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  1. Book: Impact of energy balance on cancer disparities

    Bowen, Deborah J. / Denis, Gerald V. / Berger, Nathan A.

    (Energy balance and cancer ; ; 9)

    2014  

    Author's details Deborah J. Bowen, Gerald V. Denis, Nathan A. Berger (ed.)
    Series title Energy balance and cancer ; ; 9
    Collection
    Keywords Cancer/Epidemiology ; Bioenergetics
    Subject code 614.5999
    Language English
    Size XIII, 308 S. : graf. Darst., Kt., 24 cm
    Publisher Springer
    Publishing place Cham u.a.
    Publishing country Switzerland
    Document type Book
    Note Includes bibliographical references
    HBZ-ID HT018377789
    ISBN 978-3-319-06102-3 ; 9783319061030 ; 3-319-06102-X ; 3319061038
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    2014 A 3426 available for loan (reading room) Lesesaal EG

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  2. Article ; Online: Exosomes as novel biomarkers in metabolic disease and obesity-related cancers.

    Jafari, Naser / Llevenes, Pablo / Denis, Gerald V

    Nature reviews. Endocrinology

    2022  Volume 18, Issue 6, Page(s) 327–328

    MeSH term(s) Biomarkers/metabolism ; Exosomes/metabolism ; Humans ; Metabolic Diseases/diagnosis ; Metabolic Diseases/metabolism ; Neoplasms/diagnosis ; Neoplasms/metabolism ; Obesity/complications ; Obesity/metabolism
    Chemical Substances Biomarkers
    Language English
    Publishing date 2022-04-22
    Publishing country England
    Document type Journal Article
    ZDB-ID 2489381-X
    ISSN 1759-5037 ; 1759-5029
    ISSN (online) 1759-5037
    ISSN 1759-5029
    DOI 10.1038/s41574-022-00666-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MG 93: Show issues

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  3. Article ; Online: BET Proteins Exhibit Transcriptional and Functional Opposition in the Epithelial-to-Mesenchymal Transition.

    Andrieu, Guillaume P / Denis, Gerald V

    Molecular cancer research : MCR

    2018  Volume 16, Issue 4, Page(s) 580–586

    Abstract: Transcriptional programs in embryogenesis and cancer, such as the epithelial-to-mesenchymal transition (EMT), ensure cellular plasticity, an essential feature of carcinoma progression. As effectors of signal transduction, the bromodomain and ... ...

    Abstract Transcriptional programs in embryogenesis and cancer, such as the epithelial-to-mesenchymal transition (EMT), ensure cellular plasticity, an essential feature of carcinoma progression. As effectors of signal transduction, the bromodomain and extraterminal (BET) proteins are well suited to support plasticity because they function as co-activators or co-repressors of mammalian transcriptomes. Here, using both hormone-sensitive and triple-negative breast cancer (TNBC) model systems, we systematically altered EMT transcriptional profiles by manipulating individual BET proteins and found that BRD2 positively regulates EMT, whereas BRD3 and BRD4 repress this program. Knockdown of individual BET proteins revealed independent transcriptional networks that differed from each other and from the small-molecule pan-BET inhibitor JQ1, which previously had been misleadingly asserted to be BRD4-selective. Available small-molecule pan-BET inhibitors, proposed as antiproliferative agents in cancer clinical trials, obscure these biological differences. Transcriptional profiling reveals that individual BET proteins, inhibited separately, engage in and control EMT through unique processes.
    MeSH term(s) Azepines/pharmacology ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Epithelial-Mesenchymal Transition/drug effects ; Female ; Gene Expression Profiling/methods ; Gene Expression Regulation, Neoplastic/drug effects ; Gene Knockdown Techniques ; Gene Regulatory Networks/drug effects ; Humans ; MCF-7 Cells ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/metabolism ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Triazoles/pharmacology ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/metabolism
    Chemical Substances (+)-JQ1 compound ; Azepines ; BRD2 protein, human ; BRD3 protein, human ; BRD4 protein, human ; Nuclear Proteins ; RNA-Binding Proteins ; Transcription Factors ; Triazoles ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2018-02-07
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2098788-2
    ISSN 1557-3125 ; 1541-7786
    ISSN (online) 1557-3125
    ISSN 1541-7786
    DOI 10.1158/1541-7786.MCR-17-0568
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: The crosstalk within the breast tumor microenvironment in type II diabetes: Implications for cancer disparities.

