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Article ; Online: Therapeutic high affinity T cell receptor targeting a KRAS

Poole, Andrew / Karuppiah, Vijaykumar / Hartt, Annabelle / Haidar, Jaafar N / Moureau, Sylvie / Dobrzycki, Tomasz / Hayes, Conor / Rowley, Christopher / Dias, Jorge / Harper, Stephen / Barnbrook, Keir / Hock, Miriam / Coles, Charlotte / Yang, Wei / Aleksic, Milos / Lin, Aimee Bence / Robinson, Ross / Dukes, Joe D / Liddy, Nathaniel /

Van der Kamp, Marc / Plowman, Gregory D / Vuidepot, Annelise / Cole, David K / Whale, Andrew D / Chillakuri, Chandramouli

Nature communications

2022 Volume 13, Issue 1, Page(s) 5333

Abstract: Neoantigens derived from somatic mutations are specific to cancer cells and are ideal targets for cancer immunotherapy. KRAS is the most frequently mutated oncogene and drives the pathogenesis of several cancers. Here we show the identification and ... ...

Abstract	Neoantigens derived from somatic mutations are specific to cancer cells and are ideal targets for cancer immunotherapy. KRAS is the most frequently mutated oncogene and drives the pathogenesis of several cancers. Here we show the identification and development of an affinity-enhanced T cell receptor (TCR) that recognizes a peptide derived from the most common KRAS mutant, KRAS
MeSH term(s)	Humans ; Lung Neoplasms/genetics ; Proto-Oncogene Proteins p21(ras)/genetics ; Receptors, Antigen, T-Cell/genetics
Chemical Substances	KRAS protein, human ; Receptors, Antigen, T-Cell ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
Language	English
Publishing date	2022-09-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-32811-1
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Article ; Online: Characterization of 7A5: A Human CD137 (4-1BB) Receptor Binding Monoclonal Antibody with Differential Agonist Properties That Promotes Antitumor Immunity.

Kotanides, Helen / Sattler, Rose Marie / Lebron, Maria B / Carpenito, Carmine / Shen, Juqun / Li, Jingxing / Surguladze, David / Haidar, Jaafar N / Burns, Colleen / Shen, Leyi / Inigo, Ivan / Pennello, Anthony L / Forest, Amelie / Chen, Xinlei / Chin, Darin / Sonyi, Andreas / Topper, Michael / Boucher, Lauren / Sharma, Prachi /

Zhang, Yiwei / Burtrum, Douglas / Novosiadly, Ruslan D / Ludwig, Dale L / Plowman, Gregory D / Kalos, Michael

Molecular cancer therapeutics

2021 Volume 19, Issue 4, Page(s) 988–998

Abstract: The CD137 receptor plays a key role in mediating immune response by promoting T cell proliferation, survival, and memory. Effective agonism of CD137 has the potential to reinvigorate potent antitumor immunity either alone or in combination with other ... ...

Abstract	The CD137 receptor plays a key role in mediating immune response by promoting T cell proliferation, survival, and memory. Effective agonism of CD137 has the potential to reinvigorate potent antitumor immunity either alone or in combination with other immune-checkpoint therapies. In this study, we describe the discovery and characterization of a unique CD137 agonist, 7A5, a fully human IgG1 Fc effector-null monoclonal antibody. The biological properties of 7A5 were investigated through
MeSH term(s)	Animals ; Antibodies, Monoclonal/pharmacology ; Apoptosis ; CD8-Positive T-Lymphocytes/immunology ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/immunology ; Carcinoma, Non-Small-Cell Lung/pathology ; Cell Proliferation ; Female ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/immunology ; Lung Neoplasms/pathology ; Lymphocyte Activation/immunology ; Mice ; Mice, Inbred NOD ; Mice, SCID ; NF-kappa B/metabolism ; Signal Transduction ; Tumor Cells, Cultured ; Tumor Necrosis Factor Receptor Superfamily, Member 9/immunology ; Xenograft Model Antitumor Assays
Chemical Substances	Antibodies, Monoclonal ; NF-kappa B ; TNFRSF9 protein, human ; Tumor Necrosis Factor Receptor Superfamily, Member 9
Language	English
Publishing date	2021-04-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2063563-1
ISSN	1538-8514 ; 1535-7163
ISSN (online)	1538-8514
ISSN	1535-7163
DOI	10.1158/1535-7163.MCT-19-0893
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Article ; Online: Targeting the TGFβ pathway with galunisertib, a TGFβRI small molecule inhibitor, promotes anti-tumor immunity leading to durable, complete responses, as monotherapy and in combination with checkpoint blockade.

