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  1. Article ; Online: The 2021 FASEB Virtual Science Research Conference on Nutrition, Immunity, and Inflammation: From Model Systems to Human Trials, July 27-29, 2021.

    Shaikh, Saame Raza / Stephensen, Charles B / Hursting, Stephen D / Comstock, Sarah S

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology

    2021  Volume 35, Issue 11, Page(s) e21978

    MeSH term(s) Animals ; Humans ; Immunity, Innate ; Inflammation/immunology ; Models, Biological ; Neoplasms/immunology ; Nutritional Status/immunology
    Language English
    Publishing date 2021-10-25
    Publishing country United States
    Document type Congress ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 639186-2
    ISSN 1530-6860 ; 0892-6638
    ISSN (online) 1530-6860
    ISSN 0892-6638
    DOI 10.1096/fj.202101509
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2266: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 296: Show issues

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  2. Article ; Online: The obesity-breast cancer link: a multidisciplinary perspective.

    Devericks, Emily N / Carson, Meredith S / McCullough, Lauren E / Coleman, Michael F / Hursting, Stephen D

    Cancer metastasis reviews

    2022  Volume 41, Issue 3, Page(s) 607–625

    Abstract: Obesity, exceptionally prevalent in the USA, promotes the incidence and progression of numerous cancer types including breast cancer. Complex, interacting metabolic and immune dysregulation marks the development of both breast cancer and obesity. Obesity ...

    Abstract Obesity, exceptionally prevalent in the USA, promotes the incidence and progression of numerous cancer types including breast cancer. Complex, interacting metabolic and immune dysregulation marks the development of both breast cancer and obesity. Obesity promotes chronic low-grade inflammation, particularly in white adipose tissue, which drives immune dysfunction marked by increased pro-inflammatory cytokine production, alternative macrophage activation, and reduced T cell function. Breast tissue is predominantly composed of white adipose, and developing breast cancer readily and directly interacts with cells and signals from adipose remodeled by obesity. This review discusses the biological mechanisms through which obesity promotes breast cancer, the role of obesity in breast cancer health disparities, and dietary interventions to mitigate the adverse effects of obesity on breast cancer. We detail the intersection of obesity and breast cancer, with an emphasis on the shared and unique patterns of immune dysregulation in these disease processes. We have highlighted key areas of breast cancer biology exacerbated by obesity, including incidence, progression, and therapeutic response. We posit that interception of obesity-driven breast cancer will require interventions that limit protumor signaling from obese adipose tissue and that consider genetic, structural, and social determinants of the obesity-breast cancer link. Finally, we detail the evidence for various dietary interventions to offset obesity effects in clinical and preclinical studies of breast cancer. In light of the strong associations between obesity and breast cancer and the rising rates of obesity in many parts of the world, the development of effective, safe, well-tolerated, and equitable interventions to limit the burden of obesity on breast cancer are urgently needed.
    MeSH term(s) Adipose Tissue/metabolism ; Breast Neoplasms/complications ; Breast Neoplasms/etiology ; Female ; Humans ; Inflammation/metabolism ; Obesity/complications ; Obesity/metabolism
    Language English
    Publishing date 2022-06-25
    Publishing country Netherlands
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 604857-2
    ISSN 1573-7233 ; 0167-7659
    ISSN (online) 1573-7233
    ISSN 0167-7659
    DOI 10.1007/s10555-022-10043-5
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1812: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: 1α,25-dihydroxyvitamin D reduction of MCF10A-ras cell viability in extracellular matrix detached conditions is dependent on regulation of pyruvate carboxylase.

    Sheeley, Madeline P / Kiesel, Violet A / Andolino, Chaylen / Lanman, Nadia A / Donkin, Shawn S / Hursting, Stephen D / Wendt, Michael K / Teegarden, Dorothy

    The Journal of nutritional biochemistry

    2022  Volume 109, Page(s) 109116

    Abstract: ... that the bioactive metabolite of vitamin D, 1α,25-dihydroxyvitamin D (1,25[OH] ...

