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Amanda Schech Department of Pharmacology, Division of Biostatistics, Department of Medicine and Physiology, University of Maryland School of Medicine, University of Maryland Marlene and Stewart Greenebaum Cancer Center, Baltimore, Maryland, USA

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Stephen Yu Department of Pharmacology, Division of Biostatistics, Department of Medicine and Physiology, University of Maryland School of Medicine, University of Maryland Marlene and Stewart Greenebaum Cancer Center, Baltimore, Maryland, USA

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Olga Goloubeva Department of Pharmacology, Division of Biostatistics, Department of Medicine and Physiology, University of Maryland School of Medicine, University of Maryland Marlene and Stewart Greenebaum Cancer Center, Baltimore, Maryland, USA

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John McLenithan Department of Pharmacology, Division of Biostatistics, Department of Medicine and Physiology, University of Maryland School of Medicine, University of Maryland Marlene and Stewart Greenebaum Cancer Center, Baltimore, Maryland, USA

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Gauri Sabnis Department of Pharmacology, Division of Biostatistics, Department of Medicine and Physiology, University of Maryland School of Medicine, University of Maryland Marlene and Stewart Greenebaum Cancer Center, Baltimore, Maryland, USA

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used for in vitro studies at passage number <20. Nude mouse model of diet-induced obesity All animal studies were performed according to the guidelines and approval of the Animal Care and Use Committee of the University of Maryland, Baltimore. Female

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-15-0168
Volume/Issue:
Volume 22: Issue 4
Free access
Sunmi Park Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA

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Mark C Willingham Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA

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Jun Qi Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA

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Sheue-Yann Cheng Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA

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studies ( Guigon et al . 2009 , 2010 ). Using Thrb PV/PV Pten +/ − mice, Kim et al . found that diet-induced obesity increases tumor growth and promotes anaplastic transformation in thyroid cancer ( Kim et al . 2013 b ). Further

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-18-0071
Volume/Issue:
Volume 25: Issue 10
Free access
Grant D Foglesong Department of Cancer Biology and Genetics, The Ohio State University, Columbus, Ohio, USA
The Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio, USA

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Nicholas J Queen Department of Cancer Biology and Genetics, The Ohio State University, Columbus, Ohio, USA
The Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio, USA

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Wei Huang Department of Cancer Biology and Genetics, The Ohio State University, Columbus, Ohio, USA
The Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio, USA

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Kyle J Widstrom Department of Cancer Biology and Genetics, The Ohio State University, Columbus, Ohio, USA
The Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio, USA

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Lei Cao Department of Cancer Biology and Genetics, The Ohio State University, Columbus, Ohio, USA
The Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio, USA

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( Guy et al. 1992 , Lin et al. 2003 , Juncker-Jensen et al. 2009 ). Moreover, we carried this transgene on the C57BL/6 background, because they are more prone to diet-induced obesity (DIO) when fed a high-fat diet (HFD) and have longer tumor

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-19-0075
Volume/Issue:
Volume 26: Issue 5
Free access
Leticia M Nogueira Institute of Cell and Molecular Biology, Department of Molecular Carcinogenesis, Department of Nutritional Sciences, University of Texas at Austin, Austin, Texas 78712, USA
Institute of Cell and Molecular Biology, Department of Molecular Carcinogenesis, Department of Nutritional Sciences, University of Texas at Austin, Austin, Texas 78712, USA

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Sarah M Dunlap Institute of Cell and Molecular Biology, Department of Molecular Carcinogenesis, Department of Nutritional Sciences, University of Texas at Austin, Austin, Texas 78712, USA

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Nikki A Ford Institute of Cell and Molecular Biology, Department of Molecular Carcinogenesis, Department of Nutritional Sciences, University of Texas at Austin, Austin, Texas 78712, USA

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Stephen D Hursting Institute of Cell and Molecular Biology, Department of Molecular Carcinogenesis, Department of Nutritional Sciences, University of Texas at Austin, Austin, Texas 78712, USA
Institute of Cell and Molecular Biology, Department of Molecular Carcinogenesis, Department of Nutritional Sciences, University of Texas at Austin, Austin, Texas 78712, USA
Institute of Cell and Molecular Biology, Department of Molecular Carcinogenesis, Department of Nutritional Sciences, University of Texas at Austin, Austin, Texas 78712, USA

