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  1. Book: Cancer prevention

    Bode, Ann M. / Dong, Zigang

    dietary factors and pharmacology

    (Methods in pharmacology and toxicology ; Springer protocols)

    2014  

    Author's details ed. by Ann M. Bode and Zigang Dong
    Series title Methods in pharmacology and toxicology
    Springer protocols
    Language English
    Size XV, 288 S. : Ill., graph. Darst.
    Publisher Humana Press
    Publishing place New York u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT018120378
    ISBN 978-1-4614-9226-9 ; 1-4614-9226-2 ; 9781461492276 ; 1461492270
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2014 A 43 available for loan (reading room) Lesesaal EG

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  2. Article: Recent Advances in Carcinogenesis Transcription Factors: Biomarkers and Targeted Therapies.

    Bode, Ann M / Zhang, Tianshun

    Cancers

    2023  Volume 15, Issue 19

    Abstract: Carcinogenesis, the process by which normal cells transform into cancer cells, is complex and multifaceted [ ... ]. ...

    Abstract Carcinogenesis, the process by which normal cells transform into cancer cells, is complex and multifaceted [...].
    Language English
    Publishing date 2023-09-22
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers15194673
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Targeting CDK1 in cancer: mechanisms and implications.

    Wang, Qiushi / Bode, Ann M / Zhang, Tianshun

    NPJ precision oncology

    2023  Volume 7, Issue 1, Page(s) 58

    Abstract: Cyclin dependent kinases (CDKs) are serine/threonine kinases that are proposed as promising candidate targets for cancer treatment. These proteins complexed with cyclins play a critical role in cell cycle progression. Most CDKs demonstrate substantially ... ...

    Abstract Cyclin dependent kinases (CDKs) are serine/threonine kinases that are proposed as promising candidate targets for cancer treatment. These proteins complexed with cyclins play a critical role in cell cycle progression. Most CDKs demonstrate substantially higher expression in cancer tissues compared with normal tissues and, according to the TCGA database, correlate with survival rate in multiple cancer types. Deregulation of CDK1 has been shown to be closely associated with tumorigenesis. CDK1 activation plays a critical role in a wide range of cancer types; and CDK1 phosphorylation of its many substrates greatly influences their function in tumorigenesis. Enrichment of CDK1 interacting proteins with Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis was conducted to demonstrate that the associated proteins participate in multiple oncogenic pathways. This abundance of evidence clearly supports CDK1 as a promising target for cancer therapy. A number of small molecules targeting CDK1 or multiple CDKs have been developed and evaluated in preclinical studies. Notably, some of these small molecules have also been subjected to human clinical trials. This review evaluates the mechanisms and implications of targeting CDK1 in tumorigenesis and cancer therapy.
    Language English
    Publishing date 2023-06-13
    Publishing country England
    Document type Journal Article ; Review
    ISSN 2397-768X
    ISSN 2397-768X
    DOI 10.1038/s41698-023-00407-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Metabolic reprogramming in nasopharyngeal carcinoma: Mechanisms and therapeutic opportunities.

    Liu, Qian / Bode, Ann M / Chen, Xue / Luo, Xiangjian

    Biochimica et biophysica acta. Reviews on cancer

    2023  Volume 1878, Issue 6, Page(s) 189023

    Abstract: The high prevalence of metabolic reprogramming in nasopharyngeal carcinoma (NPC) offers an abundance of potential therapeutic targets. This review delves into the distinct mechanisms underlying metabolic reprogramming in NPC, including enhanced ... ...

    Abstract The high prevalence of metabolic reprogramming in nasopharyngeal carcinoma (NPC) offers an abundance of potential therapeutic targets. This review delves into the distinct mechanisms underlying metabolic reprogramming in NPC, including enhanced glycolysis, nucleotide synthesis, and lipid metabolism. All of these changes are modulated by Epstein-Barr virus (EBV) infection, hypoxia, and tumor microenvironment. We highlight the role of metabolic reprogramming in the development of NPC resistance to standard therapies, which represents a challenging barrier in treating this malignancy. Furthermore, we dissect the state of the art in therapeutic strategies that target these metabolic changes, evaluating the successes and failures of clinical trials and the strategies to tackle resistance mechanisms. By providing a comprehensive overview of the current knowledge and future directions in this field, this review sets the stage for new therapeutic avenues in NPC.
    MeSH term(s) Humans ; Nasopharyngeal Carcinoma/metabolism ; Nasopharyngeal Carcinoma/pathology ; Epstein-Barr Virus Infections/complications ; Carcinoma/metabolism ; Nasopharyngeal Neoplasms/metabolism ; Nasopharyngeal Neoplasms/pathology ; Herpesvirus 4, Human/metabolism ; Tumor Microenvironment
    Language English
    Publishing date 2023-11-16
    Publishing country Netherlands
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2918802-7
    ISSN 1879-2561 ; 0304-419X
    ISSN (online) 1879-2561
    ISSN 0304-419X
    DOI 10.1016/j.bbcan.2023.189023
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 7162: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: Are FDA-Approved Sunscreen Components Effective in Preventing Solar UV-Induced Skin Cancer?

