David A. Tuveson
Cold Spring Harbor Laboratory
CancerInternal medicinePathologyOncologyStromal cellImmunologyTumor microenvironmentPancreasMetastasisPancreatic cancerGemcitabineAdenocarcinomaKRASPancreatic ductal adenocarcinomaOrganoidCancer researchCarcinogenesisMedicineBiologyCell biologyCancer cell
320Publications
95H-index
44.5kCitations
Publications 317
Newest
#1Ledong Wan (CSHL: Cold Spring Harbor Laboratory)
#2Kuan-Ting Lin (CSHL: Cold Spring Harbor Laboratory)H-Index: 14
Last. Adrian R. Krainer (CSHL: Cold Spring Harbor Laboratory)H-Index: 110
view all 7 authors...
KRAS is recurrently mutated in pancreatic ductal adenocarcinoma (PDAC), triggering the formation of acinar-to-ductal metaplasia (ADM) and pancreatic intraepithelial neoplasia (PanIN). However, the majority of pancreatic cells from KC (LSL-KrasG12D/+; Pdx-1-Cre) mice carrying the KrasG12D mutation remain morphologically normal for a long time, suggesting the existence of compensatory feedback mechanisms that buffer KrasG12D signaling, and that additional steps are required for disrupting cell hom...
Source
#1Ledong Wan (CSHL: Cold Spring Harbor Laboratory)
#2Kuan-Ting Lin (CSHL: Cold Spring Harbor Laboratory)H-Index: 14
Last. Adrian R. Krainer (CSHL: Cold Spring Harbor Laboratory)H-Index: 110
view all 8 authors...
The gene encoding KRAS GTPase is recurrently mutated in pancreatic ductal adenocarcinoma (PDAC), triggering the formation of precursor lesions, i.e., acinar-to-ductal metaplasia (ADM) and pancreatic intraepithelial neoplasia (PanIN). However, the majority of pancreatic cells from KC (LSL-KrasG12D/+; Pdx-1-Cre) mice expressing the KrasG12D mutation remain morphologically normal for a long time, suggesting the existence of compensatory feedback mechanisms that buffer aberrant KrasG12D signaling, a...
Source
#1L. Shaashua (Weizmann Institute of Science)H-Index: 1
#2Meirav Pevsner-Fischer (Weizmann Institute of Science)H-Index: 26
Last. Han Sang Kim (Yonsei University)H-Index: 17
view all 25 authors...
Abstract null Cancer-associated fibroblasts (CAFs) give rise to desmoplastic stroma, which supports tumor progression and metastasis, and comprises up to 90% of the tumor mass in pancreatic cancer. Recent work by us and others has shown that CAFs are transcriptionally rewired by adjacent cancer cells to form heterogeneous subtypes. Whether this rewiring is differentially affected by different driver mutations in cancer cells is largely unknown. Here we address this question by dissecting and com...
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#1Tuo Hu (Eppley Institute for Research in Cancer and Allied Diseases)H-Index: 7
#2Surendra K. Shukla (Eppley Institute for Research in Cancer and Allied Diseases)H-Index: 16
Last. Kuldeep S. Attri (Eppley Institute for Research in Cancer and Allied Diseases)H-Index: 10
view all 31 authors...
ABSTRACT null Background & Aims null SIRT5 plays pleiotropic roles via post-translational modifications, serving as a tumor suppressor, or an oncogene, in different tumors. However, the role SIRT5 plays in the initiation and progression of pancreatic ductal adenocarcinoma (PDAC) remains unknown. null Methods null Published datasets and tissue arrays with SIRT5 staining were used to investigate the clinical relevance of SIRT5 in PDAC. Furthermore, to define the role of SIRT5 in the carcinogenesis...
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#1Nina SteeleH-Index: 8
#2Giulia BiffiH-Index: 16
Last. Ela ElyadaH-Index: 10
view all 31 authors...
Source
Pancreatic ductal adenocarcinoma (PDAC) patients have a 5-year survival rate of only 8% largely due to late diagnosis and insufficient therapeutic options. Neutrophils are among the most abundant immune cell type within the PDAC tumor microenvironment (TME), and are associated with a poor clinical prognosis. However, despite recent advances in understanding neutrophil biology in cancer, therapies targeting tumor-associated neutrophils are lacking. Here, we demonstrate, using pre-clinical mouse m...
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Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy with limited treatment options. Although activating mutations of the KRAS GTPase are the predominant dependency present in >90% of PDAC patients, targeting KRAS mutants directly has been challenging in PDAC. Similarly, strategies targeting known KRAS downstream effectors have had limited clinical success due to feedback mechanisms, alternate pathways, and dose-limiting toxicities in normal tissues. Therefore, identifying additional f...
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#1David A. Tuveson (CSHL: Cold Spring Harbor Laboratory)H-Index: 95
Summary: Cancer models have helped solve many mysteries of cancer research, and are poised to bring our understanding to the next level as we dissect the relevance of cancer-associated alleles and heterocellular interactions. However, the ability of cancer models to correctly identify new therapeutic methods has been less fruitful, and a reconsideration of model designs and model applications should help develop more effective approaches for patients.
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: Pancreatic ductal adenocarcinoma (PDAC) has one of the poorest prognoses of all malignancies, with a 5-year survival rate <8%.1,2 Suspicious lesions are typically diagnosed via endoscopic ultrasound-guided fine-needle aspiration or endoscopic ultrasound-guided fine-needle biopsy (EUS-FNB).3 Fewer needle passes decreases the risk of postprocedure complications, including pancreatitis and hemorrhage, while allowing additional needle passes to be used for adjuvant tissue testing, such as organoid...
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#1Nina Steele (UM: University of Michigan)H-Index: 8
#2Giulia Biffi (University of Cambridge)H-Index: 16
Last. Marina Pasca di Magliano (UM: University of Michigan)H-Index: 33
view all 35 authors...
Purpose: Pancreatic ductal adenocarcinoma (PDAC) is a deadly disease characterized by an extensive fibroinflammatory stroma, which includes abundant cancer-associated fibroblast (CAF) populations. PDAC CAFs are heterogeneous, but the nature of this heterogeneity is incompletely understood. The Hedgehog (HH) pathway functions in PDAC in a paracrine manner, with ligands secreted by cancer cells signaling to stromal cells in the microenvironment. Previous reports investigating the role of HH signal...
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