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  1. 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
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1812: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  2. 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
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Revealing molecular pathways for cancer cell fitness through a genetic screen of the cancer translatome.

    Kuzuoglu-Ozturk, Duygu / Hu, Zhiqiang / Rama, Martina / Devericks, Emily / Weiss, Jacob / Chiang, Gary G / Worland, Stephen T / Brenner, Steven E / Goodarzi, Hani / Gilbert, Luke A / Ruggero, Davide

    Cell reports

    2021  Volume 35, Issue 13, Page(s) 109321

    Abstract: The major cap-binding protein eukaryotic translation initiation factor 4E (eIF4E), an ancient protein required for translation of all eukaryotic genomes, is a surprising yet potent oncogenic driver. The genetic interactions that maintain the oncogenic ... ...

    Abstract The major cap-binding protein eukaryotic translation initiation factor 4E (eIF4E), an ancient protein required for translation of all eukaryotic genomes, is a surprising yet potent oncogenic driver. The genetic interactions that maintain the oncogenic activity of this key translation factor remain unknown. In this study, we carry out a genome-wide CRISPRi screen wherein we identify more than 600 genetic interactions that sustain eIF4E oncogenic activity. Our data show that eIF4E controls the translation of Tfeb, a key executer of the autophagy response. This autophagy survival response is triggered by mitochondrial proteotoxic stress, which allows cancer cell survival. Our screen also reveals a functional interaction between eIF4E and a single anti-apoptotic factor, Bcl-xL, in tumor growth. Furthermore, we show that eIF4E and the exon-junction complex (EJC), which is involved in many steps of RNA metabolism, interact to control the migratory properties of cancer cells. Overall, we uncover several cancer-specific vulnerabilities that provide further resolution of the cancer translatome.
    MeSH term(s) 5' Untranslated Regions/genetics ; Animals ; Apoptosis/genetics ; Autophagy ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/metabolism ; CRISPR-Cas Systems/genetics ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Eukaryotic Initiation Factor-4E/genetics ; Eukaryotic Initiation Factor-4E/metabolism ; Exons/genetics ; Genetic Testing ; Genome, Human ; Humans ; Male ; Metalloendopeptidases/metabolism ; Mice ; Mitochondria/metabolism ; Mitochondrial Proteins/metabolism ; Neoplasms/genetics ; Neoplasms/pathology ; Peptide Hydrolases/metabolism ; Protein Biosynthesis/genetics ; Signal Transduction/genetics ; Stress, Physiological ; bcl-X Protein/metabolism
    Chemical Substances 5' Untranslated Regions ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; Eukaryotic Initiation Factor-4E ; Mitochondrial Proteins ; TFEB protein, human ; bcl-X Protein ; Peptide Hydrolases (EC 3.4.-) ; Metalloendopeptidases (EC 3.4.24.-) ; PMPCB protein, human (EC 3.4.24.-)
    Language English
    Publishing date 2021-06-30
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2021.109321
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: ERα is an RNA-binding protein sustaining tumor cell survival and drug resistance.

    Xu, Yichen / Huangyang, Peiwei / Wang, Ying / Xue, Lingru / Devericks, Emily / Nguyen, Hao G / Yu, Xiuyan / Oses-Prieto, Juan A / Burlingame, Alma L / Miglani, Sohit / Goodarzi, Hani / Ruggero, Davide

    Cell

    2021  Volume 184, Issue 20, Page(s) 5215–5229.e17

    Abstract: Estrogen receptor α (ERα) is a hormone receptor and key driver for over 70% of breast cancers that has been studied for decades as a transcription factor. Unexpectedly, we discover that ERα is a potent non-canonical RNA-binding protein. We show that ERα ... ...