    Ennis, Christina S / Llevenes, Pablo / Qiu, Yuhan / Dries, Ruben / Denis, Gerald V

    Frontiers in endocrinology

    2022  Volume 13, Page(s) 1044670

    Abstract: Obesity-driven (type 2) diabetes (T2D), the most common metabolic disorder, both increases the incidence of all molecular subtypes of breast cancer and decreases survival in postmenopausal women. Despite this clear link, T2D and the associated ... ...

    Abstract Obesity-driven (type 2) diabetes (T2D), the most common metabolic disorder, both increases the incidence of all molecular subtypes of breast cancer and decreases survival in postmenopausal women. Despite this clear link, T2D and the associated dysfunction of diverse tissues is often not considered during the standard of care practices in oncology and, moreover, is treated as exclusion criteria for many emerging clinical trials. These guidelines have caused the biological mechanisms that associate T2D and breast cancer to be understudied. Recently, it has been illustrated that the breast tumor microenvironment (TME) composition and architecture, specifically the surrounding cellular and extracellular structures, dictate tumor progression and are directly relevant for clinical outcomes. In addition to the epithelial cancer cell fraction, the breast TME is predominantly made up of cancer-associated fibroblasts, adipocytes, and is often infiltrated by immune cells. During T2D, signal transduction among these cell types is aberrant, resulting in a dysfunctional breast TME that communicates with nearby cancer cells to promote oncogenic processes, cancer stem-like cell formation, pro-metastatic behavior and increase the risk of recurrence. As these cells are non-malignant, despite their signaling abnormalities, data concerning their function is never captured in DNA mutational databases, thus we have limited insight into mechanism from publicly available datasets. We suggest that abnormal adipocyte and immune cell exhaustion within the breast TME in patients with obesity and metabolic disease may elicit greater transcriptional plasticity and cellular heterogeneity within the expanding population of malignant epithelial cells, compared to the breast TME of a non-obese, metabolically normal patient. These challenges are particularly relevant to cancer disparities settings where the fraction of patients seen within the breast medical oncology practice also present with co-morbid obesity and metabolic disease. Within this review, we characterize the changes to the breast TME during T2D and raise urgent molecular, cellular and translational questions that warrant further study, considering the growing prevalence of T2D worldwide.
    MeSH term(s) Humans ; Female ; Tumor Microenvironment/physiology ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/metabolism ; Breast Neoplasms/pathology ; Adipocytes/metabolism ; Obesity/complications ; Obesity/metabolism
    Language English
    Publishing date 2022-12-01
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 2592084-4
    ISSN 1664-2392
    ISSN 1664-2392
    DOI 10.3389/fendo.2022.1044670
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  5. Article ; Online: The Association Between Metabolic Derangement and Wound Complications in Elective Plastic Surgery.

    Sergesketter, Amanda R / Geng, Yisong / Shammas, Ronnie L / Denis, Gerald V / Bachelder, Robin / Hollenbeck, Scott T

    The Journal of surgical research

    2022  Volume 278, Page(s) 39–48

    Abstract: Introduction: The incidence of metabolically unhealthy obesity is rising nationally. In this study, we compare wound and overall complications between metabolically unhealthy obese and healthy patients undergoing elective plastic surgery and model how ... ...

    Abstract Introduction: The incidence of metabolically unhealthy obesity is rising nationally. In this study, we compare wound and overall complications between metabolically unhealthy obese and healthy patients undergoing elective plastic surgery and model how operative time influences a complication risk.
    Methods: Patients undergoing elective breast and body plastic surgery procedures in the 2009-2019 National Surgical Quality Improvement Program (NSQIP) dataset were identified. Complications were compared between metabolically unhealthy obese (body mass index [BMI] > 30 with diabetes and/or hypertension) versus metabolically healthy obese patients (BMI > 30 without diabetes or hypertension). Logistic regression was used to model the probability of wound complications across operative times stratified by metabolic status.
    Results: Of 139,352 patients, 13.4% (n = 18,663) had metabolically unhealthy obesity and 23.8% (n = 33,135) had metabolically healthy obesity. Compared to metabolically healthy patients, metabolically unhealthy patients had higher incidence of wound complications (6.9% versus 5.6%; P < 0.001) and adverse events (12.4% versus 9.6%; P < 0.001), in addition to higher 30-d readmission, returns to the operating room, and length of stay (all P < 0.001). After adjustment, BMI (Odds ratio [OR] 7.86), hypertension (OR 1.15), and diabetes (OR 1.25) were independent risk factors for wound complications (all P < 0.001). Among metabolically unhealthy patients, the operative time was log-linear with a wound complication risk (OR 1.21; P < 0.001).
    Conclusions: Diabetes and hypertension are additive risk factors with obesity for wound complications in elective plastic surgery. Among patients with metabolically unhealthy obesity, a risk of wound complications increases logarithmically with operative time. This distinction with regard to metabolic state might explain the unclear impact of obesity on surgical outcomes within existing surgical literature.
    MeSH term(s) Body Mass Index ; Humans ; Hypertension/complications ; Hypertension/epidemiology ; Obesity/complications ; Obesity/epidemiology ; Obesity/metabolism ; Obesity, Metabolically Benign/complications ; Obesity, Metabolically Benign/epidemiology ; Risk Factors ; Surgery, Plastic
    Language English
    Publishing date 2022-05-16
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80170-7
    ISSN 1095-8673 ; 0022-4804
    ISSN (online) 1095-8673
    ISSN 0022-4804
    DOI 10.1016/j.jss.2022.03.017
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 178: Show issues Location:
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  6. Article ; Online: "Obesity-Associated" Breast Cancer in Lean Women: Metabolism and Inflammation as Critical Modifiers of Risk.