    Abstract An emerging hallmark of cancer is cellular metabolic reprogramming to adapt to varying cellular environments. Throughout the process of metastasis cancer cells gain anchorage independence which confers survival characteristics when detached from the extracellular matrix (ECM). Previous work demonstrates that the bioactive metabolite of vitamin D, 1α,25-dihydroxyvitamin D (1,25[OH]
    MeSH term(s) Aspartic Acid ; Cell Survival ; Doxycycline ; Extracellular Matrix ; Glucose/metabolism ; Glutamic Acid ; Glutamine/metabolism ; Glutamine/pharmacology ; Malates ; Pyruvate Carboxylase/genetics ; Pyruvate Carboxylase/metabolism ; RNA, Messenger/metabolism ; RNA, Small Interfering/metabolism ; Vitamin D/analogs & derivatives ; Vitamin D/pharmacology
    Chemical Substances Malates ; RNA, Messenger ; RNA, Small Interfering ; Glutamine (0RH81L854J) ; Vitamin D (1406-16-2) ; Aspartic Acid (30KYC7MIAI) ; Glutamic Acid (3KX376GY7L) ; 1,25-dihydroxyvitamin D (66772-14-3) ; malic acid (817L1N4CKP) ; Pyruvate Carboxylase (EC 6.4.1.1) ; Glucose (IY9XDZ35W2) ; Doxycycline (N12000U13O)
    Language English
    Publishing date 2022-08-04
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1014929-6
    ISSN 1873-4847 ; 0955-2863
    ISSN (online) 1873-4847
    ISSN 0955-2863
    DOI 10.1016/j.jnutbio.2022.109116
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2838: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article: Increased Ammonium Toxicity in Response to Exogenous Glutamine in Metastatic Breast Cancer Cells.

    Kiesel, Violet A / Sheeley, Madeline P / Donkin, Shawn S / Wendt, Michael K / Hursting, Stephen D / Teegarden, Dorothy

    Metabolites

    2022  Volume 12, Issue 5

    Abstract: Several cancers, including breast cancers, show dependence on glutamine metabolism. The purpose of the present study was to determine the mechanistic basis and impact of differential glutamine metabolism in nonmetastatic and metastatic murine mammary ... ...

    Abstract Several cancers, including breast cancers, show dependence on glutamine metabolism. The purpose of the present study was to determine the mechanistic basis and impact of differential glutamine metabolism in nonmetastatic and metastatic murine mammary cancer cells. Universally labeled
    Language English
    Publishing date 2022-05-23
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2662251-8
    ISSN 2218-1989
    ISSN 2218-1989
    DOI 10.3390/metabo12050469
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  5. Article: Hypoxia-Mediated ATF4 Induction Promotes Survival in Detached Conditions in Metastatic Murine Mammary Cancer Cells.

    Kiesel, Violet A / Sheeley, Madeline P / Hicks, Emily M / Andolino, Chaylen / Donkin, Shawn S / Wendt, Michael K / Hursting, Stephen D / Teegarden, Dorothy

    Frontiers in oncology

    2022  Volume 12, Page(s) 767479

    Abstract: Regions of hypoxia are common in solid tumors and drive changes in gene expression that increase risk of cancer metastasis. Tumor cells must respond to the stress of hypoxia by activating genes to modify cell metabolism and antioxidant response to ... ...

    Abstract Regions of hypoxia are common in solid tumors and drive changes in gene expression that increase risk of cancer metastasis. Tumor cells must respond to the stress of hypoxia by activating genes to modify cell metabolism and antioxidant response to improve survival. The goal of the current study was to determine the effect of hypoxia on cell metabolism and markers of oxidative stress in metastatic (metM-Wnt
    Language English
    Publishing date 2022-06-30
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2649216-7
    ISSN 2234-943X
    ISSN 2234-943X
    DOI 10.3389/fonc.2022.767479
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  6. Article: Obesity, Diabetes and Cancer: A Mechanistic Perspective.

