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  1. Article: A sensible approach to targeting STAT3-mediated transcription.

    Bhola, Neil E / Johnson, Daniel E / Grandis, Jennifer R

    Annals of translational medicine

    2016  Volume 4, Issue Suppl 1, Page(s) S57

    Language English
    Publishing date 2016-11-04
    Publishing country China
    Document type Journal Article ; Comment
    ZDB-ID 2893931-1
    ISSN 2305-5847 ; 2305-5839
    ISSN (online) 2305-5847
    ISSN 2305-5839
    DOI 10.21037/atm.2016.10.51
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Discovery and Characterization of ZL-2201, a Potent, Highly Selective, and Orally Bioavailable Small-molecule DNA-PK Inhibitor.

    Lal, Shruti / Bhola, Neil E / Sun, Bee-Chun / Chen, Yuping / Huang, Tom / Morton, Vivian / Chen, Kevin X / Xia, Shanghua / Zhang, Haoyu / Parikh, Nehal S / Ye, Qiuping / Veiby, O Petter / Bellovin, David I / Ji, Yuhua

    Cancer research communications

    2023  Volume 3, Issue 9, Page(s) 1731–1742

    Abstract: DNA-dependent protein kinase (DNA-PK), a driver of the non-homologous end-joining (NHEJ) DNA damage response pathway, plays an instrumental role in repairing double-strand breaks (DSB) induced by DNA-damaging poisons. We evaluate ZL-2201, an orally ... ...

    Abstract DNA-dependent protein kinase (DNA-PK), a driver of the non-homologous end-joining (NHEJ) DNA damage response pathway, plays an instrumental role in repairing double-strand breaks (DSB) induced by DNA-damaging poisons. We evaluate ZL-2201, an orally bioavailable, highly potent, and selective pharmacologic inhibitor of DNA-PK activity, for the treatment of human cancerous malignancies. ZL-2201 demonstrated greater selectivity for DNA-PK and effectively inhibited DNA-PK autophosphorylation in a concentration- and time-dependent manner. Initial data suggested a potential correlation between ataxia-telangiectasia mutated (ATM) deficiency and ZL-2201 sensitivity. More so, ZL-2201 showed strong synergy with topoisomerase II inhibitors independent of ATM status
    Significance: ZL-2201, a potent and selective DNA-PK inhibitor, can target tumor models in combination with DNA DSB-inducing agents such as radiation or doxorubicin, with potential to improve recurrent therapies in the clinic.
    MeSH term(s) Humans ; Administration, Oral ; Phosphorylation ; Animals ; DNA-Activated Protein Kinase/antagonists & inhibitors
    Chemical Substances DNA-Activated Protein Kinase (EC 2.7.11.1)
    Language English
    Publishing date 2023-09-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2767-9764
    ISSN (online) 2767-9764
    DOI 10.1158/2767-9764.CRC-23-0304
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  3. Article ; Online: Interleukin 6 is increased in preclinical HNSCC models of acquired cetuximab resistance, but is not required for maintenance of resistance.

    O'Keefe, Rachel A / Bhola, Neil E / Lee, David S / Johnson, Daniel E / Grandis, Jennifer R

    PloS one

    2020  Volume 15, Issue 1, Page(s) e0227261

    Abstract: The epidermal growth factor receptor inhibitor cetuximab is the only oncogene-targeted agent that has been FDA approved for the treatment of head and neck squamous cell carcinoma (HNSCC). Currently, there are no biomarkers used in the clinic to predict ... ...

