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  1. Article: A very long and winding road: developing novel therapeutics for metastatic tumors.

    Dent, Paul

    Oncoscience

    2024  Volume 11, Page(s) 32–33

    Language English
    Publishing date 2024-02-09
    Publishing country United States
    Document type Editorial
    ISSN 2331-4737
    ISSN 2331-4737
    DOI 10.18632/oncoscience.595
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  2. Article ; Online: Investigational CHK1 inhibitors in early phase clinical trials for the treatment of cancer.

    Dent, Paul

    Expert opinion on investigational drugs

    2019  Volume 28, Issue 12, Page(s) 1095–1100

    Abstract: ... ...

    Abstract Introduction
    MeSH term(s) Animals ; Antineoplastic Agents/administration & dosage ; Antineoplastic Agents/adverse effects ; Antineoplastic Agents/pharmacology ; Antineoplastic Combined Chemotherapy Protocols/administration & dosage ; Antineoplastic Combined Chemotherapy Protocols/adverse effects ; Antineoplastic Combined Chemotherapy Protocols/pharmacology ; Checkpoint Kinase 1/antagonists & inhibitors ; Checkpoint Kinase 1/metabolism ; Drug Development ; Drugs, Investigational/adverse effects ; Drugs, Investigational/pharmacology ; Humans ; Neoplasms/drug therapy ; Neoplasms/enzymology ; Protein Kinase Inhibitors/administration & dosage ; Protein Kinase Inhibitors/adverse effects ; Protein Kinase Inhibitors/pharmacology
    Chemical Substances Antineoplastic Agents ; Drugs, Investigational ; Protein Kinase Inhibitors ; CHEK1 protein, human (EC 2.7.11.1) ; Checkpoint Kinase 1 (EC 2.7.11.1)
    Language English
    Publishing date 2019-11-29
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1182884-5
    ISSN 1744-7658 ; 0967-8298 ; 1354-3784
    ISSN (online) 1744-7658
    ISSN 0967-8298 ; 1354-3784
    DOI 10.1080/13543784.2019.1694661
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  3. Article ; Online: GZ17-6.02 interacts with proteasome inhibitors to kill multiple myeloma cells.

    Booth, Laurence / Roberts, Jane L / West, Cameron / Dent, Paul

    Oncotarget

    2024  Volume 15, Page(s) 159–174

    Abstract: GZ17-6.02, a synthetically manufactured compound containing isovanillin, harmine and curcumin, has undergone phase I evaluation in patients with solid tumors (NCT03775525) with a recommended phase 2 dose (RP2D) of 375 mg PO BID. GZ17-6.02 was more ... ...

    Abstract GZ17-6.02, a synthetically manufactured compound containing isovanillin, harmine and curcumin, has undergone phase I evaluation in patients with solid tumors (NCT03775525) with a recommended phase 2 dose (RP2D) of 375 mg PO BID. GZ17-6.02 was more efficacious as a single agent at killing multiple myeloma cells than had previously been observed in solid tumor cell types. GZ17-6.02 interacted with proteasome inhibitors in a greater than additive fashion to kill myeloma cells and alone it killed inhibitor-resistant cells to a similar extent. The drug combination of GZ17-6.02 and bortezomib activated ATM, the AMPK and PERK and inactivated ULK1, mTORC1, eIF2α, NFκB and the Hippo pathway. The combination increased ATG13 S318 phosphorylation and the expression of Beclin1, ATG5, BAK and BIM, and reduced the levels of BCL-XL and MCL1. GZ17-6.02 interacted with bortezomib to enhance autophagosome formation and autophagic flux, and knock down of ATM, AMPKα, ULK1, Beclin1 or ATG5 significantly reduced both autophagy and tumor cell killing. Knock down of BAK and BIM significantly reduced tumor cell killing. The expression of HDACs1/2/3 was significantly reduced beyond that previously observed in solid tumor cells and required autophagy. This was associated with increased acetylation and methylation of histone H3. Combined knock down of HDACs1/2/3 caused activation of ATM and the AMPK and caused inactivation of ULK1, mTORC1, NFκB and the Hippo pathway. HDAC knock down also enhanced ATG13 phosphorylation, increased BAK levels and reduced those of BCL-XL. Collectively, our present studies support performing additional
    MeSH term(s) Humans ; Proteasome Inhibitors/pharmacology ; Multiple Myeloma/drug therapy ; Bortezomib/pharmacology ; AMP-Activated Protein Kinases ; Beclin-1 ; Antineoplastic Agents/pharmacology ; Mechanistic Target of Rapamycin Complex 1
    Chemical Substances Proteasome Inhibitors ; Bortezomib (69G8BD63PP) ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Beclin-1 ; Antineoplastic Agents ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
    Language English
    Publishing date 2024-03-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.28558
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Cell Signaling and Translational Developmental Therapeutics