    Cifarelli, V / Hursting, S D

    International journal of diabetology & vascular disease research

    2015  Volume 2015, Issue Suppl 4

    Abstract: Nearly 35% of adults and 20% of children in the United States are obese, defined as having a body mass index (BMI) ≥ 30 kg/ ... ...

    Abstract Nearly 35% of adults and 20% of children in the United States are obese, defined as having a body mass index (BMI) ≥ 30 kg/m
    Language English
    Publishing date 2015-09-28
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2781467-1
    ISSN 2328-353X
    ISSN 2328-353X
    DOI 10.19070/2328-353X-SI04001
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  7. Article ; Online: Intermittent fasting interventions to leverage metabolic and circadian mechanisms for cancer treatment and supportive care outcomes.

    Kalam, Faiza / James, Dara L / Li, Yun Rose / Coleman, Michael F / Kiesel, Violet A / Cespedes Feliciano, Elizabeth M / Hursting, Stephen D / Sears, Dorothy D / Kleckner, Amber S

    Journal of the National Cancer Institute. Monographs

    2023  Volume 2023, Issue 61, Page(s) 84–103

    Abstract: Intermittent fasting entails restricting food intake during specific times of day, days of the week, religious practice, or surrounding clinically important events. Herein, the metabolic and circadian rhythm mechanisms underlying the proposed benefits of ...

    Abstract Intermittent fasting entails restricting food intake during specific times of day, days of the week, religious practice, or surrounding clinically important events. Herein, the metabolic and circadian rhythm mechanisms underlying the proposed benefits of intermittent fasting for the cancer population are described. We summarize epidemiological, preclinical, and clinical studies in cancer published between January 2020 and August 2022 and propose avenues for future research. An outstanding concern regarding the use of intermittent fasting among cancer patients is that fasting often results in caloric restriction, which can put patients already prone to malnutrition, cachexia, or sarcopenia at risk. Although clinical trials do not yet provide sufficient data to support the general use of intermittent fasting in clinical practice, this summary may be useful for patients, caregivers, and clinicians who are exploring intermittent fasting as part of their cancer journey for clinical outcomes and symptom management.
    MeSH term(s) Humans ; Obesity ; Intermittent Fasting ; Caloric Restriction/adverse effects ; Diet, Reducing/adverse effects ; Diet, Reducing/methods ; Circadian Rhythm ; Neoplasms/diagnosis ; Neoplasms/epidemiology ; Neoplasms/therapy
    Language English
    Publishing date 2023-05-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ISSN 1745-6614
    ISSN (online) 1745-6614
    DOI 10.1093/jncimonographs/lgad008
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  8. Article: Pyruvate carboxylase and cancer progression.

    Kiesel, Violet A / Sheeley, Madeline P / Coleman, Michael F / Cotul, Eylem Kulkoyluoglu / Donkin, Shawn S / Hursting, Stephen D / Wendt, Michael K / Teegarden, Dorothy

    Cancer & metabolism

    2021  Volume 9, Issue 1, Page(s) 20

    Abstract: Pyruvate carboxylase (PC) is a mitochondrial enzyme that catalyzes the ATP-dependent carboxylation of pyruvate to oxaloacetate (OAA), serving to replenish the tricarboxylic acid (TCA) cycle. In nonmalignant tissue, PC plays an essential role in ... ...