    Abstract The epidermal growth factor receptor inhibitor cetuximab is the only oncogene-targeted agent that has been FDA approved for the treatment of head and neck squamous cell carcinoma (HNSCC). Currently, there are no biomarkers used in the clinic to predict which HNSCC tumors will respond to cetuximab, and even in tumors that regress with treatment, acquired resistance occurs in the majority of cases. Though a number of mechanisms of acquired resistance to cetuximab have been identified in preclinical studies, no therapies targeting these resistance pathways have yet been effectively translated into the clinic. To address this unmet need, we examined the role of the cytokine interleukin 6 (IL-6) in acquired cetuximab resistance in preclinical models of HNSCC. We found that IL-6 secretion was increased in PE/CA-PJ49 cells that had acquired resistance to cetuximab compared to the parental cells from which they were derived. However, addition of exogenous IL-6 to parental cells did not promote cetuximab resistance, and inhibition of the IL-6 pathway did not restore cetuximab sensitivity in the cetuximab-resistant cells. Further examination of the IL-6 pathway revealed that expression of IL6R, which encodes a component of the IL-6 receptor, was decreased in cetuximab-resistant cells compared to parental cells, and that treatment of the cetuximab-resistant cells with exogenous IL-6 did not induce phosphorylation of signal transducer and activator of transcription 3, suggesting that the IL-6 pathway was functionally impaired in the cetuximab-resistant cells. These findings demonstrate that, even if IL-6 is increased in the context of cetuximab resistance, it is not necessarily required for maintenance of the resistant phenotype, and that targeting the IL-6 pathway may not restore sensitivity to cetuximab in cetuximab-refractory HNSCC.
    MeSH term(s) Antibodies, Monoclonal, Humanized/pharmacology ; Antibodies, Monoclonal, Humanized/therapeutic use ; Antineoplastic Combined Chemotherapy Protocols/pharmacology ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Carbazoles ; Cell Line, Tumor ; Cetuximab/pharmacology ; Cetuximab/therapeutic use ; Cisplatin/pharmacology ; Cisplatin/therapeutic use ; Drug Resistance, Neoplasm/drug effects ; Drug Resistance, Neoplasm/immunology ; Drug Screening Assays, Antitumor ; ErbB Receptors/antagonists & inhibitors ; Gene Knockdown Techniques ; Head and Neck Neoplasms/drug therapy ; Head and Neck Neoplasms/immunology ; Head and Neck Neoplasms/pathology ; Humans ; Interleukin-6/genetics ; Interleukin-6/immunology ; Interleukin-6/metabolism ; Phosphorylation ; RNA, Small Interfering/metabolism ; Receptors, Interleukin-6/antagonists & inhibitors ; Receptors, Interleukin-6/genetics ; Receptors, Interleukin-6/immunology ; Receptors, Interleukin-6/metabolism ; Recombinant Proteins/immunology ; STAT3 Transcription Factor/metabolism ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Signal Transduction/immunology ; Squamous Cell Carcinoma of Head and Neck/drug therapy ; Squamous Cell Carcinoma of Head and Neck/immunology ; Squamous Cell Carcinoma of Head and Neck/pathology
    Chemical Substances Antibodies, Monoclonal, Humanized ; CBLC137 ; Carbazoles ; IL6 protein, human ; IL6R protein, human ; Interleukin-6 ; RNA, Small Interfering ; Receptors, Interleukin-6 ; Recombinant Proteins ; STAT3 Transcription Factor ; STAT3 protein, human ; EGFR protein, human (EC 2.7.10.1) ; ErbB Receptors (EC 2.7.10.1) ; tocilizumab (I031V2H011) ; Cetuximab (PQX0D8J21J) ; Cisplatin (Q20Q21Q62J)
    Language English
    Publishing date 2020-01-08
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0227261
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  4. Article ; Online: PD-L1 is upregulated via BRD2 in head and neck squamous cell carcinoma models of acquired cetuximab resistance.

    Bhola, Neil E / Njatcha, Christian / Hu, Lanlin / Lee, Eliot D / Shiah, Jamie V / Kim, Mi-Ok / Johnson, Daniel E / Grandis, Jennifer R

    Head & neck

    2021  Volume 43, Issue 11, Page(s) 3364–3373

    Abstract: Background: Tumor models resistant to EGFR tyrosine kinase inhibitors or cisplatin express higher levels of the immune checkpoint molecule PD-L1. We sought to determine whether PD-L1 expression is elevated in head and neck squamous cell carcinoma (HNSCC) ...