    Dent, Paul

    Reference Module in Chemistry, Molecular Sciences and Chemical Engineering

    Abstract: The relationships between drug pharmacodynamics and subsequent changes in cellular signaling processes are complex. Many in vitro cell signaling studies often use drug concentrations above physiologically safe drug levels achievable in a patient's plasma. ...

    Abstract The relationships between drug pharmacodynamics and subsequent changes in cellular signaling processes are complex. Many in vitro cell signaling studies often use drug concentrations above physiologically safe drug levels achievable in a patient's plasma. Drug companies develop agents to inhibit or modify the activities of specific target enzymes, often without a full consideration that their compounds have additional unknown targets. These two negative sequelae, when published together, become impediments against successful developmental therapeutics and translation because this data distorts our understanding of signaling mechanisms and reduces the probability of successfully translating drug-based concepts from the bench to the bedside. This article will discuss cellular signaling in isolation and as it relates to extant single and combined therapeutic drug interventions. This will lead to a hypothetical series standardized sequential approaches describing a rigorous concept to drug development and clinical translation.
    Keywords covid19
    Publisher Elsevier; PMC
    Document type Article ; Online
    DOI 10.1016/b978-0-12-820472-6.00002-5
    Database COVID19

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  5. Book: Remodelling hospitals and health professions in Europe

    Dent, Mike

    medicine, nursing and the state

    2003  

    Author's details Mike Dent
    Keywords Hospital Restructuring ; Nursing Service, Hospital / organization & administration ; Quality Assurance, Health Care / organization & administration ; Health services administration/Employee participation ; Europe
    Subject code 362.1094
    Language English
    Size XVI, 208 S.
    Publisher Palgrave Macmillan
    Publishing place Basingstoke, Hampshire u.a.
    Publishing country Great Britain
    Document type Book
    HBZ-ID HT013445919
    ISBN 0-333-76067-0 ; 978-0-333-76067-3
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    2006 A 5245 order for loan Magazin

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  6. Article ; Online: GZ17-6.02 interacts with bexarotene to kill mycosis fungoides cells.

    Booth, Michael R / Booth, Laurence / Roberts, Jane L / West, Cameron / Dent, Paul

    Oncotarget

    2024  Volume 15, Page(s) 124–133

    Abstract: GZ17-6.02, composed of curcumin, harmine and isovanillin, has undergone phase I evaluation in patients with solid tumors (NCT03775525) with an RP2D of 375 mg PO BID. The biology of GZ17-6.02 in malignant T cells and in particular those derived from ... ...

