C. Quéva

发表

Targeted Deletion of the S-Phase-Specific Myc Antagonist Mad3 Sensitizes Neuronal and Lymphoid Cells to Radiation-Induced Apoptosis

R. Eisenman, G. McArthur, C. Quéva, 2001, Molecular and Cellular Biology.

Dwarfism and dysregulated proliferation in mice overexpressing the MYC antagonist MAD1.

R. Eisenman, G. McArthur, C. Quéva, 1999, Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research.

The Mad protein family links transcriptional repression to cell differentiation.

R. Eisenman, Carol D. Laherty, C. Grandori, 1998, Cold Spring Harbor symposia on quantitative biology.

Mnt, a novel Max-interacting protein is coexpressed with Myc in proliferating cells and mediates repression at Myc binding sites.

R. Eisenman, C. Quéva, P. Hurlin, 1997, Genes & development.

Expression patterns of c-myb and of v-myb induced myeloid-1 (mim-1) gene during the development of the chick embryo.

T. Graf, B. Vandenbunder, S. Ness, 1992, Development.

The ETS1 transcription factor is expressed during epithelial-mesenchymal transitions in the chick embryo and is activated in scatter factor-stimulated MDCK epithelial cells.

B. Vandenbunder, C. Quéva, D. Stéhelin, 1997, Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research.

Arming oHSV with ULBP3 drives abscopal immunity in lymphocyte-depleted glioblastoma.

A. M. Houghton, P. Grandi, M. Weller, 2019, JCI insight.

Discovery of AMG 925, a FLT3 and CDK4 dual kinase inhibitor with preferential affinity for the activated state of FLT3.

K. Pattabiraman, Zhulun Wang, C. Quéva, 2014, Journal of medicinal chemistry.

Mad3 and Mad4: novel Max-interacting transcriptional repressors that suppress c-myc dependent transformation and are expressed during neural and epidermal differentiation.

N. Copeland, N. Jenkins, R. Eisenman, 1996, The EMBO journal.

Combination Effects of B Cell Receptor Pathway Inhibitors (Entospletinib, ONO/GS-4059, and Idelalisib) and a BCL-2 Inhibitor in Primary CLL Cells

C. Quéva, D. Tumas, M. Axelrod, 2015 .

Combination of Idelalisib and ONO/GS-4059 in Lymphoma Cell Lines Sensitive and Resistant to BTK Inhibitors

Jia Liu, C. Quéva, Peng Yue, 2015 .

ONCR-177, an Oncolytic HSV-1 Designed to Potently Activate Systemic Antitumor Immunity

B. Haines, C. Quéva, L. Lerner, 2020, Cancer Immunology Research.

Idelalisib: First-in-Class PI3K Delta Inhibitor for the Treatment of Chronic Lymphocytic Leukemia, Small Lymphocytic Leukemia, and Follicular Lymphoma

V. Gandhi, C. Quéva, Qingshan Yang, 2015, Clinical Cancer Research.

Idelalisib for the treatment of B-cell malignancies

V. Gandhi, C. Quéva, S. Ramanathan, 2015 .

Mnt: a novel Max-interacting protein and Myc antagonist.

R. Eisenman, C. Quéva, P. Hurlin, 1997, Current topics in microbiology and immunology.

A novel ex vivo high-throughput assay reveals antiproliferative effects of idelalisib and ibrutinib in chronic lymphocytic leukemia

Marcos González, K. Stamatopoulos, R. Rosenquist, 2018, Oncotarget.

Effects of GABA agonists on body temperature regulation in GABAB(1)−/− mice

C. Quéva, J. Mattsson, Susanne Elg, 2003, British journal of pharmacology.

The relationship between cell proliferation and the transcription of the nuclear oncogenes c-myc, c-myb and c-ets-1 during feather morphogenesis in the chick embryo.

B. Vandenbunder, C. Quéva, D. Stéhelin, 1991, Development.

Design of an Interferon-Resistant Oncolytic HSV-1 Incorporating Redundant Safety Modalities for Improved Tolerability

B. Haines, C. Quéva, J. Glorioso, 2020, Molecular therapy oncolytics.

Mad3 and Mad4: novel Max‐interacting transcriptional repressors that suppress c‐myc dependent transformation and are expressed during neural and epidermal differentiation.

