WEE1 Inhibition Enhances Anti-Apoptotic Dependency as a Result of Premature Mitotic Entry and DNA Damage (original) (raw)
WEE1 inhibition synergizes with CHOP chemotherapy and radiation therapy through induction of premature mitotic entry and DNA damage in diffuse large B-cell lymphoma
Mathilde de Jong
Therapeutic Advances in Hematology
View PDFchevron_right
University of Groningen WEE1 inhibition synergizes with CHOP chemotherapy and radiation therapy through induction of premature mitotic entry and DNA damage in diffuse large B-cell lymphoma de Jong
Mathilde de Jong
2020
View PDFchevron_right
Chemotherapy-induced differential cell cycle arrest in B cell lymphomas affects their sensitivity to Wee1 inhibition
alexa silva
Haematologica, 2017
View PDFchevron_right
WEE1 kinase inhibition reverses G2/M cell cycle checkpoint activation to sensitize cancer cells to immunotherapy
Anthony Saleh
OncoImmunology, 2018
View PDFchevron_right
Preclinical evaluation of the WEE1 inhibitor MK-1775 as single-agent anticancer therapy
S. Fawell, Stuart Shumway
Molecular cancer therapeutics, 2013
View PDFchevron_right
A regimen combining the Wee1 inhibitor AZD1775 with HDAC inhibitors targets human acute myeloid leukemia cells harboring various genetic mutations
Maciej Kmieciak
Leukemia, 2014
View PDFchevron_right
Targeting WEE1 to enhance conventional therapies for acute lymphoblastic leukemia
Carmen Baldazzi
Journal of hematology & oncology, 2018
View PDFchevron_right
Cellular responses to a prolonged delay in mitosis are determined by a DNA damage response controlled by Bcl-2 family proteins
Victor Wang
View PDFchevron_right
Tumor cell-selective cytotoxicity by targeting cell cycle checkpoints
Andrew Burgess
2003
View PDFchevron_right
Combined Inhibition of Smoothened and the DNA Damage Checkpoint WEE1 Exerts Antitumor Activity in Cholangiocarcinoma
Mirella Pastore
Molecular Cancer Therapeutics, 2022
View PDFchevron_right
p21(WAF1) modulates drug-induced apoptosis and cell cycle arrest in B-cell precursor acute lymphoblastic leukemia
Carwyn Davies
Cell cycle (Georgetown, Tex.), 2015
View PDFchevron_right
Novel DNA Damage Checkpoints Mediating Cell Death Induced by the NEDD8-Activating Enzyme Inhibitor MLN4924
David Bouck
Cancer Research, 2013
View PDFchevron_right
Cell Cycle Checkpoint and DNA Damage Response Defects as Anticancer Targets: From Molecular Mechanisms to Therapeutic Opportunities
Nikolas Haass
Stress Response Pathways in Cancer, 2014
View PDFchevron_right
Cell survival, cell death and cell cycle pathways are interconnected: Implications for cancer therapy
Soumya Panigrahi, Marek Los
Drug Resistance Updates, 2007
View PDFchevron_right
Transcriptional repression of WEE1 by Kruppel-like factor 2 is involved in DNA damage-induced apoptosis
Hextan Ngan
Oncogene, 2005
View PDFchevron_right
Targeting DNA Repair, Cell Cycle, and Tumor Microenvironment in B Cell Lymphoma
Mathilde de Jong
Cells, 2020
View PDFchevron_right
Cell cycle checkpoint in cancer: a therapeutically targetable double-edged sword
Rosa Della Monica
Journal of experimental & clinical cancer research : CR, 2016
View PDFchevron_right
Data from Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress
mason bartels
View PDFchevron_right
Tumor cell-specific cytotoxicity by targeting cell cycle checkpoints
Andrew Burgess
Faseb Journal, 2003
View PDFchevron_right
CHK1 plays a critical role in the anti-leukemic activity of the wee1 inhibitor MK-1775 in acute myeloid leukemia cells
Jeffrey Taub
Journal of hematology & oncology, 2014
View PDFchevron_right
Importance of DNA damage checkpoints in the pathogenesis of human cancers
Angela Poehlmann
Pathology - Research and Practice, 2010
View PDFchevron_right
Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress
mason bartels
Molecular Cancer Therapeutics, 2021
View PDFchevron_right
miR-16 and miR-26a target checkpoint kinases Wee1 and Chk1 in response to p53 activation by genotoxic stress
Mircea Ivan, D. Tentler
Cell Death and Disease, 2013
View PDFchevron_right
The cyclin-dependent kinase inhibitor 5, 6-dichloro-1-beta-D-ribofuranosylbenzimidazole induces nongenotoxic, DNA replication-independent apoptosis of normal and leukemic cells, regardless of their p53 status
Luca Orlando
BMC Cancer, 2009
View PDFchevron_right
Cancer: A cell cycle defect
Thabiso Langa
View PDFchevron_right
26 DNA Damage Response Pathways and Cell Cycle Checkpoints in
Gabriele Zoppoli
View PDFchevron_right
PromotesCell Survival due to theReversibility of Its Cell-Cycle Checkpoints
Lois Resnick-Silverman
2014
View PDFchevron_right
Prolonged mitotic arrest triggers partial activation of apoptosis, resulting in DNA damage and p53 induction
Alexander Loewer
Molecular Biology of the Cell, 2012
View PDFchevron_right
Constitutive activation of the DNA damage response pathway as a novel therapeutic target in diffuse large B-cell lymphoma
Beatrice Casadei
Oncotarget, 2014
View PDFchevron_right
Prolonged mitotic arrest induced by Wee1 inhibition sensitizes breast cancer cells to paclitaxel
Dawn Macdonald
Oncotarget, 2017
View PDFchevron_right
G2/M checkpoint stringency is a key parameter in the sensitivity of AML cells to genotoxic stress
Christine Didier
Oncogene, 2008
View PDFchevron_right
Lack of Bcl11b tumor suppressor results in vulnerability to DNA replication stress and damages
Yutaka Aoyagi
Oncogene, 2007
View PDFchevron_right
Pharmacological targeting the ATR–CHK1–WEE1 axis involves balancing cell growth stimulation and apoptosis
Victor Wang
View PDFchevron_right
Bcl-2 blocks 2-methoxyestradiol induced leukemia cell apoptosis by a p27Kip1-dependent G1/S cell cycle arrest in conjunction with NF-κB activation
Andreas Constantinou
Biochemical Pharmacology, 2009
View PDFchevron_right
Functional inhibition of BCL2 is needed to increase the susceptibility to apoptosis to SMO inhibitors in diffuse large B-cell lymphoma of germinal center subtype
Kranthi Kunkalla
Annals of Hematology, 2013
View PDFchevron_right