    Abstract GZ17-6.02, composed of curcumin, harmine and isovanillin, has undergone phase I evaluation in patients with solid tumors (NCT03775525) with an RP2D of 375 mg PO BID. The biology of GZ17-6.02 in malignant T cells and in particular those derived from mycosis fungoides (MF) patients, has not been studied. GZ17-6.02 alone and in combination with standard-of-care agents was effective in killing MF cells. All three components are necessary for optimal killing of MF cells. GZ17-6.02 activated ATM, the AMPK, NFκB and PERK and inactivated ERK1/2, AKT, ULK1, mTORC1, eIF2α, and reduced the expression of BCL-XL and MCL1. GZ17-6.02 increased ATG13 S318 phosphorylation and the expression of Beclin1, ATG5, BAK and BIM. GZ17-6.02 in a dose-dependent fashion enhanced autophagosome formation and autophagic flux, and tumor cell killing. Signaling by ATM and AMPK were both required for efficient killing but not for the dose-response effect whereas ER stress (eIF2α) and macroautophagy (Beclin1, ATG5) were required for both efficient killing and the dose-response. Knock down of the death receptor CD95 reduced killing by ~20% and interacted with autophagy inhibition to further reduce killing, collectively, by ~70%. Inhibition of autophagy and knock down of death-mediators downstream of the mitochondrion, AIF and caspase 3, almost abolished tumor cell killing. Hence in MF cells, GZ17-6.02 is a multi-factorial killer, utilizing ER stress, macroautophagy, death receptor signaling and directly causing mitochondrial dysfunction.
    MeSH term(s) Humans ; Bexarotene/pharmacology ; AMP-Activated Protein Kinases ; Beclin-1/genetics ; Antineoplastic Agents ; Mycosis Fungoides ; Skin Neoplasms/drug therapy ; Skin Neoplasms/genetics ; Receptors, Death Domain
    Chemical Substances Bexarotene (A61RXM4375) ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Beclin-1 ; Antineoplastic Agents ; Receptors, Death Domain
    Language English
    Publishing date 2024-02-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.28557
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  7. Article ; Online: Autophagy as a therapeutic mechanism to kill drug-resistant cancer cells.

    Booth, Laurence / Roberts, Jane L / Poklepovic, Andrew / Dent, Paul

    Anti-cancer drugs

    2023  Volume 35, Issue 2, Page(s) 177–182

    Abstract: Herein we discuss multiple pre-clinical projects developed by our group that have been translated into patients at Massey Cancer Center. Our work has used multi-kinase inhibitors, for example, sorafenib, regorafenib and neratinib, and combined with ... ...

    Abstract Herein we discuss multiple pre-clinical projects developed by our group that have been translated into patients at Massey Cancer Center. Our work has used multi-kinase inhibitors, for example, sorafenib, regorafenib and neratinib, and combined with additional agents, for example, histone deacetylase inhibitors, the thymidylate synthase inhibitor pemetrexed, and PDE5 inhibitors. In broad-brush terms, our experience has been that these drug combinations enhance signaling by ATM-AMPK-ULK-1 and decrease signaling from growth factor receptors and RAS proteins, thereby lowering the activities of the intracellular signaling kinase ERK1/2, AKT, mTOR and p70 S6K . This collectively results in reduced protein synthesis and the induction of an endoplasmic reticulum stress response alongside autophagosome formation and autophagic flux. The rupture of autolysosomes, releasing proteases such as cathepsin B into the cytosol results in the cleavage and activation of the toxic BH3 domain protein BID which cooperates with BAX, BAK and BIM to cause mitochondrial dysfunction, leading to the release of cytochrome c and AIF, which then execute the tumor cell. For each of our two-drug combinations, we then performed additional laboratory-based studies to define the development of evolutionary resistance mechanisms, with the long-term concept of performing new three-drug clinical trials to prolong therapeutic efficacy and disease control.
    MeSH term(s) Humans ; Sorafenib ; Signal Transduction ; Histone Deacetylase Inhibitors/pharmacology ; Autophagy ; Drug Combinations ; Cell Line, Tumor ; Neoplasms/drug therapy
    Chemical Substances Sorafenib (9ZOQ3TZI87) ; Histone Deacetylase Inhibitors ; Drug Combinations
    Language English
    Publishing date 2023-10-16
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1065301-6
    ISSN 1473-5741 ; 0959-4973
    ISSN (online) 1473-5741
    ISSN 0959-4973
    DOI 10.1097/CAD.0000000000001549
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  8. Article ; Online: A novel combination of isovanillin, curcumin, and harmine (GZ17-6.02) enhances cell death and alters signaling in actinic keratoses cells when compared to individual components and two-component combinations.