Holmgaard, Rikke B / Schaer, David A / Li, Yanxia / Castaneda, Stephen P / Murphy, Mary Y / Xu, Xiaohong / Inigo, Ivan / Dobkin, Julie / Manro, Jason R / Iversen, Philip W / Surguladze, David / Hall, Gerald E / Novosiadly, Ruslan D / Benhadji, Karim A / Plowman, Gregory D / Kalos, Michael / Driscoll, Kyla E

Journal for immunotherapy of cancer

2018 Volume 6, Issue 1, Page(s) 47

Abstract: Background: TGFβ signaling plays a pleotropic role in tumor biology, promoting tumor proliferation, invasion and metastasis, and escape from immune surveillance. Inhibiting TGFβ's immune suppressive effects has become of particular interest as a way to ... ...

Abstract	Background: TGFβ signaling plays a pleotropic role in tumor biology, promoting tumor proliferation, invasion and metastasis, and escape from immune surveillance. Inhibiting TGFβ's immune suppressive effects has become of particular interest as a way to increase the benefit of cancer immunotherapy. Here we utilized preclinical models to explore the impact of the clinical stage TGFβ pathway inhibitor, galunisertib, on anti-tumor immunity at clinically relevant doses. Results: In vitro treatment with galunisertib reversed TGFβ and regulatory T cell mediated suppression of human T cell proliferation. In vivo treatment of mice with established 4T1-LP tumors resulted in strong dose-dependent anti-tumor activity with close to 100% inhibition of tumor growth and complete regressions upon cessation of treatment in 50% of animals. This effect was CD8+ T cell dependent, and led to increased T cell numbers in treated tumors. Mice with durable regressions rejected tumor rechallenge, demonstrating the establishment of immunological memory. Consequently, mice that rejected immunogenic 4T1-LP tumors were able to resist rechallenge with poorly immunogenic 4 T1 parental cells, suggesting the development of a secondary immune response via antigen spreading as a consequence of effective tumor targeting. Combination of galunisertib with PD-L1 blockade resulted in improved tumor growth inhibition and complete regressions in colon carcinoma models, demonstrating the potential synergy when cotargeting TGFβ and PD-1/PD-L1 pathways. Combination therapy was associated with enhanced anti-tumor immune related gene expression profile that was accelerated compared to anti-PD-L1 monotherapy. Conclusions: Together these data highlight the ability of galunisertib to modulate T cell immunity and the therapeutic potential of combining galunisertib with current PD-1/L1 immunotherapy.
MeSH term(s)	Animals ; Combined Modality Therapy/methods ; Disease Models, Animal ; Female ; Humans ; Immunotherapy/methods ; Male ; Mice ; Pyrazoles/pharmacology ; Pyrazoles/therapeutic use ; Quinolines/pharmacology ; Quinolines/therapeutic use ; Transforming Growth Factor beta/drug effects
Chemical Substances	Pyrazoles ; Quinolines ; Transforming Growth Factor beta ; LY-2157299 (700874-72-2)
Language	English
Publishing date	2018-06-04
Publishing country	England
Document type	Journal Article
ZDB-ID	2719863-7
ISSN	2051-1426 ; 2051-1426
ISSN (online)	2051-1426
ISSN	2051-1426
DOI	10.1186/s40425-018-0356-4
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Article: Mouse PDX Trial Suggests Synergy of Concurrent Inhibition of RAF and EGFR in Colorectal Cancer with

Yao, Yung-Mae M / Donoho, Gregory P / Iversen, Philip W / Zhang, Youyan / Van Horn, Robert D / Forest, Amelie / Novosiadly, Ruslan D / Webster, Yue Wang / Ebert, Philip / Bray, Steven / Ting, Jason C / Aggarwal, Amit / Henry, James R / Tiu, Ramon V / Plowman, Gregory D / Peng, Sheng-Bin

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

2017 Volume 23, Issue 18, Page(s) 5547–5560

Abstract: Purpose: ...