    Abstract Estrogen receptor α (ERα) is a hormone receptor and key driver for over 70% of breast cancers that has been studied for decades as a transcription factor. Unexpectedly, we discover that ERα is a potent non-canonical RNA-binding protein. We show that ERα RNA binding function is uncoupled from its activity to bind DNA and critical for breast cancer progression. Employing genome-wide cross-linking immunoprecipitation (CLIP) sequencing and a functional CRISPRi screen, we find that ERα-associated mRNAs sustain cancer cell fitness and elicit cellular responses to stress. Mechanistically, ERα controls different steps of RNA metabolism. In particular, we demonstrate that ERα RNA binding mediates alternative splicing of XBP1 and translation of the eIF4G2 and MCL1 mRNAs, which facilitates survival upon stress conditions and sustains tamoxifen resistance of cancer cells. ERα is therefore a multifaceted RNA-binding protein, and this activity transforms our knowledge of post-transcriptional regulation underlying cancer development and drug response.
    MeSH term(s) Animals ; Base Sequence ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Cell Survival/drug effects ; Cell Survival/genetics ; Disease Progression ; Drug Resistance, Neoplasm/drug effects ; Drug Resistance, Neoplasm/genetics ; Estrogen Receptor alpha/chemistry ; Estrogen Receptor alpha/metabolism ; Eukaryotic Initiation Factor-4G/genetics ; Eukaryotic Initiation Factor-4G/metabolism ; Female ; Gene Expression Regulation, Neoplastic/drug effects ; Genomics ; Humans ; Mice, Inbred NOD ; Myeloid Cell Leukemia Sequence 1 Protein/genetics ; Myeloid Cell Leukemia Sequence 1 Protein/metabolism ; Oncogenes ; Protein Binding/drug effects ; Protein Domains ; RNA Splicing/genetics ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; RNA-Binding Proteins/metabolism ; Stress, Physiological/drug effects ; Stress, Physiological/genetics ; Tamoxifen/pharmacology ; X-Box Binding Protein 1/metabolism ; Mice
    Chemical Substances EIF4G2 protein, human ; Estrogen Receptor alpha ; Eukaryotic Initiation Factor-4G ; MCL1 protein, human ; Myeloid Cell Leukemia Sequence 1 Protein ; RNA, Messenger ; RNA-Binding Proteins ; X-Box Binding Protein 1 ; XBP1 protein, human ; Tamoxifen (094ZI81Y45)
    Language English
    Publishing date 2021-09-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2021.08.036
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1167: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Zs.MG 58: Show issues

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  5. Article: ERα is an RNA-binding protein sustaining tumor cell survival and drug resistance

    Xu, Yichen / Huangyang, Peiwei / Wang, Ying / Xue, Lingru / Devericks, Emily / Nguyen, Hao G. / Yu, Xiuyan / Oses-Prieto, Juan A. / Burlingame, Alma L. / Miglani, Sohit / Goodarzi, Hani / Ruggero, Davide

    Cell. 2021 Sept. 30, v. 184, no. 20

    2021  

    Abstract: Estrogen receptor α (ERα) is a hormone receptor and key driver for over 70% of breast cancers that has been studied for decades as a transcription factor. Unexpectedly, we discover that ERα is a potent non-canonical RNA-binding protein. We show that ERα ... ...

    Abstract Estrogen receptor α (ERα) is a hormone receptor and key driver for over 70% of breast cancers that has been studied for decades as a transcription factor. Unexpectedly, we discover that ERα is a potent non-canonical RNA-binding protein. We show that ERα RNA binding function is uncoupled from its activity to bind DNA and critical for breast cancer progression. Employing genome-wide cross-linking immunoprecipitation (CLIP) sequencing and a functional CRISPRi screen, we find that ERα-associated mRNAs sustain cancer cell fitness and elicit cellular responses to stress. Mechanistically, ERα controls different steps of RNA metabolism. In particular, we demonstrate that ERα RNA binding mediates alternative splicing of XBP1 and translation of the eIF4G2 and MCL1 mRNAs, which facilitates survival upon stress conditions and sustains tamoxifen resistance of cancer cells. ERα is therefore a multifaceted RNA-binding protein, and this activity transforms our knowledge of post-transcriptional regulation underlying cancer development and drug response.
    Keywords DNA ; RNA-binding proteins ; breast neoplasms ; breasts ; carcinogenesis ; cell viability ; crosslinking ; drug resistance ; estrogen receptors ; metabolism ; neoplasm cells ; neoplasm progression ; precipitin tests ; tamoxifen
    Language English
    Dates of publication 2021-0930
    Size p. 5215-5229.e17.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2021.08.036
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

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  6. Article ; Online: Modest Decreases in Endogenous All-

    Yang, Di / Vuckovic, Marta G / Smullin, Carolyn P / Kim, Myeongcheol / Lo, Christabel Pui-See / Devericks, Emily / Yoo, Hong Sik / Tintcheva, Milena / Deng, Yinghua / Napoli, Joseph L

    Diabetes

    2018  Volume 67, Issue 4, Page(s) 662–673

    Abstract: Pharmacological dosing of all- ...