    Denis, Gerald V / Palmer, Julie R

    Cancer prevention research (Philadelphia, Pa.)

    2017  Volume 10, Issue 5, Page(s) 267–269

    Abstract: Why is obesity only weakly associated with certain "obesity-driven" cancers? Recent population studies identify cohorts of high body mass index (BMI) subjects with unexpectedly reduced risk for breast and colon cancer, and normal BMI subjects with ... ...

    Abstract Why is obesity only weakly associated with certain "obesity-driven" cancers? Recent population studies identify cohorts of high body mass index (BMI) subjects with unexpectedly reduced risk for breast and colon cancer, and normal BMI subjects with unexpectedly elevated risk for breast cancer, provoking hard thinking about cellular and molecular mechanisms that most strongly couple obesity to cancer occurrence or progression. Emerging work suggests that abnormal metabolism and its associated chronic inflammation make the difference. Type II diabetes, for example, is a chronic inflammatory disease with specific imbalances in T-cell and myeloid-origin cytokines. Inflammation is elevated systemically, measured through blood biomarkers, and locally in adipose tissue. Here, cytokines and chemokines likely modify tumor microenvironments in dangerous ways. High BMI subjects with low inflammation and less disturbed metabolism appear to have reduced risk for certain obesity-associated cancers, whereas lean or slightly overweight subjects with high inflammation and metabolic abnormalities have elevated risk. This latter phenotype is prevalent among South Asian adults and suggests we are not monitoring certain normal weight adults sufficiently for risks of "obesity-associated" cancers. Profiling of patient metabolism and inflammation should accompany measures of body composition when considering cancer risk; the evidence base for these refinements must be extended through new, prospective observational studies.
    Language English
    Publishing date 2017-05
    Publishing country United States
    Document type Editorial
    ZDB-ID 2434717-6
    ISSN 1940-6215 ; 1940-6207
    ISSN (online) 1940-6215
    ISSN 1940-6207
    DOI 10.1158/1940-6207.CAPR-17-0083
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6766: Show issues Location:
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  7. Article ; Online: Novel forms of prostate cancer chemoresistance to successful androgen deprivation therapy demand new approaches: Rationale for targeting BET proteins.

    Mori, Joakin O / Shafran, Jordan S / Stojanova, Marija / Katz, Mark H / Gignac, Gretchen A / Wisco, Jonathan J / Heaphy, Christopher M / Denis, Gerald V

    The Prostate

    2022  Volume 82, Issue 10, Page(s) 1005–1015

    Abstract: In patients with prostate cancer, the duration of remission after treatment with androgen deprivation therapies (ADTs) varies dramatically. Clinical experience has demonstrated difficulties in predicting individual risk for progression due to ... ...