Abstract	Purpose:
Language	English
Publishing date	2017-09-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-16-3250
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Article ; Online: Bispecific Targeting of PD-1 and PD-L1 Enhances T-cell Activation and Antitumor Immunity.

Kotanides, Helen / Li, Yiwen / Malabunga, Maria / Carpenito, Carmine / Eastman, Scott W / Shen, Yang / Wang, George / Inigo, Ivan / Surguladze, David / Pennello, Anthony L / Persaud, Krishnadatt / Hindi, Sagit / Topper, Michael / Chen, Xinlei / Zhang, Yiwei / Bulaon, Danielle K / Bailey, Tim / Lao, Yanbin / Han, Bing /

Torgerson, Stacy / Chin, Darin / Sonyi, Andreas / Haidar, Jaafar N / Novosiadly, Ruslan D / Moxham, Christopher M / Plowman, Gregory D / Ludwig, Dale L / Kalos, Michael

Cancer immunology research

2020 Volume 8, Issue 10, Page(s) 1300–1310

Abstract: The programmed cell death protein 1 receptor (PD-1) and programmed death ligand 1 (PD-L1) coinhibitory pathway suppresses T-cell-mediated immunity. We hypothesized that cotargeting of PD-1 and PD-L1 with a bispecific antibody molecule could provide an ... ...

Abstract	The programmed cell death protein 1 receptor (PD-1) and programmed death ligand 1 (PD-L1) coinhibitory pathway suppresses T-cell-mediated immunity. We hypothesized that cotargeting of PD-1 and PD-L1 with a bispecific antibody molecule could provide an alternative therapeutic approach, with enhanced antitumor activity, compared with monospecific PD-1 and PD-L1 antibodies. Here, we describe LY3434172, a bispecific IgG1 mAb with ablated Fc immune effector function that targets both human PD-1 and PD-L1. LY3434172 fully inhibited the major inhibitory receptor-ligand interactions in the PD-1 pathway. LY3434172 enhanced functional activation of T cells
MeSH term(s)	Animals ; Antibodies, Bispecific/immunology ; Antibodies, Bispecific/pharmacology ; B7-H1 Antigen/antagonists & inhibitors ; B7-H1 Antigen/immunology ; CHO Cells ; Cricetulus ; Female ; Humans ; Immunotherapy/methods ; Lymphocyte Activation ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Molecular Targeted Therapy ; Programmed Cell Death 1 Receptor/antagonists & inhibitors ; Programmed Cell Death 1 Receptor/immunology ; T-Lymphocytes/immunology ; Xenograft Model Antitumor Assays
Chemical Substances	Antibodies, Bispecific ; B7-H1 Antigen ; CD274 protein, human ; PDCD1 protein, human ; Programmed Cell Death 1 Receptor
Language	English
Publishing date	2020-07-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2732489-8
ISSN	2326-6074 ; 2326-6066
ISSN (online)	2326-6074
ISSN	2326-6066
DOI	10.1158/2326-6066.CIR-20-0304
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Article ; Online: Oncogenic BRAF Deletions That Function as Homodimers and Are Sensitive to Inhibition by RAF Dimer Inhibitor LY3009120.

Chen, Shih-Hsun / Zhang, Youyan / Van Horn, Robert D / Yin, Tinggui / Buchanan, Sean / Yadav, Vipin / Mochalkin, Igor / Wong, Swee Seong / Yue, Yong Gang / Huber, Lysiane / Conti, Ilaria / Henry, James R / Starling, James J / Plowman, Gregory D / Peng, Sheng-Bin

Cancer discovery

2016 Volume 6, Issue 3, Page(s) 300–315

Abstract: Unlabelled: We have identified previously undiscovered BRAF in-frame deletions near the αC-helix region of the kinase domain in pancreatic, lung, ovarian, and thyroid cancers. These deletions are mutually exclusive with KRAS mutations and occur in 4.21% ...

