About: David Tuveson

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An Entity of Type : wikibase:Item, within Data Space : wikidata.demo.openlinksw.com associated with source document(s)

American cancer biologist

Attributes	Values
rdf:type	Item
owl:sameAs	David Tuveson
description	wetenschapper (nl) науковець (uk) American cancer biologist (en)
rdfs:label	David Tuveson (en) David Tuveson (es) David Tuveson (nl) David Tuveson (sq) David Tuveson (ast)
skos:prefLabel	David Tuveson (en) David Tuveson (es) David Tuveson (nl) David Tuveson (sq) David Tuveson (ast)
name	David Tuveson (en) David Tuveson (es) David Tuveson (nl) David Tuveson (sq) David Tuveson (ast)
given name	wds:Q23417102-A2CD39B6-EE8D-4942-AA41-B927275A2B58
given name	David
instance of	wds:Q23417102-844BE2BD-5C08-4ABD-A20B-2195AE521986
instance of	Homo sapiens
Academic Tree ID	wds:Q23417102-b455f3f6-4c4a-4add-5131-abe1fe68672c
Google Knowledge Graph ID	wds:Q23417102-C54F922D-D477-49D1-A3D5-3F1B60B03560
Google Knowledge Graph ID	http://g.co/kg/g/11bxjvqr5g
Academic Tree ID	99383
Google Knowledge Graph ID	/g/11bxjvqr5g
Google Scholar author ID	wds:Q23417102-7164F430-9D62-42C1-8B3A-71CCEDC694FB
Google Scholar author ID	G48jb_QAAAAJ
skos:altLabel	David Arthur Tuveson (en)
occupation	wds:Q23417102-9E94ADB2-D2D8-49F6-92A2-5B72DE35089A
employer	wds:Q23417102-ECA05AF0-B07F-43A0-961B-C3A54C532511
sex or gender	wds:Q23417102-937BCDC7-2DD2-4529-8613-FEDE44A78F2D
on focus list of Wikimedia project	wds:Q23417102-4CD0FDBB-D226-4F1A-AB32-015D823D392C
date of birth	wds:Q23417102-E4B8F90D-B366-4A9B-AE54-44B64B0FE86D
educated at	wds:Q23417102-51433F12-0447-4148-B18F-9E43B490041D wds:Q23417102-84FA1A12-79F5-470F-B30B-2B17C98C71D7
family name	wds:Q23417102-423D428B-A8CF-40EF-8029-2C6340BE6D7D
occupation	scientist
employer	Cold Spring Harbor Laboratory
sex or gender	male
on focus list of Wikimedia project	WikiProject COVID-19
date of birth	1966-01-01 00:00:00Z (xsd:dateTime)
educated at	Johns Hopkins School of Medicine Massachusetts Institute of Technology
family name	Tuveson
ORCID iD	wds:Q23417102-67C6507D-7567-4CF7-A1A2-0CF6A4418D46
ORCID iD	https://orcid.org/0000-0002-8017-2712
ORCID iD	0000-0002-8017-2712
is owl:sameAs of	David Tuveson
is about of	David Tuveson https://www.wikidata.org/wiki/Special:EntityData/Q23417102 David Tuveson
is author of	Retinoic acid-induced pancreatic stellate cell quiescence reduces paracrine Wnt-β-catenin signaling to slow tumor progression Conditional expression of oncogenic K-ras from its endogenous promoter induces a myeloproliferative disease Pancreatic cancer genomes reveal aberrations in axon guidance pathway genes Maximizing mouse cancer models Efficacy and safety of imatinib mesylate in advanced gastrointestinal stromal tumors Oncogene-induced Nrf2 transcription promotes ROS detoxification and tumorigenesis Demonstration of a genetic therapeutic index for tumors expressing oncogenic BRAF by the kinase inhibitor SB-590885 Mutant V599EB-Raf regulates growth and vascular development of malignant melanoma tumors Suppression of BRAF(V599E) in human melanoma abrogates transformation SPARC independent drug delivery and antitumour effects of nab-paclitaxel in genetically engineered mice Predictive in vivo animal models and translation to clinical trials Exome sequencing identifies frequent mutation of the SWI/SNF complex gene PBRM1 in renal carcinoma Anti-tumour efficacy of capecitabine in a genetically engineered mouse model of pancreatic cancer Targeting CXCL12 from FAP-expressing carcinoma-associated fibroblasts synergizes with anti-PD-L1 immunotherapy in pancreatic cancer Crosstalk between the canonical NF-κB and Notch signaling pathways inhibits Pparγ expression and promotes pancreatic cancer progression in mice Gamma secretase inhibition promotes hypoxic necrosis in mouse pancreatic ductal adenocarcinoma The deubiquitinase USP9X suppresses pancreatic ductal adenocarcinoma Hyaluronan impairs vascular function and drug delivery in a mouse model of pancreatic cancer nab-Paclitaxel potentiates gemcitabine activity by reducing cytidine deaminase levels in a mouse model of pancreatic cancer CTGF antagonism with mAb FG-3019 enhances chemotherapy response without increasing drug delivery in murine ductal pancreas cancer Germline Brca2 heterozygosity promotes Kras(G12D) -driven carcinogenesis in a murine model of familial pancreatic cancer Impaired JNK signaling cooperates with KrasG12D expression to accelerate pancreatic ductal adenocarcinoma. The use of GEM models for experimental cancer therapeutics Cathepsin B promotes the progression of pancreatic ductal adenocarcinoma in mice Twist induces an epithelial-mesenchymal transition to facilitate tumor metastasis In vivo identification of tumor- suppressive PTEN ceRNAs in an oncogenic BRAF-induced mouse model of melanoma Vitamin D receptor-mediated stromal reprogramming suppresses pancreatitis and enhances pancreatic cancer therapy Pathology of genetically engineered mouse models of pancreatic exocrine cancer: consensus report and recommendations. C-Raf is required for the initiation of lung cancer by K-Ras(G12D). The differential effects of mutant p53 alleles on advanced murine lung cancer Kras(G12D) and Smad4/Dpc4 haploinsufficiency cooperate to induce mucinous cystic neoplasms and invasive adenocarcinoma of the pancreas Somatic activation of oncogenic Kras in hematopoietic cells initiates a rapidly fatal myeloproliferative disorder Expression of oncogenic K-ras from its endogenous promoter leads to a partial block of erythroid differentiation and hyperactivation of cytokine-dependent signaling pathways Ras redux: rethinking how and where Ras acts. Pancreatic cancer in mice and man: the Penn Workshop 2004 ATP citrate lyase inhibition can suppress tumor cell growth Endogenous oncogenic K-ras(G12D) stimulates proliferation and widespread neoplastic and developmental defects. The promise and perils of antioxidants for cancer patients Mutant p53 gain of function in two mouse models of Li-Fraumeni syndrome SCRIB expression is deregulated in human prostate cancer, and its deficiency in mice promotes prostate neoplasia Finding and killing the CRABs of pancreatic cancer. Direct histological processing of EUS biopsies enables rapid molecular biomarker analysis for interventional pancreatic cancer trials Fibroblast heterogeneity in the cancer wound BRAF inhibitor resistance mediated by the AKT pathway in an oncogenic BRAF mouse melanoma model Restoration of p53 function leads to tumour regression in vivo

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