    Abstract Pyruvate carboxylase (PC) is a mitochondrial enzyme that catalyzes the ATP-dependent carboxylation of pyruvate to oxaloacetate (OAA), serving to replenish the tricarboxylic acid (TCA) cycle. In nonmalignant tissue, PC plays an essential role in controlling whole-body energetics through regulation of gluconeogenesis in the liver, synthesis of fatty acids in adipocytes, and insulin secretion in pancreatic β cells. In breast cancer, PC activity is linked to pulmonary metastasis, potentially by providing the ability to utilize glucose, fatty acids, and glutamine metabolism as needed under varying conditions as cells metastasize. PC enzymatic activity appears to be of particular importance in cancer cells that are unable to utilize glutamine for anaplerosis. Moreover, PC activity also plays a role in lipid metabolism and protection from oxidative stress in cancer cells. Thus, PC activity may be essential to link energy substrate utilization with cancer progression and to enable the metabolic flexibility necessary for cell resilience to changing and adverse conditions during the metastatic process.
    Language English
    Publishing date 2021-04-30
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2700141-6
    ISSN 2049-3002
    ISSN 2049-3002
    DOI 10.1186/s40170-021-00256-7
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  9. Article: Intermittent energy restriction inhibits tumor growth and enhances paclitaxel response in a transgenic mouse model of endometrial cancer.

    Zhao, Ziyi / Wang, Jiandong / Kong, Weimin / Fang, Ziwei / Coleman, Michael / Milne, Ginger / Burkett, Wesley C / Newton, Meredith A / Lee, Douglas / Deng, Beor / Shen, Xiaochang / Suo, Hongyan / Sun, Wenchuan / Hursting, Stephen / Zhou, Chunxiao / Bae-Jump, Victoria L

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Objective: Overweight/obesity is the strongest risk factor for endometrial cancer (EC), and weight management can reduce that risk and improve survival. We aimed to establish the differential abilities of intermittent energy restriction (IER) and low- ... ...

    Abstract Objective: Overweight/obesity is the strongest risk factor for endometrial cancer (EC), and weight management can reduce that risk and improve survival. We aimed to establish the differential abilities of intermittent energy restriction (IER) and low-fat diet (LFD), alone and in combination with paclitaxel, to reverse the procancer effects of high-fat diet (HFD)-induced obesity in a mouse model of EC.
    Methods: Lkb1
    Results: HFD-IER and HFD-LFD, relative to HFD, reduced body weight; reversed obesity-induced alterations in serum insulin, leptin and inflammatory factors; and decreased tumor incidence and mass, often to levels emulating those associated with continuous LFD. Concurrent paclitaxel, versus placebo, enhanced tumor suppression in each group, with greatest benefit in HFD-IER. The diets produced distinct tumoral gene expression and metabolic profiles, with HFD-IER associated with a more favorable (antitumor) metabolic and inflammatory environment.
    Conclusion: In
    Language English
    Publishing date 2024-02-07
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.02.02.578679
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Mechanistic Targets and Nutritionally Relevant Intervention Strategies to Break Obesity-Breast Cancer Links.

    Bustamante-Marin, Ximena M / Merlino, Jenna L / Devericks, Emily / Carson, Meredith S / Hursting, Stephen D / Stewart, Delisha A

    Frontiers in endocrinology

    2021  Volume 12, Page(s) 632284

    Abstract: The worldwide prevalence of overweight and obesity has tripled since 1975. In the United States, the percentage of adults who are obese exceeds 42.5%. Individuals with obesity often display multiple metabolic perturbations, such as insulin resistance and ...

    Abstract The worldwide prevalence of overweight and obesity has tripled since 1975. In the United States, the percentage of adults who are obese exceeds 42.5%. Individuals with obesity often display multiple metabolic perturbations, such as insulin resistance and persistent inflammation, which can suppress the immune system. These alterations in homeostatic mechanisms underlie the clinical parameters of metabolic syndrome, an established risk factor for many cancers, including breast cancer. Within the growth-promoting, proinflammatory milieu of the obese state, crosstalk between adipocytes, immune cells and breast epithelial cells occurs
    MeSH term(s) Breast Neoplasms/metabolism ; Energy Metabolism/physiology ; Humans ; Inflammation/metabolism ; Insulin Resistance/physiology ; Metabolic Syndrome/metabolism ; Obesity/metabolism ; Risk Factors
    Language English
    Publishing date 2021-03-17
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2592084-4
    ISSN 1664-2392
    ISSN 1664-2392
    DOI 10.3389/fendo.2021.632284
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