    Abstract Background: Tumor models resistant to EGFR tyrosine kinase inhibitors or cisplatin express higher levels of the immune checkpoint molecule PD-L1. We sought to determine whether PD-L1 expression is elevated in head and neck squamous cell carcinoma (HNSCC) models of acquired cetuximab resistance and whether the expression is regulated by bromodomain and extraterminal domain (BET) proteins.
    Methods: Expression of PD-L1 was assessed in HNSCC cell line models of acquired cetuximab resistance. Proteolysis targeting chimera (PROTAC)- and RNAi-mediated targeting were used to assess the role of BET proteins.
    Results: Cetuximab-resistant HNSCC cells expressed elevated PD-L1 compared to cetuximab-sensitive controls. Treatment with the BET inhibitor JQ1, the BET PROTAC MZ1, or RNAi-mediated knockdown of BRD2 decreased PD-L1 expression. Knockdown of BRD2 also reduced the elevated levels of PD-L1 seen in a model of acquired cisplatin resistance.
    Conclusions: PD-L1 is significantly elevated in HNSCC models of acquired cetuximab and cisplatin resistance where BRD2 is the primary regulator.
    MeSH term(s) B7-H1 Antigen/genetics ; Cell Line, Tumor ; Cetuximab/pharmacology ; Drug Resistance, Neoplasm/genetics ; Head and Neck Neoplasms/drug therapy ; Head and Neck Neoplasms/genetics ; Humans ; Squamous Cell Carcinoma of Head and Neck/drug therapy ; Squamous Cell Carcinoma of Head and Neck/genetics ; Transcription Factors
    Chemical Substances B7-H1 Antigen ; BRD2 protein, human ; CD274 protein, human ; Transcription Factors ; Cetuximab (PQX0D8J21J)
    Language English
    Publishing date 2021-08-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 645165-2
    ISSN 1097-0347 ; 0148-6403 ; 1043-3074
    ISSN (online) 1097-0347
    ISSN 0148-6403 ; 1043-3074
    DOI 10.1002/hed.26827
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  5. Article ; Online: Correction: Cross-talk Signaling between HER3 and HPV16 E6 and E7 Mediates Resistance to PI3K Inhibitors in Head and Neck Cancer.

    Brand, Toni M / Hartmann, Stefan / Bhola, Neil E / Li, Hua / Zeng, Yan / O'Keefe, Rachel A / Ranall, Max V / Bandyopadhyay, Sourav / Soucheray, Margaret / Krogan, Nevan J / Kemp, Carolyn / Duvvuri, Umamaheswar / LaVallee, Theresa / Johnson, Daniel E / Ozbun, Michelle A / Bauman, Julie E / Grandis, Jennifer R

    Cancer research

    2022  Volume 82, Issue 17, Page(s) 3187

    Language English
    Publishing date 2022-09-02
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-22-1308
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  6. Article ; Online: Editor's Note: Cross-talk Signaling between HER3 and HPV16 E6 and E7 Mediates Resistance to PI3K Inhibitors in Head and Neck Cancer.

    Brand, Toni M / Hartmann, Stefan / Bhola, Neil E / Li, Hua / Zeng, Yan / O'Keefe, Rachel A / Ranall, Max V / Bandyopadhyay, Sourav / Soucheray, Margaret / Krogan, Nevan J / Kemp, Carolyn / Duvvuri, Umamaheswar / LaVallee, Theresa / Johnson, Daniel E / Ozbun, Michelle A / Bauman, Julie E / Grandis, Jennifer R

    Cancer research

    2022  Volume 82, Issue 17, Page(s) 3188

    Language English
    Publishing date 2022-09-02
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-22-1307
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  7. Article: HGF/Met Signaling in Head and Neck Cancer: Impact on the Tumor Microenvironment.

    Hartmann, Stefan / Bhola, Neil E / Grandis, Jennifer R

    Clinical cancer research : an official journal of the American Association for Cancer Research

    2016  Volume 22, Issue 16, Page(s) 4005–4013

    Abstract: Studies to date have revealed several major molecular alterations that contribute to head and neck squamous cell carcinoma (HNSCC) initiation, progression, metastatic spread, and therapeutic failure. The EGFR is the only FDA-approved therapeutic target, ... ...