Abstract	Unlabelled: We have identified previously undiscovered BRAF in-frame deletions near the αC-helix region of the kinase domain in pancreatic, lung, ovarian, and thyroid cancers. These deletions are mutually exclusive with KRAS mutations and occur in 4.21% of KRAS wild-type pancreatic cancer. siRNA knockdown in cells harboring BRAF deletions showed that the MAPK activity and cell growth are BRAF dependent. Structurally, the BRAF deletions are predicted to shorten the β3/αC-helix loop and hinder its flexibility by locking the helix in the active αC-helix-in conformation that favors dimer formation. Expression of L485-P490-deleted BRAF is able to transform NIH/3T3 cells in a BRAF dimer-dependent manner. BRAF homodimer is confirmed to be the dominant RAF dimer by proximity ligation assays in BRAF deletion cells, which are resistant to the BRAF inhibitor vemurafenib and sensitive to LY3009120, a RAF dimer inhibitor. In tumor models with BRAF deletions, LY3009120 has shown tumor growth regression, whereas vemurafenib is inactive. Significance: This study discovered oncogenic BRAF deletions with a distinct activation mechanism dependent on the BRAF dimer formation in tumor cells. LY3009120 is active against these cells and represents a potential treatment option for patients with cancer with these BRAF deletions, or other atypical BRAF mutations where BRAF functions as a dimer.
MeSH term(s)	Animals ; Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; Cell Transformation, Neoplastic/genetics ; Disease Models, Animal ; Drug Resistance, Neoplasm ; Ectopic Gene Expression ; Gene Deletion ; Gene Expression ; Humans ; MAP Kinase Signaling System ; Mice ; Models, Molecular ; Phenylurea Compounds/pharmacology ; Protein Conformation ; Protein Interaction Domains and Motifs/genetics ; Protein Kinase Inhibitors/chemistry ; Protein Kinase Inhibitors/pharmacology ; Protein Multimerization ; Proto-Oncogene Proteins B-raf/antagonists & inhibitors ; Proto-Oncogene Proteins B-raf/chemistry ; Proto-Oncogene Proteins B-raf/genetics ; Pyrimidines/pharmacology ; Xenograft Model Antitumor Assays
Chemical Substances	Antineoplastic Agents ; LY3009120 ; Phenylurea Compounds ; Protein Kinase Inhibitors ; Pyrimidines ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1)
Language	English
Publishing date	2016-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-15-0896
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Article: Evolution of protein kinase signaling from yeast to man.

Manning, Gerard / Plowman, Gregory D / Hunter, Tony / Sudarsanam, Sucha

Trends in biochemical sciences

2002 Volume 27, Issue 10, Page(s) 514–520

Abstract: Protein phosphorylation controls many cellular processes, especially those involved in intercellular communication and coordination of complex functions. To explore the evolution of protein phosphorylation, we compared the protein kinase complements (' ... ...

Abstract	Protein phosphorylation controls many cellular processes, especially those involved in intercellular communication and coordination of complex functions. To explore the evolution of protein phosphorylation, we compared the protein kinase complements ('kinomes') of budding yeast, worm and fly, with known human kinases. We classify kinases into putative orthologous groups with conserved functions and discuss kinase families and pathways that are unique, expanded or lost in each lineage. Fly and human share several kinase families involved in immunity, neurobiology, cell cycle and morphogenesis that are absent from worm, suggesting that these functions might have evolved after the divergence of nematodes from the main metazoan lineage.
MeSH term(s)	Animals ; Evolution, Molecular ; Humans ; Phosphorylation ; Phylogeny ; Protein Kinases/genetics ; Protein Kinases/immunology ; Protein Kinases/metabolism ; Protein Structure, Tertiary ; Saccharomyces cerevisiae/enzymology ; Sequence Homology ; Signal Transduction/physiology
Chemical Substances	Protein Kinases (EC 2.7.-)
Language	English
Publishing date	2002-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	194216-5
ISSN	1362-4326 ; 0968-0004 ; 0376-5067
ISSN (online)	1362-4326
ISSN	0968-0004 ; 0376-5067
DOI	10.1016/s0968-0004(02)02179-5
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Article ; Online: Tumor cell expression of vascular endothelial growth factor receptor 2 is an adverse prognostic factor in patients with squamous cell carcinoma of the lung.