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mice ( n =105) were administered a diet-induced obesity (DIO) regimen consisting of ad libitum access to a 60 kcal % fat diet (D12492; Research Diets, Inc., New Brunswick, NJ, USA) for 8 weeks. Mice were then randomized to receive a control diet ( n

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-11-0213
Volume/Issue:
Volume 19: Issue 1
Free access
Srilatha Swami Department of Medicine-Endocrinology, Stanford University School of Medicine, Stanford, CA, USA

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Aruna V Krishnan Department of Pediatrics-Endocrinology, Stanford University School of Medicine, Stanford, CA, USA

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Jasmaine Williams Department of Pediatrics-Endocrinology, Stanford University School of Medicine, Stanford, CA, USA
Cancer Biology Program, Stanford University School of Medicine, Stanford, CA, USA

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Abhishek Aggarwal Department of Pediatrics-Endocrinology, Stanford University School of Medicine, Stanford, CA, USA

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Megan A Albertelli Department of Comparative Medicine, Stanford University School of Medicine, Stanford, CA, USA

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Ronald L Horst Heartland Assays Inc, Ames, IA, USA

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Brian J Feldman Department of Pediatrics-Endocrinology, Stanford University School of Medicine, Stanford, CA, USA
Cancer Biology Program, Stanford University School of Medicine, Stanford, CA, USA
Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA, USA
Stanford Cancer Institute, Stanford University School of Medicine, Stanford, CA, USA

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David Feldman Department of Medicine-Endocrinology, Stanford University School of Medicine, Stanford, CA, USA
Stanford Cancer Institute, Stanford University School of Medicine, Stanford, CA, USA

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have examined the ability of calcitriol and dietary vitamin D supplementation to alter the growth of mouse mammary tumor virus Mmtv-Wnt1 in an ovariectomized (OVX), diet-induced obesity (DIO) model and compared the effects in obese mice to lean mice

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-15-0557
Volume/Issue:
Volume 23: Issue 4
Free access
Nikki A Ford Department of Nutritional Sciences, Department of Molecular Carcinogenesis, Dell Pediatric Research Institute, University of Texas, 1400 Barbara Jordan Boulevard, DPRI 2.834, Austin, Texas 78722, USA

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Nomeli P Nunez Department of Nutritional Sciences, Department of Molecular Carcinogenesis, Dell Pediatric Research Institute, University of Texas, 1400 Barbara Jordan Boulevard, DPRI 2.834, Austin, Texas 78722, USA

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Valerie B Holcomb Department of Nutritional Sciences, Department of Molecular Carcinogenesis, Dell Pediatric Research Institute, University of Texas, 1400 Barbara Jordan Boulevard, DPRI 2.834, Austin, Texas 78722, USA

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Stephen D Hursting Department of Nutritional Sciences, Department of Molecular Carcinogenesis, Dell Pediatric Research Institute, University of Texas, 1400 Barbara Jordan Boulevard, DPRI 2.834, Austin, Texas 78722, USA
Department of Nutritional Sciences, Department of Molecular Carcinogenesis, Dell Pediatric Research Institute, University of Texas, 1400 Barbara Jordan Boulevard, DPRI 2.834, Austin, Texas 78722, USA

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decreases progression of mammary and many other tumor types in various animal models ( Nunez et al . 2008 , Hursting & Berger 2010 , Hursting et al . 2010 ). The effects of dietary energy balance alterations, such as CR and diet-induced obesity (DIO), on

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-12-0329
Volume/Issue:
Volume 20: Issue 1
Free access
Jiyoung Park Department of Internal Medicine, Department of Cell Biology, Simmons Cancer Center, Touchstone Diabetes Center

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Philipp E Scherer Department of Internal Medicine, Department of Cell Biology, Simmons Cancer Center, Touchstone Diabetes Center
Department of Internal Medicine, Department of Cell Biology, Simmons Cancer Center, Touchstone Diabetes Center
Department of Internal Medicine, Department of Cell Biology, Simmons Cancer Center, Touchstone Diabetes Center