    Abstract Studies to date have revealed several major molecular alterations that contribute to head and neck squamous cell carcinoma (HNSCC) initiation, progression, metastatic spread, and therapeutic failure. The EGFR is the only FDA-approved therapeutic target, yet responses to cetuximab have been limited. Activation and cross-talk of cellular receptors and consequent activation of different signaling pathways contribute to limited activity of blockade of a single pathway. The hepatocyte growth factor (HGF) receptor, Met, has been implicated in HNSCC tumorigenesis and EGFR inhibitor resistance. HGF, the sole ligand of Met, is overexpressed in the tumor microenvironment. The role of HGF/Met signaling in proliferation, metastasis, and angiogenesis has been investigated in HNSCC, leading to clinical trials with various Met inhibitors and HGF antibodies. However, the role of the HGF/Met signaling axis in mediating the tumor microenvironment has been relatively understudied in HNSCC. In this review, we discuss the functional roles of Met and HGF in HNSCC with a focus on the tumor microenvironment and the immune system. Clin Cancer Res; 22(16); 4005-13. ©2016 AACR.
    MeSH term(s) Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Carcinoma, Squamous Cell/drug therapy ; Carcinoma, Squamous Cell/etiology ; Carcinoma, Squamous Cell/metabolism ; Carcinoma, Squamous Cell/pathology ; Clinical Trials as Topic ; Drug Evaluation, Preclinical ; Head and Neck Neoplasms/drug therapy ; Head and Neck Neoplasms/etiology ; Head and Neck Neoplasms/metabolism ; Head and Neck Neoplasms/pathology ; Hepatocyte Growth Factor/metabolism ; Humans ; Molecular Targeted Therapy ; Prognosis ; Proto-Oncogene Proteins c-met/metabolism ; Signal Transduction/drug effects ; Squamous Cell Carcinoma of Head and Neck ; Treatment Outcome ; Tumor Microenvironment
    Chemical Substances Antineoplastic Agents ; Hepatocyte Growth Factor (67256-21-7) ; MET protein, human (EC 2.7.10.1) ; Proto-Oncogene Proteins c-met (EC 2.7.10.1)
    Language English
    Publishing date 2016-07-01
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1225457-5
    ISSN 1557-3265 ; 1078-0432
    ISSN (online) 1557-3265
    ISSN 1078-0432
    DOI 10.1158/1078-0432.CCR-16-0951
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  8. Article ; Online: Corrigendum to: The H1047R PIK3CA oncogene induces a senescence-like state, pleiotropy and acute HSP90 dependency in HER2+ mammary epithelial cells.

    Chakrabarty, Anindita / Surendran, Sreeraj / Bhola, Neil E / Mishra, Vishnu S / Wani, Tasaduq Hussain / Baghel, Khemraj S / Arteaga, Carlos L / Garg, Rohini / Chowdhury, Goutam

    Carcinogenesis

    2021  Volume 42, Issue 8, Page(s) 1131

    Language English
    Publishing date 2021-08-06
    Publishing country England
    Document type Published Erratum
    ZDB-ID 603134-1
    ISSN 1460-2180 ; 0143-3334
    ISSN (online) 1460-2180
    ISSN 0143-3334
    DOI 10.1093/carcin/bgab065
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  9. Article ; Online: Correction: Treatment of Triple-Negative Breast Cancer with TORC1/2 Inhibitors Sustains a Drug-Resistant and Notch-Dependent Cancer Stem Cell Population.

    Bhola, Neil E / Jansen, Valerie M / Koch, James P / Li, Hua / Formisano, Luigi / Williams, Janice A / Grandis, Jennifer R / Arteaga, Carlos L

    Cancer research

    2019  Volume 79, Issue 4, Page(s) 875

    Language English
    Publishing date 2019-02-12
    Publishing country United States
    Document type Journal Article ; Published Erratum
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-18-4087
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  10. Article ; Online: Correction: Human Papillomavirus Regulates HER3 Expression in Head and Neck Cancer: Implications for Targeted HER3 Therapy in HPV

    Brand, Toni M / Hartmann, Stefan / Bhola, Neil E / Peyser, Noah D / Li, Hua / Zeng, Yan / Wechsler, Erin Isaacson / Ranall, Max V / Bandyopadhyay, Sourav / Duvvuri, Umamaheswar / LaVallee, Theresa M / Jordan, Richard C K / Johnson, Daniel E / Grandis, Jennifer R

    Clinical cancer research : an official journal of the American Association for Cancer Research

    2021  Volume 27, Issue 14, Page(s) 4129

    Language English
    Publishing date 2021-07-16
    Publishing country United States
    Document type Journal Article ; Published Erratum
    ZDB-ID 1225457-5
    ISSN 1557-3265 ; 1078-0432
    ISSN (online) 1557-3265
    ISSN 1078-0432
    DOI 10.1158/1078-0432.CCR-21-2141
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