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.2 Poorly differentiated NEC 62% ATM, ATRX, CDK12, MSH6, NOTCH3, RAD50, CREBBP, TSC2, SMARCA4 Carboplatin + etoposide (two cycles) PD 5 51, Female Pancreatic tail, stage 4, G2 Bone, RP LNs 1 Capecitabine + temozolomide 2.5 4.6 4
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, type 1, E-cadherin (epithelial) and junction plakoglobin in ATC cell lines. Two genes frequently epigenetically silenced through CpG island promoter methylation are the RAS association domain family 1A gene ( RASSF1A ) and the CDK inhibitor, p16 INK4 α
Human Cancer Genetics Program, Division of Pathology, Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA
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4 miR-29 7q32 DNA methylation Mcl-1 miR-34a 1p36 Regulation of cell cycle SIRT1 CDK4 miR-34b/c 11q23 Regulation of proliferation and adhesion-independent cell growth CDK6 miR-106b-25 7q22 Regulates E2F1 involved
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(triple-negative human breast cancer PDX line) were treated with different dosages of SI-12 for 2 weeks. Images were taken at the end of treatment and the organoid number was counted and analyzed accordingly. (B) Combination treatment with SI-12 and CDK4
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strategy for MEN1 tumors. However, a recent integrative genomics study in Men1 -depleted pancreatic islets from 2-month-old mice, the CDK genes were not among the menin–MLL1/MLL2 target genes ( Lin et al . 2015 ). An experimental approach using H3K4me3
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MEK and CDK4/6 was effective in a preclinical study using patient colorectal xenografts ( Lee et al. 2016 ) and thus represents another option for a subset of NET patients harboring KRAS or NRAS mutations. Previous small studies with imatinib
The Breast Cancer Now Toby Robins Research Centre, The Institute of Cancer Research, London, UK
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The Breast Cancer Now Toby Robins Research Centre, The Institute of Cancer Research, London, UK
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treatment, and eventually die from the disease ( D’Souza et al. 2018 ). The response can occur sequentially with different endocrine agents. The duration of response is increased by combination with other agents, such as cyclin-dependent kinase 4/6 (CDK4
Department of Medical Biophysics University of Toronto, Toronto, Ontario, Canada
Division of Neurosurgery Toronto Western Hospital, 399 Bathurst Street, 4W-439, Toronto, Ontario, Canada M5T 2S8
Ontario Cancer Institute Princess Margaret Hospital, Toronto, Ontario, Canada
Endocrine Oncology Site Group Princess Margaret Hospital, Toronto, Ontario, Canada
Department of Laboratory Medicine and Pathobiology University of Toronto, Toronto, Ontario, Canada
Institute of Medical Science
Department of Medical Biophysics University of Toronto, Toronto, Ontario, Canada
Division of Neurosurgery Toronto Western Hospital, 399 Bathurst Street, 4W-439, Toronto, Ontario, Canada M5T 2S8
Ontario Cancer Institute Princess Margaret Hospital, Toronto, Ontario, Canada
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Department of Laboratory Medicine and Pathobiology University of Toronto, Toronto, Ontario, Canada
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Department of Medical Biophysics University of Toronto, Toronto, Ontario, Canada
Division of Neurosurgery Toronto Western Hospital, 399 Bathurst Street, 4W-439, Toronto, Ontario, Canada M5T 2S8
Ontario Cancer Institute Princess Margaret Hospital, Toronto, Ontario, Canada
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Department of Laboratory Medicine and Pathobiology University of Toronto, Toronto, Ontario, Canada
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Department of Medical Biophysics University of Toronto, Toronto, Ontario, Canada
Division of Neurosurgery Toronto Western Hospital, 399 Bathurst Street, 4W-439, Toronto, Ontario, Canada M5T 2S8
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Department of Laboratory Medicine and Pathobiology University of Toronto, Toronto, Ontario, Canada
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Department of Medical Biophysics University of Toronto, Toronto, Ontario, Canada
Division of Neurosurgery Toronto Western Hospital, 399 Bathurst Street, 4W-439, Toronto, Ontario, Canada M5T 2S8
Ontario Cancer Institute Princess Margaret Hospital, Toronto, Ontario, Canada
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Department of Laboratory Medicine and Pathobiology University of Toronto, Toronto, Ontario, Canada