    Bordeaux, Zachary A / Kwatra, Shawn G / Booth, Laurence / Dent, Paul

    Anti-cancer drugs

    2023  Volume 34, Issue 4, Page(s) 544–550

    Abstract: Actinic keratosis is a pre-malignant skin disease caused by excessive exposure to ultraviolet light. The present studies further defined the biology of a novel combination of isovanillin, curcumin, and harmine in actinic keratosis cells in vitro . An ... ...

    Abstract Actinic keratosis is a pre-malignant skin disease caused by excessive exposure to ultraviolet light. The present studies further defined the biology of a novel combination of isovanillin, curcumin, and harmine in actinic keratosis cells in vitro . An oral formulation (GZ17-6.02) and topical preparation (GZ21T) comprised of the same fixed, stoichiometric ratio have been developed. Together, the three active ingredients killed actinic keratosis cells more effectively than any of its component parts as either individual agents or when combined in pairs. The three active ingredients caused greater levels of DNA damage than any of its component parts as either individual agents or when combined in pairs. As a single agent, compared to isolated components, GZ17-6.02/GZ21T caused significantly greater activation of PKR-like endoplasmic reticulum kinase, the AMP-dependent protein kinase, and ULK1 and significantly reduced the activities of mTORC1, AKT, and YAP. Knockdown of the autophagy-regulatory proteins ULK1, Beclin1, or ATG5 significantly reduced the lethality of GZ17-6.02/GZ21T alone. Expression of an activated mammalian target of rapamycin mutant suppressed autophagosome formation and autophagic flux and reduced tumor cell killing. Blockade of both autophagy and death receptor signaling abolished drug-induced actinic keratosis cell death. Our data demonstrate that the unique combination of isovanillin, curcumin, and harmine represents a novel therapeutic with the potential to treat actinic keratosis in a manner different from the individual components or pairs of the components.
    MeSH term(s) Humans ; Keratosis, Actinic ; Curcumin/pharmacology ; Harmine/pharmacology ; Antineoplastic Agents ; Cell Death
    Chemical Substances Curcumin (IT942ZTH98) ; Harmine (4FHH5G48T7) ; isovanillin (4A9N90H9X6) ; Antineoplastic Agents
    Language English
    Publishing date 2023-02-24
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1065301-6
    ISSN 1473-5741 ; 0959-4973
    ISSN (online) 1473-5741
    ISSN 0959-4973
    DOI 10.1097/CAD.0000000000001425
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  9. Article ; Online: Cellular responses after (neratinib plus pemetrexed) exposure in NSCLC cells.

    Booth, Laurence / Poklepovic, Andrew / Hancock, John F / Dent, Paul

    Anti-cancer drugs

    2023  Volume 34, Issue 9, Page(s) 1025–1034

    Abstract: We previously demonstrated that neratinib interacted with pemetrexed to kill non-small cell lung cancer (NSCLC) cells. From developing other drug combinations, we observed that several days following exposure, cells activated survival mechanisms to ... ...