    Bode, Ann M / Roh, Eunmiri

    Cells

    2020  Volume 9, Issue 7

    Abstract: Solar ultraviolet (SUV) exposure is a major risk factor in the etiology of cutaneous squamous cell carcinoma (cSCC). People commonly use sunscreens to prevent SUV-induced skin damage and cancer. Nonetheless, the prevalence of cSCC continues to increase ... ...

    Abstract Solar ultraviolet (SUV) exposure is a major risk factor in the etiology of cutaneous squamous cell carcinoma (cSCC). People commonly use sunscreens to prevent SUV-induced skin damage and cancer. Nonetheless, the prevalence of cSCC continues to increase every year, suggesting that commercially available sunscreens might not be used appropriately or are not completely effective. In the current study, a solar simulated light (SSL)-induced cSCC mouse model was used to investigate the efficacy of eight commonly used FDA-approved sunscreen components against skin carcinogenesis. First, we tested FDA-approved sunscreen components for their ability to block UVA or UVB irradiation by using VITRO-SKIN (a model that mimics human skin properties), and then the efficacy of FDA-approved sunscreen components was investigated in an SSL-induced cSCC mouse model. Our results identified which FDA-approved sunscreen components or combinations are effective in preventing cSCC development. Not surprisingly, the results indicated that sunscreen combinations that block both UVA and UVB significantly suppressed the formation of cutaneous papillomas and cSCC development and decreased the activation of oncoproteins and the expression of COX-2, keratin 17, and EGFR in SSL-exposed SKH-1 (Crl:SKH1-
    MeSH term(s) Animals ; Cell Proliferation/drug effects ; Drug Approval ; Female ; Humans ; Mice, Hairless ; Oncogenes ; Phosphorylation/drug effects ; Protein Kinases/metabolism ; Skin/drug effects ; Skin/radiation effects ; Skin Neoplasms/etiology ; Skin Neoplasms/pathology ; Skin Neoplasms/prevention & control ; Sunscreening Agents/chemistry ; Sunscreening Agents/pharmacology ; Ultraviolet Rays ; United States ; United States Food and Drug Administration
    Chemical Substances Sunscreening Agents ; Protein Kinases (EC 2.7.-)
    Language English
    Publishing date 2020-07-11
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells9071674
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Fyn-mediated phosphorylation of Menin disrupts telomere maintenance in stem cells.

    Paul, Souren / McCourt, Preston M / Le, Le Thi My / Ryu, Joohyun / Czaja, Wioletta / Bode, Ann M / Contreras-Galindo, Rafael / Dong, Zigang

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Telomeres protect chromosome ends and determine the replication potential of dividing cells. The canonical telomere sequence TTAGGG is synthesized by telomerase holoenzyme, which maintains telomere length in proliferative stem cells. Although the core ... ...

    Abstract Telomeres protect chromosome ends and determine the replication potential of dividing cells. The canonical telomere sequence TTAGGG is synthesized by telomerase holoenzyme, which maintains telomere length in proliferative stem cells. Although the core components of telomerase are well-defined, mechanisms of telomerase regulation are still under investigation. We report a novel role for the Src family kinase Fyn, which disrupts telomere maintenance in stem cells by phosphorylating the scaffold protein Menin. We found that Fyn knockdown prevented telomere erosion in human and mouse stem cells, validating the results with four telomere measurement techniques. We show that Fyn phosphorylates Menin at tyrosine 603 (Y603), which increases Menin's SUMO1 modification, C-terminal stability, and importantly, its association with the telomerase RNA component (TR). Using mass spectrometry, immunoprecipitation, and immunofluorescence experiments we found that SUMO1-Menin decreases TR's association with telomerase subunit Dyskerin, suggesting that Fyn's phosphorylation of Menin induces telomerase subunit mislocalization and may compromise telomerase function at telomeres. Importantly, we find that Fyn inhibition reduces accelerated telomere shortening in human iPSCs harboring mutations for dyskeratosis congenita.
    Language English
    Publishing date 2024-03-19
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.10.04.560876
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Endometriosis: Cell Death and Cell Signaling Machinery.

    Carbone, Ginearosa / Nelson, Katherine / Baumgartner, Claire / Bode, Ann M / Takahashi, Akimasa / Chefetz, Ilana

    Endocrinology

    2023  Volume 164, Issue 6

    Abstract: Endometriosis is an estrogen-dependent disorder defined as the deposition and growth of endometrial tissue outside the uterus, including but not limited to the pelvic peritoneum, rectovaginal septum, and ovaries. Endometriosis is a substantial ... ...