N. Copeland, N. Jenkins, R. Eisenman, 1995, The EMBO journal.

Mlx, a Novel Max-like BHLHZip Protein That Interacts with the Max Network of Transcription Factors*

D. Ayer, C. Quéva, A. Billin, 1999, The Journal of Biological Chemistry.

Targeted disruption of the MYC antagonist MAD1 inhibits cell cycle exit during granulocyte differentiation

R. Eisenman, Philippe Soriano, G. McArthur, 1998, The EMBO journal.

expressed during neural and epidermal differentiation

N. Copeland, N. Jenkins, R. Eisenman, 2004 .

Preclinical Evaluation of AMG 925, a FLT3/CDK4 Dual Kinase Inhibitor for Treating Acute Myeloid Leukemia

Alexander Kamb, John Eksterowicz, C. Quéva, 2014, Molecular Cancer Therapeutics.

p54c-ets-1 and p68c-ets-1, the two transcription factors encoded by the c-ets-1 locus, are differentially expressed during the development of the chick embryo.

D. Leprince, B. Vandenbunder, C. Quéva, 1993, Oncogene.

Expression of the transcription factor c-Ets1 correlates with the occurrence of invasive processes during normal and pathological development.

B. Vandenbunder, C. Quéva, D. Stéhelin, 1994, Invasion & metastasis.

Development of a new fully human anti-CD20 monoclonal antibody for the treatment of B-cell malignancies

Mohammad Tabrizi, Gadi Gazit Bornstein, Larry L. Green, 2007, Investigational New Drugs.

AZD7762, a novel checkpoint kinase inhibitor, drives checkpoint abrogation and potentiates DNA-targeted therapies

Stephen Green, B. Caleb, G. Schwartz, 2008, Molecular Cancer Therapeutics.

Macrophage migration inhibitory factor produced by the tumour stroma but not by tumour cells regulates angiogenesis in the B16-F10 melanoma model

Emily J. Girard, C. Quéva, C. Strathdee, 2012, British Journal of Cancer.

PI3Kδ inhibitor idelalisib in combination with BTK inhibitor ONO/GS-4059 in diffuse large B cell lymphoma with acquired resistance to PI3Kδ and BTK inhibitors

C. Quéva, K. Keegan, S. Tannheimer, 2017, PloS one.

Oncolytic HSV Vectors and Anti-Tumor Immunity.

Joseph W. Jackson, M. Caligiuri, E. Holland, 2020, Current issues in molecular biology.

Development of intravenously administered synthetic RNA virus immunotherapy for the treatment of cancer

T. Ashburn, B. Haines, C. Quéva, 2021, Nature Communications.

Sequential expression of the MAD family of transcriptional repressors during differentiation and development

R. Eisenman, K. Foley, C. Quéva, 1998, Oncogene.

Amphicoup-TF, a nuclear orphan receptor of the lancelet Branchiostoma floridae, is implicated in retinoic acid signalling pathways

V. Laudet, L. Holland, C. Quéva, 2000, Development Genes and Evolution.

Peptibodies: A flexible alternative format to antibodies

Tom Boone, T. Boone, C. Quéva, 2012, mAbs.

Abstract 1683: A novel adenosine A2A receptor antagonist optimized for high potency in adenosine-rich tumor microenvironment boosts antitumor immunity

C. Quéva, V. Bol, B. Gomes, 2017 .

Returns to the East: German internal migrations and local development in East Germany

C. Quéva, 2018 .

Seneca Valley virus replicons are packaged in trans and have the capacity to overcome the limitations of viral transgene expression

C. Quéva, L. Lerner, Jennifer S. Lee, 2023, Molecular therapy oncolytics.

Does the transcription factor c-ets1 take part in the regulation of angiogenesis and tumor invasion?

B. Vandenbunder, C. Quéva, D. Stéhelin, 1994, Folia biologica.

The PI3K Delta Selective Inhibitor Idelalisib Minimally Interferes with Immune Effector Function and B Cell Depletion Mediated By Obinutuzumab (GA101) and Rituximab

C. Klein, M. Bacac, C. Quéva, 2014 .

PI3Kδ Inhibitor Idelalisib Inhibits AKT Signaling In Myelofibrosis Patients On Chronic JAK Inhibitor Therapy

C. Quéva, J. Gotlib, S. Coutre, 2013 .

Oncolytic HSV Vectors and Anti-Tumor Immunity.

M. Caligiuri, C. Quéva, J. Glorioso, 2020, Current issues in molecular biology.

Discovery of AMG 925, a FLT3 and CDK4 dual kinase inhibitor with preferential affinity for the activated state of FLT3.

K. Pattabiraman, Zhulun Wang, C. Quéva, 2014, Journal of medicinal chemistry.

AZD7762, a novel checkpoint kinase inhibitor, drives checkpoint abrogation and potentiates DNA-targeted therapies

B. Caleb, G. Schwartz, J. Janetka, 2008, Molecular Cancer Therapeutics.

Cooperation of oncolytic virotherapy with VEGF-neutralizing antibody treatment in IDH wildtype glioblastoma dependends on MMP9.

M. Weller, Sonali Arora, C. Quéva, 2019, Neuro-oncology.