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addition, diet-induced obese mouse models have been used to modulate leptin levels in vivo . From these diet studies, it is apparent that mammary tumors grow faster under high-fat diet conditions. Consistent with a possible involvement of leptin, obese

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-11-0163
Volume/Issue:
Volume 18: Issue 4
Free access
Yvonne Fierz Division of Endocrinology, Diabetes and Bone Diseases, The Samuel Bronfman Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA

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Ruslan Novosyadlyy Division of Endocrinology, Diabetes and Bone Diseases, The Samuel Bronfman Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA

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Archana Vijayakumar Division of Endocrinology, Diabetes and Bone Diseases, The Samuel Bronfman Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA

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Shoshana Yakar Division of Endocrinology, Diabetes and Bone Diseases, The Samuel Bronfman Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA

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Derek LeRoith Division of Endocrinology, Diabetes and Bone Diseases, The Samuel Bronfman Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA

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poorly understood. The mTOR pathway plays a critical role in adipogenesis ( Wullschleger et al . 2006 ), and treatment with rapamycin has been shown to protect from high-fat diet-induced obesity ( Chang et al . 2009 a , b ). Moreover, S6 kinase

Article Type:
Research Article
DOI:
https://doi.org/10.1677/ERC-10-0091
Volume/Issue:
Volume 17: Issue 4
Free access
Emma H Allott Department of Epidemiology, Lineberger Comprehensive Cancer Center, Department of Nutrition, CB 7435, University of North Carolina at Chapel Hill, 135 Dauer Drive, Chapel Hill, North Carolina 27599, USA
Department of Epidemiology, Lineberger Comprehensive Cancer Center, Department of Nutrition, CB 7435, University of North Carolina at Chapel Hill, 135 Dauer Drive, Chapel Hill, North Carolina 27599, USA

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Stephen D Hursting Department of Epidemiology, Lineberger Comprehensive Cancer Center, Department of Nutrition, CB 7435, University of North Carolina at Chapel Hill, 135 Dauer Drive, Chapel Hill, North Carolina 27599, USA
Department of Epidemiology, Lineberger Comprehensive Cancer Center, Department of Nutrition, CB 7435, University of North Carolina at Chapel Hill, 135 Dauer Drive, Chapel Hill, North Carolina 27599, USA

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genetically-engineered mice, and thus murine models of hormone receptor-positive breast cancer may not be fully representative of human luminal breast cancer ( Herschkowitz et al . 2007 , Borowsky 2011 ). Nonetheless, diet-induced obesity has been

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-15-0400
Volume/Issue:
Volume 22: Issue 6
Free access
Tiffany Scully Hormones and Cancer Laboratories, Kolling Institute, University of Sydney, Royal North Shore Hospital, St Leonards, New South Wales, Australia

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Carolyn D Scott Hormones and Cancer Laboratories, Kolling Institute, University of Sydney, Royal North Shore Hospital, St Leonards, New South Wales, Australia

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Sue M Firth Hormones and Cancer Laboratories, Kolling Institute, University of Sydney, Royal North Shore Hospital, St Leonards, New South Wales, Australia

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Lisa M Sedger School of Life Sciences, Faculty of Science, University of Technology Sydney, Ultimo, New South Wales, Australia

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John E Pintar Department of Neuroscience and Cell Biology, Rutgers Robert Wood Johnson Medical School, New Jersey, USA

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Stephen M Twigg Charles Perkins Centre, Sydney Medical School, University of Sydney, New South Wales, Australia

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Robert C Baxter Hormones and Cancer Laboratories, Kolling Institute, University of Sydney, Royal North Shore Hospital, St Leonards, New South Wales, Australia

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, diet-induced obesity has been linked to the decreased development of an anti-tumour immune response through the impairment of dendritic cell function ( James et al. 2012 ). In addition to these mechanisms, obesity may also potentially influence immune

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-17-0384
Volume/Issue:
Volume 25: Issue 2
Free access