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Igryl S Cordero-Hernandez Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA

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Alicia C Ross Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA

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Arvind Dasari Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA

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Daniel M Halperin Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA

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Beth Chasen Department of Nuclear Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA

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James C Yao Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA

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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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Robert C Smallridge Division of Endocrinology, Department of Cancer Biology, Department of Internal Medicine

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Laura A Marlow Division of Endocrinology, Department of Cancer Biology, Department of Internal Medicine

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John A Copland Division of Endocrinology, Department of Cancer Biology, Department of Internal Medicine

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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

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Andrea Vecchione Human Cancer Genetics Program, Division of Pathology, Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA
Human Cancer Genetics Program, Division of Pathology, Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA

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Carlo M Croce 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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Li Qin Department of Molecular and Cellular Biology and Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas, USA

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Jianwei Chen Department of Pharmacology and Chemical Biology, Baylor College of Medicine, Houston, Texas, USA

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Dong Lu Department of Pharmacology and Chemical Biology, Baylor College of Medicine, Houston, Texas, USA

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Prashi Jain Department of Molecular and Cellular Biology and Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas, USA

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Yang Yu Department of Molecular and Cellular Biology and Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas, USA

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David Cardenas Department of Molecular and Cellular Biology and Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas, USA

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Xiaohui Peng Department of Molecular and Cellular Biology and Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas, USA

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Xiaobin Yu Department of Molecular and Cellular Biology and Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas, USA

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Jianming Xu Department of Molecular and Cellular Biology and Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas, USA

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Jin Wang Department of Pharmacology and Chemical Biology, Baylor College of Medicine, Houston, Texas, USA

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Bert W O’Malley Department of Molecular and Cellular Biology and Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas, USA

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David M Lonard Department of Molecular and Cellular Biology and Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas, USA

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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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Koen M A Dreijerink Department of Endocrinology VU University Medical Center, Amsterdam, The Netherlands

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H T Marc Timmers German Cancer Consortium (DKTK) partner site Freiburg German Cancer Research Center (DKFZ) and Department of Urology, Medical Center-University of Freiburg, Freiburg, Germany

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Myles Brown Department of Medical Oncology Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA

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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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Marianne E Pavel Medical Department, Division of Hepatology and Gastroenterology including Metabolic Diseases, Campus Virchow Klinikum, Charité University Medicine, Berlin, Germany

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Christine Sers Institute of Pathology, Charité University Medicine, Berlin, Germany

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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

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Anastasia Alataki Ralph Lauren Centre for Breast Cancer Research, Royal Marsden Hospital and The Institute of Cancer Research, London, UK
The Breast Cancer Now Toby Robins Research Centre, The Institute of Cancer Research, London, UK

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Mitch Dowsett Ralph Lauren Centre for Breast Cancer Research, Royal Marsden Hospital and The Institute of Cancer Research, London, UK
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

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Eric Monsalves 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

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

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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Kyle Juraschka 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

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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Toru Tateno 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

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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Sameer Agnihotri 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

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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Sylvia L Asa 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

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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Shereen Ezzat 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

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

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

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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Gelareh Zadeh 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

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

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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Xumeng Wang Department of Surgical Oncology of The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China

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Tianxing Ying Department of Surgical Oncology of The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China

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Jimeng Yuan Department of Surgical Oncology of The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China

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Yue Wang Department of Surgical Oncology of The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China

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Xingyun Su Department of Surgical Oncology of The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China

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Shitu Chen Department of Surgical Oncology of The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China

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Yurong Zhao Institute of Environmental Medicine and Hepatobiliary and Pancreatic Surgery of The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
Zhejiang Laboratory for Systems & Precision Medicine, Zhejiang University Medical Center, Hangzhou, China

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Yuanyuan Zhao Institute of Environmental Medicine and Hepatobiliary and Pancreatic Surgery of The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
Zhejiang Laboratory for Systems & Precision Medicine, Zhejiang University Medical Center, Hangzhou, China

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Jinghao Sheng Zhejiang Laboratory for Systems & Precision Medicine, Zhejiang University Medical Center, Hangzhou, China
Institute of Environmental Medicine of Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, China

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Lisong Teng Department of Surgical Oncology of The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China

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Chi Luo Institute of Environmental Medicine and Hepatobiliary and Pancreatic Surgery of The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
Zhejiang Laboratory for Systems & Precision Medicine, Zhejiang University Medical Center, Hangzhou, China

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Weibin Wang Department of Surgical Oncology of The First Affiliated Hospital, Zhejiang University School of Medicine, 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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Bing Cheng Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore

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Karen Crasta Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore
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

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