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Pancreatic Neoplasms: HELP
Articles by Marco Dal Molin
Based on 5 articles published since 2010
(Why 5 articles?)
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Between 2010 and 2020, Marco Dal Molin wrote the following 5 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Editorial Very long-term survival in pancreatic cancer. 2015

Molin, Marco Dal / Wood, Laura D. ·Gastrointestinal and Liver Pathology Department, Johns Hopkins University, Baltimore, MD, USA. ·Aging (Albany NY) · Pubmed #26143583.

ABSTRACT: -- No abstract --

2 Article Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. 2017

Genovese, Giannicola / Carugo, Alessandro / Tepper, James / Robinson, Frederick Scott / Li, Liren / Svelto, Maria / Nezi, Luigi / Corti, Denise / Minelli, Rosalba / Pettazzoni, Piergiorgio / Gutschner, Tony / Wu, Chia-Chin / Seth, Sahil / Akdemir, Kadir Caner / Leo, Elisabetta / Amin, Samirkumar / Molin, Marco Dal / Ying, Haoqiang / Kwong, Lawrence N / Colla, Simona / Takahashi, Koichi / Ghosh, Papia / Giuliani, Virginia / Muller, Florian / Dey, Prasenjit / Jiang, Shan / Garvey, Jill / Liu, Chang-Gong / Zhang, Jianhua / Heffernan, Timothy P / Toniatti, Carlo / Fleming, Jason B / Goggins, Michael G / Wood, Laura D / Sgambato, Alessandro / Agaimy, Abbas / Maitra, Anirban / Roberts, Charles W M / Wang, Huamin / Viale, Andrea / DePinho, Ronald A / Draetta, Giulio F / Chin, Lynda. ·Department of Genomic Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · Institute for Applied Cancer Science, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · European Institute of Oncology, Milano 20141, Italy. · Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangzhou, 510060, China. · Istituto di Patologia Generale, Universitá Cattolica del Sacro Cuore, Rome 00168, Italy. · Graduate program in Structural and Computational Biology and Molecular Biophysics, Baylor College of Medicine, Houston, Texas 77030, USA. · Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University, Baltimore, Maryland 21287, USA. · Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · Office of Technology Commercialization, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · Department of Cancer Systems Imaging, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · Department of Cancer Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · ORBIT Platform, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · Department of Surgical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · Department of Pathology, Friedrich Alexander University Erlangen-Nuremberg, University Hospital, Erlangen 91054, Germany. · Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · Sheikh Ahmed Bin Zayed Al Nahyan Center for Pancreatic Cancer Research, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. · Comprehensive Cancer Center and Department of Oncology, St Jude Children's Research Hospital, Memphis, Tennessee 77027, USA. ·Nature · Pubmed #28178232.

ABSTRACT: Malignant neoplasms evolve in response to changes in oncogenic signalling. Cancer cell plasticity in response to evolutionary pressures is fundamental to tumour progression and the development of therapeutic resistance. Here we determine the molecular and cellular mechanisms of cancer cell plasticity in a conditional oncogenic Kras mouse model of pancreatic ductal adenocarcinoma (PDAC), a malignancy that displays considerable phenotypic diversity and morphological heterogeneity. In this model, stochastic extinction of oncogenic Kras signalling and emergence of Kras-independent escaper populations (cells that acquire oncogenic properties) are associated with de-differentiation and aggressive biological behaviour. Transcriptomic and functional analyses of Kras-independent escapers reveal the presence of Smarcb1-Myc-network-driven mesenchymal reprogramming and independence from MAPK signalling. A somatic mosaic model of PDAC, which allows time-restricted perturbation of cell fate, shows that depletion of Smarcb1 activates the Myc network, driving an anabolic switch that increases protein metabolism and adaptive activation of endoplasmic-reticulum-stress-induced survival pathways. Increased protein turnover renders mesenchymal sub-populations highly susceptible to pharmacological and genetic perturbation of the cellular proteostatic machinery and the IRE1-α-MKK4 arm of the endoplasmic-reticulum-stress-response pathway. Specifically, combination regimens that impair the unfolded protein responses block the emergence of aggressive mesenchymal subpopulations in mouse and patient-derived PDAC models. These molecular and biological insights inform a potential therapeutic strategy for targeting aggressive mesenchymal features of PDAC.