    Abstract In patients with prostate cancer, the duration of remission after treatment with androgen deprivation therapies (ADTs) varies dramatically. Clinical experience has demonstrated difficulties in predicting individual risk for progression due to chemoresistance. Drug combinations that inhibit androgen biosynthesis (e.g., abiraterone acetate) and androgen signaling (e.g., enzalutamide or apalutamide) have proven so effective that new forms of ADT resistance are emerging. In particular, prostate cancers with a neuroendocrine transcriptional signature, which demonstrate greater plasticity, and potentially, increased predisposition to metastasize, are becoming more prevalent. Notably, these subtypes had in fact been relatively rare before the widespread success of novel ADT regimens. Therefore, better understanding of these resistance mechanisms and potential alternative treatments are necessary to improve progression-free survival for patients treated with ADT. Targeting the bromodomain and extra-terminal (BET) protein family, specifically BRD4, with newer investigational agents may represent one such option. Several families of chromatin modifiers appear to be involved in ADT resistance and targeting these pathways could also offer novel approaches. However, the limited transcriptional and genomic information on ADT resistance mechanisms, and a serious lack of patient diversity in clinical trials, demand profiling of a much broader clinical and demographic range of patients, before robust conclusions can be drawn and a clear direction established.
    MeSH term(s) Androgen Antagonists/therapeutic use ; Androgens ; Cell Cycle Proteins ; Drug Resistance, Neoplasm/genetics ; Humans ; Male ; Nerve Tissue Proteins/metabolism ; Nuclear Proteins ; Prostatic Neoplasms, Castration-Resistant/drug therapy ; Prostatic Neoplasms, Castration-Resistant/genetics ; Prostatic Neoplasms, Castration-Resistant/metabolism ; Receptors, Cell Surface/metabolism ; Transcription Factors ; Treatment Outcome
    Chemical Substances Androgen Antagonists ; Androgens ; BRD4 protein, human ; Cell Cycle Proteins ; DNER protein, human ; Nerve Tissue Proteins ; Nuclear Proteins ; Receptors, Cell Surface ; Transcription Factors
    Language English
    Publishing date 2022-04-11
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 604707-5
    ISSN 1097-0045 ; 0270-4137
    ISSN (online) 1097-0045
    ISSN 0270-4137
    DOI 10.1002/pros.24351
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  8. Article ; Online: Bromodomain coactivators in cancer, obesity, type 2 diabetes, and inflammation.

    Denis, Gerald V

    Discovery medicine

    2010  Volume 10, Issue 55, Page(s) 489–499

    Abstract: Double bromodomain proteins bind to acetylated lysines in histones, bringing associated histone modification and nucleosome remodeling activity to chromatin. The ability of bromodomain regulators to alter chromatin status and control gene expression has ... ...

    Abstract Double bromodomain proteins bind to acetylated lysines in histones, bringing associated histone modification and nucleosome remodeling activity to chromatin. The ability of bromodomain regulators to alter chromatin status and control gene expression has long been appreciated to be important in the development of certain human cancers. However, bromodomain proteins have now been found also to be critical, non-redundant players in diverse, non-malignant phenotypes, directing transcriptional programs that control adipogenesis, energy metabolism and inflammation. The fact that such different processes are functionally linked by the same molecular machinery suggests a common epigenetic basis to understand and interpret the origins of several important co-morbidities, such as asthma or cancer that occurs in obesity, and complex inflammatory diseases like cardiovascular disease, systemic lupus erythematosus, rheumatoid arthritis and insulin resistance that may be built on a common pro-inflammatory foundation.
    MeSH term(s) Animals ; Diabetes Mellitus, Type 2/metabolism ; Humans ; Inflammation/metabolism ; Neoplasms/metabolism ; Nuclear Proteins/metabolism ; Obesity/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Transcription Factors
    Chemical Substances BRD2 protein, human ; Nuclear Proteins ; Transcription Factors ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2010-12-29
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2415544-5
    ISSN 1944-7930 ; 1944-7930
    ISSN (online) 1944-7930
    ISSN 1944-7930
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Inhibition of LSD1 Attenuates Oral Cancer Development and Promotes Therapeutic Efficacy of Immune Checkpoint Blockade and YAP/TAZ Inhibition.

    Alhousami, Thabet / Diny, Michael / Ali, Faiza / Shin, Jennifer / Kumar, Gaurav / Kumar, Vikas / Campbell, Joshua D / Noonan, Vikki / Hanna, Glenn J / Denis, Gerald V / Monti, Stefano / Kukuruzinska, Maria A / Varelas, Xaralabos / Bais, Manish V

    Molecular cancer research : MCR

    2022  Volume 20, Issue 5, Page(s) 712–721

    Abstract: Lysine-specific demethylase 1 (LSD1) is a histone demethylase that contributes to the etiology of oral squamous cell carcinoma (OSCC) in part by promoting cancer stem cell phenotypes. The molecular signals regulated by LSD1, or acting with LSD1, are ... ...

