Our data demonstrate that higher endoxifen levels were associated with lower hot flash severity scores thus hot flash symptoms may not be predictive of tamoxifen efficacy.
Response to: ‘<i>HLA-A* 31:01</i> is not associated with the development of methotrexate pneumonitis in the UK population: results from a genome wide association study’ by Bluett <i>et al</i>
Authors: Hiroshi Furukawa, Shomi Oka, Kota Shimada, Naoyuki Tsuchiya, Shigeto Tohma
Journal: Annals of the Rheumatic Diseases (2017)

We appreciate the comments by Bluett et al 1 on our report of an association of HLA-A*31:01 with methotrexate-induced interstitial lung disease (ILD) in patients with rheumatoid arthritis (RA).2 They have tried to reveal the genetic factors associated with methotrexate-induced ILD, but found no significant association except three suggestive loci in chromosome 1, 9 and 14. This study did not show the association of A*31:01 with methotrexate-induced ILD, though the p value of the analysis was still 0.21 in spite of the small sample size with 62 cases and 175 controls. The meta-analysis with our previous study2 or other forthcoming HLA association studies on methotrexate-induced ILD may reveal more conclusive results in the future.

Genetic factors would be involved in the pathogenesis of methotrexate-induced ILD, because the susceptibility of methotrexate-induced ILD in Japanese patients with RA are thought to be higher than other ethnic groups or patients with other autoimmune diseases.3 4 However, there are few reports of genome-wide association study of drug-induced ILD.5 Since the prevalence of drug-induced ILD is low and the clinical conditions of the patients with drug-induced ILD are various,6 genetic analyses …
Experimental approach to IGF-1 therapy in acute liver damage: acute injury by carbon tetrachloride in controls and mice with partial IGF-1 deficiency
Authors: L.A. Morales-Garza, J.E. Puche, R.G. de la Garza, Ú. Muñoz-Morón, I. Castilla-Cortázar
Journal: Journal of Hepatology (2017)
Secukinumab re‐initiation achieves regain of high response levels in patients who interrupt treatment for moderate to severe plaque psoriasis
Authors: A. Blauvelt, K. Reich, R.B. Warren, J.C. Szepietowski, B. Sigurgeirsson, S. K. Tyring, I. Messina, V. Bhosekar, J. Oliver, C. Papavassilis, J. Frueh, R.G.B. Langley
Journal: British Journal of Dermatology (2017)

Clinical trials of biologic therapies in psoriasis usually evaluate fixed dosing regimens. It is well-known, however, that patients prescribed biologics may occasionally need to interrupt therapy for reasons such as surgery, changes in healthcare coverage, or pregnancy.1 Consequently, dermatologists need to know whether interruption of biologic therapy may be associated with diminished response upon retreatment. We analyzed data from a randomised withdrawal trial of secukinumab in subjects with moderate to severe plaque psoriasis to ascertain the effects of retreatment.

This article is protected by copyright. All rights reserved.
External validation of the ITA.LI.CA prognostic system for patients with hepatocellular carcinoma: a multicenter cohort study
Authors: M. Borzio, E. Dionigi, A. Rossini, M. Marignani, R. Sacco, I. De Sio, E. Bertolini, G. Francica, A. Giacomin, G. Parisi, S. Vicari, A. Toldi, A. Salmi, S. Boccia, A. Maringhini, F. Fornari
Journal: Journal of Hepatology (2017)
Dendritic cells pulsed with an anti-idiotype antibody mimicking Her-2 induced protective antitumor immunity in mice transgenic for human Her-2
Authors: Asim Saha, Palash Mallick, Sunil Chatterjee, Kenneth Foon, Wei-Zen Wei, Malaya Chatterjee
Journal: Cancer Research (2008)