    Abstract Endometriosis is an estrogen-dependent disorder defined as the deposition and growth of endometrial tissue outside the uterus, including but not limited to the pelvic peritoneum, rectovaginal septum, and ovaries. Endometriosis is a substantial contributor to pelvic pain and subfertility and has been associated with an increased incidence of certain cancers, including ovarian. Appropriate treatment of endometriosis can reduce morbidity, but generally is used only to address symptoms, since no cure currently exists. Multifactorial etiologies for endometriosis have been proposed, with significant evidence for genetic, immune, and environmental causes. Recent advances suggest that molecular signaling and programmed cell death pathways are involved in endometriosis, suggesting avenues for future curative treatments. The goal of this review is to examine the pathologic processes of endometriosis, focusing on cell signaling and cell death pathways, stem cells, treatment regimens, and future directions surrounding this gynecologic disorder.
    MeSH term(s) Female ; Humans ; Endometriosis/pathology ; Peritoneum/metabolism ; Peritoneum/pathology ; Uterus/metabolism ; Signal Transduction ; Cell Death
    Language English
    Publishing date 2023-05-20
    Publishing country United States
    Document type Review ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 427856-2
    ISSN 1945-7170 ; 0013-7227
    ISSN (online) 1945-7170
    ISSN 0013-7227
    DOI 10.1210/endocr/bqad057
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.72: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  8. Article: Recent advances in precision oncology research.

    Bode, Ann M / Dong, Zigang

    NPJ precision oncology

    2018  Volume 2, Page(s) 11

    Language English
    Publishing date 2018-04-16
    Publishing country England
    Document type Editorial
    ISSN 2397-768X
    ISSN 2397-768X
    DOI 10.1038/s41698-018-0055-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Roles of regulator of chromosome condensation 2 in cancer: Beyond its regulatory function in cell cycle.

    Calderon-Aparicio, Ali / Bode, Ann M

    Oncology reviews

    2021  Volume 15, Issue 1, Page(s) 525

    Abstract: Regulator of chromosome condensation 2 (RCC2) is an essential protein in order for mitosis to proceed properly. It localizes in the centrosome of chromosomes where is involved in chromosome segregation and cytokinesis. Furthermore, RCC2 associates with ... ...

    Abstract Regulator of chromosome condensation 2 (RCC2) is an essential protein in order for mitosis to proceed properly. It localizes in the centrosome of chromosomes where is involved in chromosome segregation and cytokinesis. Furthermore, RCC2 associates with integrin networks at the plasma membrane where participates in the control of cell movement. Because of its known role in cell cycle, RCC2 has been linked with cancer progression. Several reports show that RCC2 induces cancer hallmarks, but the mechanisms explaining how RCC2 exerts these roles are widely unknown. Here, we aim to summarize the main findings explaining the roles and mechanisms of RCC2 in cancer promotion. RCC2 is overexpressed in different cancers, including glioblastoma, lung, ovarian, and esophageal which is related to proliferation, migration, invasion promotion
    Language English
    Publishing date 2021-03-19
    Publishing country Italy
    Document type Journal Article
    ZDB-ID 2390302-8
    ISSN 1970-5565 ; 1970-5565 ; 1970-5557
    ISSN (online) 1970-5565
    ISSN 1970-5565 ; 1970-5557
    DOI 10.4081/oncol.2021.525
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6550: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  10. Article ; Online: Are FDA-Approved Sunscreen Components Effective in Preventing Solar UV-Induced Skin Cancer?

    Ann M. Bode / Eunmiri Roh

    Cells, Vol 9, Iss 1674, p

    2020  Volume 1674

    Abstract: Solar ultraviolet (SUV) exposure is a major risk factor in the etiology of cutaneous squamous cell carcinoma (cSCC). People commonly use sunscreens to prevent SUV-induced skin damage and cancer. Nonetheless, the prevalence of cSCC continues to increase ... ...

    Abstract Solar ultraviolet (SUV) exposure is a major risk factor in the etiology of cutaneous squamous cell carcinoma (cSCC). People commonly use sunscreens to prevent SUV-induced skin damage and cancer. Nonetheless, the prevalence of cSCC continues to increase every year, suggesting that commercially available sunscreens might not be used appropriately or are not completely effective. In the current study, a solar simulated light (SSL)-induced cSCC mouse model was used to investigate the efficacy of eight commonly used FDA-approved sunscreen components against skin carcinogenesis. First, we tested FDA-approved sunscreen components for their ability to block UVA or UVB irradiation by using VITRO-SKIN (a model that mimics human skin properties), and then the efficacy of FDA-approved sunscreen components was investigated in an SSL-induced cSCC mouse model. Our results identified which FDA-approved sunscreen components or combinations are effective in preventing cSCC development. Not surprisingly, the results indicated that sunscreen combinations that block both UVA and UVB significantly suppressed the formation of cutaneous papillomas and cSCC development and decreased the activation of oncoproteins and the expression of COX-2, keratin 17, and EGFR in SSL-exposed SKH-1 (Crl:SKH1- Hr hr ) hairless mouse skin. Notably, several sunscreen components that were individually purported to block both UVA and UVB were ineffective alone. At least one component had toxic effects that led to a high mortality rate in mice exposed to SSL. Our findings provide new insights into the development of the best sunscreen to prevent chronic SUV-induced cSCC development.
    Keywords sunscreen ; prevention ; cutaneous squamous cell carcinoma ; skin cancer ; solar ultraviolet ; skin carcinogenesis ; Biology (General) ; QH301-705.5
    Subject code 571
    Language English
    Publishing date 2020-07-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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