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Department of Medical Biophysics University of Toronto, Toronto, Ontario, Canada
Division of Neurosurgery Toronto Western Hospital, 399 Bathurst Street, 4W-439, Toronto, Ontario, Canada M5T 2S8
Ontario Cancer Institute Princess Margaret Hospital, Toronto, Ontario, Canada
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Department of Laboratory Medicine and Pathobiology University of Toronto, Toronto, Ontario, Canada
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Department of Medical Biophysics University of Toronto, Toronto, Ontario, Canada
Division of Neurosurgery Toronto Western Hospital, 399 Bathurst Street, 4W-439, Toronto, Ontario, Canada M5T 2S8
Ontario Cancer Institute Princess Margaret Hospital, Toronto, Ontario, Canada
Endocrine Oncology Site Group Princess Margaret Hospital, Toronto, Ontario, Canada
Department of Laboratory Medicine and Pathobiology University of Toronto, Toronto, Ontario, Canada
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Department of Medical Biophysics University of Toronto, Toronto, Ontario, Canada
Division of Neurosurgery Toronto Western Hospital, 399 Bathurst Street, 4W-439, Toronto, Ontario, Canada M5T 2S8
Ontario Cancer Institute Princess Margaret Hospital, Toronto, Ontario, Canada
Endocrine Oncology Site Group Princess Margaret Hospital, Toronto, Ontario, Canada
Department of Laboratory Medicine and Pathobiology University of Toronto, Toronto, Ontario, Canada
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Department of Medical Biophysics University of Toronto, Toronto, Ontario, Canada
Division of Neurosurgery Toronto Western Hospital, 399 Bathurst Street, 4W-439, Toronto, Ontario, Canada M5T 2S8
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Department of Laboratory Medicine and Pathobiology University of Toronto, Toronto, Ontario, Canada
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Department of Medical Biophysics University of Toronto, Toronto, Ontario, Canada
Division of Neurosurgery Toronto Western Hospital, 399 Bathurst Street, 4W-439, Toronto, Ontario, Canada M5T 2S8
Ontario Cancer Institute Princess Margaret Hospital, Toronto, Ontario, Canada
Endocrine Oncology Site Group Princess Margaret Hospital, Toronto, Ontario, Canada
Department of Laboratory Medicine and Pathobiology University of Toronto, Toronto, Ontario, Canada
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Department of Medical Biophysics University of Toronto, Toronto, Ontario, Canada
Division of Neurosurgery Toronto Western Hospital, 399 Bathurst Street, 4W-439, Toronto, Ontario, Canada M5T 2S8
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Endocrine Oncology Site Group Princess Margaret Hospital, Toronto, Ontario, Canada
Department of Laboratory Medicine and Pathobiology University of Toronto, Toronto, Ontario, Canada
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1 and the CDKs (CDK4 and CDK6) remain unaffected. The dual PI3K/mTOR inhibitor NVP may be a more potent agent at abrogating PA cell cycle progression by attenuating both cyclins D1 and D3. The KIP1/CIP family of CDK inhibitors (CKDI) negatively
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Zhejiang Laboratory for Systems & Precision Medicine, Zhejiang University Medical Center, Hangzhou, China
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Zhejiang Laboratory for Systems & Precision Medicine, Zhejiang University Medical Center, Hangzhou, China
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Institute of Environmental Medicine of Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, China
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Zhejiang Laboratory for Systems & Precision Medicine, Zhejiang University Medical Center, Hangzhou, China
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exposure to PLX4032, H4K12La occupancies along the promoters of CDK1 , CCNE1, and AURKB were substantially reduced ( Fig. 4B ), and in line with their mRNA expression pattern, such reduction was dramatically restored by concomitant treatment with ethyl
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School of Biological Sciences, Nanyang Technological University, Singapore, Singapore
A*STAR Institute of Molecular and Cell Biology, Singapore, Singapore
Department of Medicine, Imperial College London, London, UK
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-dependent kinase1 (Cdk1) has been postulated to control both cell death and mitotic exit. Studies have shown that phosphorylation of the apoptotic initiator protease caspase-9 at Thr125 by Cdk1/cyclin B1 reduced its activity, thus protecting mitotic cells from