AACR Annual Meeting-- Apr 12-16, 2008; San Diego, CA

5293 

The ErbB-2 (Her-2) proto-oncogene is overexpressed in 20-30% of human breast cancers and is associated with high recurrence risk. The oncogenic potential of Her-2, together with its elevated expression in tumors, cell surface localization, and immunogenicity in some patients, make this oncoprotein an ideal target for immunotherapy. A number of different approaches have been investigated in both human and animal studies in an attempt to develop an effective Her-2 vaccine. To test the efficacy of immune-based strategies in eliciting an antitumor response, we have developed and characterized a murine monoclonal anti-idiotype (Id) antibody, 6D12 that mimics a specific epitope of Her-2 and can be used as a surrogate antigen for Her-2. Anti-Id 6D12 vaccine also induced protective Her-2 specific antitumor immunity in immunocompetent C57BL/6 mice. Since Her-2 is a self-antigen and the amino acid sequence is typically unmodified in human cancer, immune tolerance to this tumor-associated antigen is expected in human. Therefore, in the present study we have tested the vaccine potential of anti-Id 6D12 in tolerant hosts. We have demonstrated that immunization of human Her-2 transgenic mice with bone marrow-derived mature dendritic cells (DCs) loaded with 6D12 could reverse Her-2 unresponsiveness and result in the induction of Her-2-specific humoral and cellular immune responses and protection against tumors expressing Her-2. The presence of anti-Her-2 antibodies in immunized mice were determined by ELISA and flow cytometry. Antibody dependent cellular cytotoxicity against human Her-2 transfected EL4 cells (EL4-Her-2) was also observed in presence of immune sera. Immune-splenic lymphocytes when stimulated in vitro , showed increased proliferative CD4+ Th1 type T-cell responses and secreted significantly high levels of Th1 cytokines (IFN-γ, IL-2, TNF-α) and low levels of Th2 cytokines (IL-4, IL-10). Antigen-specific proliferative responses were dependent on the functions of CD4, MHC II, B7-2, CD40, CD28, and CD25. Her-2 transgenic mice immunized with 6D12 were protected against a challenge with lethal doses of EL4-Her-2 cells, whereas no protection was observed against parental EL4 cells or when mice were immunized with an unrelated anti-Id antibody and challenged with EL-4-Her-2 cells. These findings suggest that 6D12-DC vaccinations were able to break immune tolerance to Her-2 and induced protective antitumor immune responses in this murine model transgenic for human Her-2. Supported by the NIH grant RO1 CA91878 and a pilot grant from The Barrett Cancer Center, Cincinnati, Ohio.
The long-term outcomes of patients with the Barcelona Clinic Liver Cancer stage 0 hepatocellular carcinoma after radiofrequency ablation therapy
Authors: P.-C. Lee, C.-W. Su, Y.-Y. Chiou, P.-C. Chen, C.-Y. Chang, Y.-H. Huang, T.-I. Huo, M.-C. Hou, H.-C. Lin, J.-C. Wu
Journal: Journal of Hepatology (2017)
Liver stiffness and serum fibrosis biomarker variations after DAAs treatment: predictive role in hepatocellular carcinoma development in in cirrhotic patients
Authors: F. Ravaioli, G. Mazzella, P. Andreone, F. Conti, S. Brillanti, F. Buonfiglioli, I. Serio, G. Verucchi, M.L.B. Reggiani, G. Marasco, A. Colecchia, D. Festi
Journal: Journal of Hepatology (2017)
Evaluation of potential futility in alcoholic hepatitis – multicentre study
Authors: R. Barosa, C. Teixeira, A. Antunes, J. Pinto, J. Branco, P. Marcos, S. Marques, A.P. Oliveira, H. Guerreiro, A. Banhudo, A. Martins, J. Reis, H. Vasconcelos, C. Chagas, C. Fonseca, R. Palma
Journal: Journal of Hepatology (2017)
Overexpression of arrest-defective protein 1 in dysplastic hepatic nodule as a possible marker of malignant potential
Authors: H.J. Kang, D. Lee, Y.-H. Chung, J.H. Seo, J.-H. Park, H.S. Lee, J. Choi, M.-K. Jang, S.H. Ryu, Y.J. Lee, E. Yu, K.-W. Kim
Journal: Journal of Hepatology (2017)
Hepatocyte microvesicle levels predict 6-month survival in patients with cirrhosis: results of a prospective study on 242 patients
Authors: A. Payancé, G. Silva-Junior, J. Bissonnette, M. Tanguy, O. Roux, C. Levi, O. Nekachtali, A. Baiges, V.H. Gea, D. Lebrec, R. Moreau, D. Valla, F. Durand, C.M. Boulanger, J.-C. Garcia-Pagan, P.-E. Rautou
Journal: Journal of Hepatology (2017)
Inhibition of Human Erythropoiesis during Inflammation Is Mediated By High Mobility Group Box Protein 1 (HMGB1) through Decreased Commitment of Hematopoietic Stem Cells to the Erythroid Lineage and By Increased Apoptosis of Terminally Differentiating Erythroblasts
Authors: Brian M. Dulmovits, Julien Papoin, John Hale, Jian Hua Li, Huan Yang, Betty Diamond, Kevin J. Tracey, Narla Mohandas, Jeffrey M Lipton, Lionel Blanc
Journal: Blood (2016)
Abstract 15520: The Association of a Genetic Risk Score With Presence of Polyvascular Disease
Authors: Zi Ye, Erin Austin, Adelaide M Arruda-Olson, Iftikhar J Kullo
Journal: Circulation (2015)