Holzer, Timothy R / Fulford, Angie D / Nedderman, Drew M / Umberger, Tara S / Hozak, Rebecca R / Joshi, Adarsh / Melemed, Symantha A / Benjamin, Laura E / Plowman, Gregory D / Schade, Andrew E / Ackermann, Bradley L / Konrad, Robert J / Nasir, Aejaz

PloS one

2013 Volume 8, Issue 11, Page(s) e80292

Abstract: A robust immunohistochemical (IHC) assay for VEGFR2 was developed to investigate its utility for patient tailoring in clinical trials. The sensitivity, specificity, and selectivity of the IHC assay were established by siRNA knockdown, immunoblotting, ... ...

Abstract	A robust immunohistochemical (IHC) assay for VEGFR2 was developed to investigate its utility for patient tailoring in clinical trials. The sensitivity, specificity, and selectivity of the IHC assay were established by siRNA knockdown, immunoblotting, mass spectrometry, and pre-absorption experiments. Characterization of the assay included screening a panel of multiple human cancer tissues and an independent cohort of non-small cell lung carcinoma (NSCLC, n = 118) characterized by TTF-1, p63, CK5/6, and CK7 IHC. VEGFR2 immunoreactivity was interpreted qualitatively (VEGFR2 positive/negative) in blood vessels and by semi-quantitative evaluation using H-scores in tumor cells (0-300). Associations were determined among combinations of VEGFR2 expression in blood vessels and tumor cells, and clinico-pathologic characteristics (age, sex, race, histologic subtype, disease stage) and overall survival using Kaplan-Meier analyses and appropriate statistical models. VEGFR2 expression both in blood vessels and in tumor cells in carcinomas of the lung, cervix, larynx, breast, and others was demonstrated. In the validation cohort, 99/118 (83.9%) NSCLC tissues expressed VEGFR2 in the blood vessels and 46/118 (39.0%) showed high tumor cell positivity (H-score ≥10). Vascular and tumor cell expression were inversely correlated (p = 0.0175). High tumor cell expression of VEGFR2 was associated with a 3.7-fold reduction in median overall survival in lung squamous-cell carcinoma (SCC, n = 25, p = 0.0134). The inverse correlation between vascular and tumor cell expression of VEGFR2 and the adverse prognosis associated with high VEGFR2 expression in immunohistochemically characterized pulmonary SCC are new findings with potential therapeutic implications. The robustness of this novel IHC assay will support further evaluation of its utility for patient tailoring in clinical trials of antiangiogenic agents.
MeSH term(s)	Aged ; Aged, 80 and over ; Carcinoma, Squamous Cell/metabolism ; Cell Line, Tumor ; Female ; Humans ; In Vitro Techniques ; Kaplan-Meier Estimate ; Lung Neoplasms/metabolism ; Male ; Middle Aged ; Prognosis ; Vascular Endothelial Growth Factor Receptor-2/metabolism
Chemical Substances	Vascular Endothelial Growth Factor Receptor-2 (EC 2.7.10.1)
Language	English
Publishing date	2013-11-14
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0080292
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Article ; Online: ERK Inhibitor LY3214996 Targets ERK Pathway-Driven Cancers: A Therapeutic Approach Toward Precision Medicine.

Bhagwat, Shripad V / McMillen, William T / Cai, Shufen / Zhao, Baohui / Whitesell, Matthew / Shen, Weihua / Kindler, Lisa / Flack, Robert S / Wu, Wenjuan / Anderson, Bryan / Zhai, Yan / Yuan, Xiu-Juan / Pogue, Meghann / Van Horn, Robert D / Rao, Xi / McCann, Denis / Dropsey, Andrew J / Manro, Jason / Walgren, Jennie /

Yuen, Eunice / Rodriguez, Michael J / Plowman, Gregory D / Tiu, Ramon V / Joseph, Sajan / Peng, Sheng-Bin

Molecular cancer therapeutics

2019 Volume 19, Issue 2, Page(s) 325–336

Abstract: The ERK pathway is critical in oncogenesis; aberrations in components of this pathway are common in approximately 30% of human cancers. ERK1/2 (ERK) regulates cell proliferation, differentiation, and survival and is the terminal node of the pathway. BRAF- ...