    Abstract Lysine-specific demethylase 1 (LSD1) is a histone demethylase that contributes to the etiology of oral squamous cell carcinoma (OSCC) in part by promoting cancer stem cell phenotypes. The molecular signals regulated by LSD1, or acting with LSD1, are poorly understood, particularly in the development of OSSC. In this study, we show that conditional deletion of the Lsd1 gene or pharmacologic inhibition of LSD1 in the tongue epithelium leads to reduced development of OSCC following exposure to the tobacco carcinogen 4NQO. LSD1 inhibition attenuated proliferation and clonogenic survival and showed an additive effect when combined with the YAP inhibitor Verteporfin. Interestingly, LSD1 inhibition upregulated the expression of PD-L1, leading to immune checkpoint inhibitor therapy responses.
    Implications: Collectively, our studies reveal a critical role for LSD1 in OSCC development and identification of tumor growth targeting strategies that can be combined with LSD1 inhibition for improved therapeutic application.
    MeSH term(s) Carcinoma, Squamous Cell ; Head and Neck Neoplasms ; Histone Demethylases/genetics ; Humans ; Immune Checkpoint Inhibitors ; Mouth Neoplasms/chemically induced ; Mouth Neoplasms/drug therapy ; Mouth Neoplasms/genetics ; Squamous Cell Carcinoma of Head and Neck/drug therapy ; Squamous Cell Carcinoma of Head and Neck/genetics
    Chemical Substances Immune Checkpoint Inhibitors ; Histone Demethylases (EC 1.14.11.-)
    Language English
    Publishing date 2022-01-30
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2098788-2
    ISSN 1557-3125 ; 1541-7786
    ISSN (online) 1557-3125
    ISSN 1541-7786
    DOI 10.1158/1541-7786.MCR-21-0310
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5744: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    ab Jg. 2022: Lesesaal (EG)

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  10. Article ; Online: BRD4 Regulates Metastatic Potential of Castration-Resistant Prostate Cancer through AHNAK.

    Shafran, Jordan S / Andrieu, Guillaume P / Györffy, Balázs / Denis, Gerald V

    Molecular cancer research : MCR

    2019  Volume 17, Issue 8, Page(s) 1627–1638

    Abstract: The inevitable progression of advanced prostate cancer to castration resistance, and ultimately to lethal metastatic disease, depends on primary or acquired resistance to conventional androgen deprivation therapy (ADT) and accumulated resistance ... ...

    Abstract The inevitable progression of advanced prostate cancer to castration resistance, and ultimately to lethal metastatic disease, depends on primary or acquired resistance to conventional androgen deprivation therapy (ADT) and accumulated resistance strategies to evade androgen receptor (AR) suppression. In prostate cancer cells, AR adaptations that arise in response to ADT are not singular, but diverse, and include gene amplification, mutation, and even complete loss of receptor expression. Collectively, each of these AR adaptations contributes to a complex, heterogeneous, ADT-resistant tumor. Here, we examined prostate cancer cell lines that model common castration-resistant prostate cancer (CRPC) subtypes, each with different AR composition, and focused on novel regulators of tumor progression, the Bromodomain and Extraterminal (BET) family of proteins. We found that BRD4 regulates cell migration across all models of CRPC, regardless of aggressiveness and AR status, whereas BRD2 and BRD3 only regulate migration and invasion in less aggressive models that retain AR expression or signaling. BRD4, a coregulator of gene transcription, controls migration and invasion through transcription of AHNAK, a large scaffolding protein linked to promotion of metastasis in a diverse set of cancers. Furthermore, treatment of CRPC cell lines with low doses of MZ1, a small-molecule, BRD4-selective degrader, inhibits metastatic potential. Overall, these results reveal a novel BRD4-AHNAK pathway that may be targetable to treat metastatic CRPC (mCRPC). IMPLICATIONS: BRD4 functions as the dominant regulator of CRPC cell migration and invasion through direct transcriptional regulation of AHNAK, which together offer a novel targetable pathway to treat metastatic CRPC.
    MeSH term(s) Apoptosis ; Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Cell Movement ; Cell Proliferation ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Neoplasm Metastasis ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Neoplasm Recurrence, Local/genetics ; Neoplasm Recurrence, Local/metabolism ; Neoplasm Recurrence, Local/pathology ; Prognosis ; Prostatic Neoplasms, Castration-Resistant/genetics ; Prostatic Neoplasms, Castration-Resistant/metabolism ; Prostatic Neoplasms, Castration-Resistant/pathology ; Receptors, Androgen/genetics ; Receptors, Androgen/metabolism ; Signal Transduction ; Survival Rate ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Tumor Cells, Cultured
    Chemical Substances AHNAK protein, human ; AR protein, human ; BRD4 protein, human ; Biomarkers, Tumor ; Cell Cycle Proteins ; Membrane Proteins ; Neoplasm Proteins ; Receptors, Androgen ; Transcription Factors
    Language English
    Publishing date 2019-05-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2098788-2
    ISSN 1557-3125 ; 1541-7786
    ISSN (online) 1557-3125
    ISSN 1541-7786
    DOI 10.1158/1541-7786.MCR-18-1279
    Database MEDical Literature Analysis and Retrieval System OnLINE

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