Background: Atherosclerotic cardiovascular disease (ASCVD) often affects &gt; 1 arterial location (polyvascular disease, PVD). The risk of adverse outcomes increases with the number of arterial territories involved. The genetic susceptibility to PVD is unknown. Hypothesis: We hypothesized that a genetic risk score representing cumulative effects of susceptibility variants to ASCVD is associated with presence of PVD. Methods: We searched genome-wide association study (GWAS) catalog to identify genetic variants associated with coronary heart disease (CHD), ischemic stroke, peripheral arterial disease (PAD) or abdominal aortic aneurysm (AAA). No variants were reported to be associated with PVD in ≥ 3 arterial territories at GWAS significance. 10 loci were associated with PVD in 2 arterial territories. We calculated a multi-locus GRS using 10 lead single nuclear polymorphisms (SNP) from these distinct loci (1 per each loci) in 7486 participants in Mayo Vascular Disease Biorepository (age 68±10 years, 61% men, 31% with CHD; 27% carotid artery stenosis; 39% PAD; 14% AAA; 38% without any of these vascular diseases). Results: Of all participants 34% had PVD (2%, 10% and 22% with exact 4, 3 and 2 arterial territories involved respectively). A higher GRS was associated with greater number of arterial territories involved (P for trend of ANOVA &lt;0.001). Patients with PVD in ≥ 3 arterial locations had higher GRS compared to those with 2 arterial locations involved after adjustment for age, sex and cardiovascular risk factors (P =0.008). One unit increase in GRS was associated with 9% higher likelihood for each additional arterial territory involved after adjustment for all covariates (odds ratio from ordinal regression model= 1.09, P &lt;0.001). The result remained significant after further adjustment for combinations of AAA, CHD, carotid arterial stenosis and PAD (all P ≤ 0.01). 5 Of the 10 SNPs were each associated with presence of PVD after adjustment for all covariates (all P &lt;0.01). None of them remained significant after further adjustment for combinations of PVD in different arterial territories (all P ≥ 0.4). Conclusions: A GRS derived from 10 SNPs of ASCVD is associated with PVD,suggesting genetic contribution to the dimension of PVD that may lead to adverse outcome.
Infant Feeding and Risk of Type 1 Diabetes in Two Large Scandinavian Birth Cohorts
Authors: Nicolai A. Lund-Blix, Stine Dydensborg Sander, Ketil Størdal, Anne-Marie Nybo Andersen, Kjersti S. Rønningen, Geir Joner, Torild Skrivarhaug, Pål R. Njølstad, Steffen Husby, Lars C. Stene
Journal: Diabetes Care (2017)

Our aim was to study the relation between the duration of full and any breastfeeding and risk of type 1 diabetes.We included two population-based cohorts of children followed from birth (1996-2009) to 2014 (Denmark) or 2015 (Norway). We analyzed data from a total of 155,392 children participating in the Norwegian Mother and Child Cohort Study (MoBa) and the Danish National Birth Cohort (DNBC). Parents reported infant dietary practices when their child was 6 and 18 months old. The outcome was clinical type 1 diabetes, ascertained from nationwide childhood diabetes registries. Hazard ratios (HRs) were estimated using Cox regression.Type 1 diabetes was identified in 504 children during follow-up, and the incidence of type 1 diabetes per 100,000 person-years was 30.5 in the Norwegian cohort and 23.5 in the Danish cohort. Children who were never breastfed had a twofold increased risk of type 1 diabetes compared with those who were breastfed (HR 2.29 [95% CI 1.14-4.61] for no breastfeeding vs. any breastfeeding for ≥12 months). Among those who were breastfed, however, the incidence of type 1 diabetes was independent of duration of both full breastfeeding (HR per month 0.99 [95% CI 0.97-1.01]) and any breastfeeding (0.97 [0.92-1.03]).Suggestive evidence supports the contention that breastfeeding reduces the risk of type 1 diabetes. Among those who were breastfed, however, no evidence indicated that prolonging full or any breastfeeding was associated with a reduced risk of type 1 diabetes.