    Abstract Pharmacological dosing of all-
    MeSH term(s) Adipogenesis/drug effects ; Adipogenesis/genetics ; Adipose Tissue/metabolism ; Adiposity/genetics ; Alcohol Oxidoreductases/genetics ; Animals ; Diet, High-Fat ; Female ; Fibroblasts/metabolism ; Glucose Intolerance/metabolism ; Heterozygote ; Insulin Resistance/genetics ; Lipid Metabolism/drug effects ; Lipid Metabolism/genetics ; Liver/metabolism ; Male ; Mice ; Non-alcoholic Fatty Liver Disease/metabolism ; Oxidation-Reduction ; Receptors, Retinoic Acid/agonists ; Sex Factors ; Tretinoin/metabolism ; Tretinoin/pharmacology ; Vitamin A/metabolism
    Chemical Substances Receptors, Retinoic Acid ; Vitamin A (11103-57-4) ; Tretinoin (5688UTC01R) ; Alcohol Oxidoreductases (EC 1.1.-) ; trans-retinol dehydrogenase (EC 1.1.1.-)
    Language English
    Publishing date 2018-01-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80085-5
    ISSN 1939-327X ; 0012-1797
    ISSN (online) 1939-327X
    ISSN 0012-1797
    DOI 10.2337/db17-0946
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.175: Show issues Location:
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  7. Article ; Online: Translation control of the immune checkpoint in cancer and its therapeutic targeting.

    Xu, Yichen / Poggio, Mauro / Jin, Hyun Yong / Shi, Zhen / Forester, Craig M / Wang, Ying / Stumpf, Craig R / Xue, Lingru / Devericks, Emily / So, Lomon / Nguyen, Hao G / Griselin, Alice / Gordan, John D / Umetsu, Sarah E / Reich, Siegfried H / Worland, Stephen T / Asthana, Saurabh / Barna, Maria / Webster, Kevin R /
    Cunningham, John T / Ruggero, Davide

    Nature medicine

    2019  Volume 25, Issue 2, Page(s) 301–311

    Abstract: Cancer cells develop mechanisms to escape immunosurveillance, among which modulating the expression of immune suppressive messenger RNAs is most well-documented. However, how this is molecularly achieved remains largely unresolved. Here, we develop an in ...

    Abstract Cancer cells develop mechanisms to escape immunosurveillance, among which modulating the expression of immune suppressive messenger RNAs is most well-documented. However, how this is molecularly achieved remains largely unresolved. Here, we develop an in vivo mouse model of liver cancer to study oncogene cooperation in immunosurveillance. We show that MYC overexpression (MYC
    MeSH term(s) 5' Untranslated Regions/genetics ; Animals ; B7-H1 Antigen/metabolism ; Base Sequence ; Disease Progression ; Down-Regulation ; Eukaryotic Initiation Factor-4E/metabolism ; Gene Expression Regulation, Neoplastic ; Immune Evasion ; Immunotherapy ; Kaplan-Meier Estimate ; Liver Neoplasms/genetics ; Liver Neoplasms/immunology ; Liver Neoplasms/pathology ; Liver Neoplasms/therapy ; Mice, Inbred C57BL ; Neoplasm Metastasis ; Open Reading Frames/genetics ; Protein Biosynthesis ; Proto-Oncogene Proteins c-myc/metabolism ; Proto-Oncogene Proteins p21(ras)/metabolism ; Pyridines/pharmacology ; Pyrimidines/pharmacology ; Transcription, Genetic ; Tumor Microenvironment ; Up-Regulation/genetics
    Chemical Substances 5' Untranslated Regions ; B7-H1 Antigen ; Cd274 protein, mouse ; Eukaryotic Initiation Factor-4E ; Proto-Oncogene Proteins c-myc ; Pyridines ; Pyrimidines ; Hras protein, mouse (EC 3.6.5.2) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; tomivosertib (U2H19X4WBV)
    Language English
    Publishing date 2019-01-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1220066-9
    ISSN 1546-170X ; 1078-8956
    ISSN (online) 1546-170X
    ISSN 1078-8956
    DOI 10.1038/s41591-018-0321-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4212: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
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    Zs.MG 39: Show issues

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