Abstract	The ERK pathway is critical in oncogenesis; aberrations in components of this pathway are common in approximately 30% of human cancers. ERK1/2 (ERK) regulates cell proliferation, differentiation, and survival and is the terminal node of the pathway. BRAF- and MEK-targeted therapies are effective in BRAF V600E/K metastatic melanoma and lung cancers; however, responses are short-lived due to emergence of resistance. Reactivation of ERK signaling is central to the mechanisms of acquired resistance. Therefore, ERK inhibition provides an opportunity to overcome resistance and leads to improved efficacy. In addition,
MeSH term(s)	Animals ; Disease Models, Animal ; Female ; Humans ; Mice ; Mice, Nude ; Neoplasms/drug therapy ; Precision Medicine ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use
Chemical Substances	Protein Kinase Inhibitors
Language	English
Publishing date	2019-11-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2063563-1
ISSN	1538-8514 ; 1535-7163
ISSN (online)	1538-8514
ISSN	1535-7163
DOI	10.1158/1535-7163.MCT-19-0183
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Article ; Online: Aurora A-Selective Inhibitor LY3295668 Leads to Dominant Mitotic Arrest, Apoptosis in Cancer Cells, and Shows Potent Preclinical Antitumor Efficacy.

Du, Jian / Yan, Lei / Torres, Raquel / Gong, Xueqian / Bian, Huimin / Marugán, Carlos / Boehnke, Karsten / Baquero, Carmen / Hui, Yu-Hua / Chapman, Sonya C / Yang, Yanzhu / Zeng, Yi / Bogner, Sarah M / Foreman, Robert T / Capen, Andrew / Donoho, Gregory P / Van Horn, Robert D / Barnard, Darlene S / Dempsey, Jack A /

Beckmann, Richard P / Marshall, Mark S / Chio, Li-Chun / Qian, Yuewei / Webster, Yue W / Aggarwal, Amit / Chu, Shaoyou / Bhattachar, Shobha / Stancato, Louis F / Dowless, Michele S / Iversen, Phillip W / Manro, Jason R / Walgren, Jennie L / Halstead, Bartley W / Dieter, Matthew Z / Martinez, Ricardo / Bhagwat, Shripad V / Kreklau, Emiko L / Lallena, Maria Jose / Ye, Xiang S / Patel, Bharvin K R / Reinhard, Christoph / Plowman, Gregory D / Barda, David A / Henry, James R / Buchanan, Sean G / Campbell, Robert M

Molecular cancer therapeutics

2019 Volume 18, Issue 12, Page(s) 2207–2219

Abstract: Although Aurora A, B, and C kinases share high sequence similarity, especially within the kinase domain, they function distinctly in cell-cycle progression. Aurora A depletion primarily leads to mitotic spindle formation defects and consequently ... ...

Abstract	Although Aurora A, B, and C kinases share high sequence similarity, especially within the kinase domain, they function distinctly in cell-cycle progression. Aurora A depletion primarily leads to mitotic spindle formation defects and consequently prometaphase arrest, whereas Aurora B/C inactivation primarily induces polyploidy from cytokinesis failure. Aurora B/C inactivation phenotypes are also epistatic to those of Aurora A, such that the concomitant inactivation of Aurora A and B, or all Aurora isoforms by nonisoform-selective Aurora inhibitors, demonstrates the Aurora B/C-dominant cytokinesis failure and polyploidy phenotypes. Several Aurora inhibitors are in clinical trials for T/B-cell lymphoma, multiple myeloma, leukemia, lung, and breast cancers. Here, we describe an Aurora A-selective inhibitor, LY3295668, which potently inhibits Aurora autophosphorylation and its kinase activity
MeSH term(s)	Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Apoptosis ; Aurora Kinase A/antagonists & inhibitors ; Cell Line, Tumor ; Cell Proliferation ; Female ; HeLa Cells ; Humans ; Male ; Mitosis/drug effects
Chemical Substances	Antineoplastic Agents ; Aurora Kinase A (EC 2.7.11.1)
Language	English
Publishing date	2019-09-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2063563-1
ISSN	1538-8514 ; 1535-7163
ISSN (online)	1538-8514
ISSN	1535-7163
DOI	10.1158/1535-7163.MCT-18-0529
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