    Abstract We previously demonstrated that neratinib interacted with pemetrexed to kill non-small cell lung cancer (NSCLC) cells. From developing other drug combinations, we observed that several days following exposure, cells activated survival mechanisms to counteract drug toxicity. The present studies attempted to define mechanisms that evolve to reduce the efficacy of neratinib and pemetrexed. Neratinib and pemetrexed synergized to kill NSCLC cells expressing wild-type RAS proteins, mutant KRAS (G12S; Q61H; G12A and G12C) or mutant NRAS (Q61K) or mutant ERBB1 (L858R; L858R T790M and exon 19 deletion). Neratinib and pemetrexed interacted in a greater than additive fashion to kill after 24 h, and after a further 24 h culture in the absence of drugs. Mutant KRAS G12V was more cytoprotective than either activated MEK1 or activated AKT. Knockdown of mutant KRAS reduced drug combination killing at the 48 h timepoint. Despite culture for 24 h in the absence of the drugs, the expression and activities of ERBB1, ERBB2 and ERBB4 remained significantly lower as did the activities of mammalian target of rapamycin (mTOR) C1 and mTORC2. The drug combination reduced KRAS and NRAS levels for 24 h, however, in the absence of the drugs, RAS levels had normalized by 48 h. Expression of Beclin1 and ATG5 remained elevated and of MCL1 and BCL-XL lower. No evolutionary activations of survival signaling by ERBB3, c-KIT, c-MET or PDGFRβ or in intracellular signaling pathways were observed. These findings argue against the development of 'early' resistance mechanisms after neratinib and pemetrexed exposure. Future studies will be required to understand how NSCLC cells become resistant to neratinib and pemetrexed.
    MeSH term(s) Humans ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/genetics ; Pemetrexed/pharmacology ; ErbB Receptors ; Proto-Oncogene Proteins p21(ras) ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Mutation ; Protein Kinase Inhibitors
    Chemical Substances Pemetrexed (04Q9AIZ7NO) ; neratinib (JJH94R3PWB) ; ErbB Receptors (EC 2.7.10.1) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; Protein Kinase Inhibitors
    Language English
    Publishing date 2023-08-31
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1065301-6
    ISSN 1473-5741 ; 0959-4973
    ISSN (online) 1473-5741
    ISSN 0959-4973
    DOI 10.1097/CAD.0000000000001442
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  10. Article ; Online: Not so WEE: targeting G₂/M to kill mesothelioma cells.

    Dent, Paul

    Cancer biology & therapy

    2014  Volume 15, Issue 4, Page(s) 351–352

    Abstract: It has been known for many years that manipulation of cell cycle checkpoint function represents one approach by which the toxicity of chemotherapy and of ionizing radiation can be increased in tumor cells. (1)(-) (3) In particular, abrogation of the G 2/ ... ...

    Abstract It has been known for many years that manipulation of cell cycle checkpoint function represents one approach by which the toxicity of chemotherapy and of ionizing radiation can be increased in tumor cells. (1)(-) (3) In particular, abrogation of the G 2/M checkpoint has been shown to enhance the lethality of a wide range of toxic stresses. (1)(-) (3) Inhibition of the G 2/M checkpoint after chemotherapy/irradiation would result in tumor cells entering mitosis with damaged DNA, which would in turn result in loss of clonogenic survival (i.e., a lethal mitosis).
    MeSH term(s) Antineoplastic Agents/pharmacology ; Cell Cycle Proteins/antagonists & inhibitors ; Cisplatin/pharmacology ; G2 Phase Cell Cycle Checkpoints ; Humans ; Lung Neoplasms/drug therapy ; Mesothelioma/drug therapy ; Mesothelioma, Malignant ; Nuclear Proteins/antagonists & inhibitors ; Protein-Tyrosine Kinases/antagonists & inhibitors ; Pyrazoles/pharmacology ; Pyrimidines/pharmacology ; Pyrimidinones
    Chemical Substances Antineoplastic Agents ; Cell Cycle Proteins ; Nuclear Proteins ; Pyrazoles ; Pyrimidines ; Pyrimidinones ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; WEE1 protein, human (EC 2.7.10.2) ; adavosertib (K2T6HJX3I3) ; Cisplatin (Q20Q21Q62J)
    Language English
    Publishing date 2014-02-04
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 2146305-0
    ISSN 1555-8576 ; 1538-4047
    ISSN (online) 1555-8576
    ISSN 1538-4047
    DOI 10.4161/cbt.27851
    Database MEDical Literature Analysis and Retrieval System OnLINE

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