3 Article Liver transplant patients have a risk of progression similar to that of sporadic patients with branch duct intraductal papillary mucinous neoplasms. 2014

Lennon, Anne Marie / Victor, David / Zaheer, Atif / Ostovaneh, Mohammad Reza / Jeh, Jessica / Law, Joanna K / Rezaee, Neda / Molin, Marco Dal / Ahn, Young Joon / Wu, Wenchuan / Khashab, Mouen A / Girotra, Mohit / Ahuja, Nita / Makary, Martin A / Weiss, Matthew J / Hirose, Kenzo / Goggins, Michael / Hruban, Ralph H / Cameron, Andrew / Wolfgang, Christopher L / Singh, Vikesh K / Gurakar, Ahmet. ·Division of Gastroenterology and Hepatology, The Sol Goldman Pancreatic Cancer Research Center, The Johns Hopkins Medical Institutions, Baltimore, MD; Division of Surgery, The Sol Goldman Pancreatic Cancer Research Center, The Johns Hopkins Medical Institutions, Baltimore, MD. ·Liver Transpl · Pubmed #25155689.

ABSTRACT: Intraductal papillary mucinous neoplasms (IPMNs) have malignant potential and can progress from low- to high-grade dysplasia to invasive adenocarcinoma. The management of patients with IPMNs is dependent on their risk of malignant progression, with surgical resection recommended for patients with branch-duct IPMN (BD-IPMN) who develop high-risk features. There is increasing evidence that liver transplant (LT) patients are at increased risk of extrahepatic malignancy. However, there are few data regarding the risk of progression of BD-IPMNs in LT recipients. The aim of this study was to determine whether LT recipients with BD-IPMNs are at higher risk of developing high-risk features than patients with BD-IPMNs who did not receive a transplant. Consecutive patients who underwent an LT with BD-IPMNs were included. Patients with BD-IPMNs with no history of immunosuppression were used as controls. Progression of the BD-IPMNs was defined as development of a high-risk feature (jaundice, dilated main pancreatic duct, mural nodule, cytology suspicious or diagnostic for malignancy, cyst diameter ≥3 cm). Twenty-three LT patients with BD-IPMN were compared with 274 control patients. The median length of follow-up was 53.7 and 24.0 months in LT and control groups, respectively. Four (17.4%) LT patients and 45 (16.4%) controls developed high-risk features (P = 0.99). In multivariate analysis, progression of BD-IPMNs was associated with age at diagnosis but not with LT. There was no statistically significant difference in the risk of developing high-risk features between the LT and the control groups.

4 Article Targeted next-generation sequencing of cancer genes dissects the molecular profiles of intraductal papillary neoplasms of the pancreas. 2014

Amato, Eliana / Molin, Marco Dal / Mafficini, Andrea / Yu, Jun / Malleo, Giuseppe / Rusev, Borislav / Fassan, Matteo / Antonello, Davide / Sadakari, Yoshihiko / Castelli, Paola / Zamboni, Giuseppe / Maitra, Anirban / Salvia, Roberto / Hruban, Ralph H / Bassi, Claudio / Capelli, Paola / Lawlor, Rita T / Goggins, Michael / Scarpa, Aldo. ·ARC-Net Research Centre and Department of Pathology and Diagnostics, University and Hospital Trust of Verona, Italy. ·J Pathol · Pubmed #24604757.

ABSTRACT: Intraductal neoplasms are important precursors to invasive pancreatic cancer and provide an opportunity to detect and treat pancreatic neoplasia before an invasive carcinoma develops. The diagnostic evaluation of these lesions is challenging, as diagnostic imaging and cytological sampling do not provide accurate information on lesion classification, the grade of dysplasia or the presence of invasion. Moreover, the molecular driver gene mutations of these precursor lesions have yet to be fully characterized. Fifty-two intraductal papillary neoplasms, including 48 intraductal papillary mucinous neoplasms (IPMNs) and four intraductal tubulopapillary neoplasms (ITPNs), were subjected to the mutation assessment in 51 cancer-associated genes, using ion torrent semiconductor-based next-generation sequencing. P16 and Smad4 immunohistochemistry was performed on 34 IPMNs and 17 IPMN-associated carcinomas. At least one somatic mutation was observed in 46/48 (96%) IPMNs; 29 (60%) had multiple gene alterations. GNAS and/or KRAS mutations were found in 44/48 (92%) of IPMNs. GNAS was mutated in 38/48 (79%) IPMNs, KRAS in 24/48 (50%) and these mutations coexisted in 18/48 (37.5%) of IPMNs. RNF43 was the third most commonly mutated gene and was always associated with GNAS and/or KRAS mutations, as were virtually all the low-frequency mutations found in other genes. Mutations in TP53 and BRAF genes (10% and 6%) were only observed in high-grade IPMNs. P16 was lost in 7/34 IPMNs and 9/17 IPMN-associated carcinomas; Smad4 was lost in 1/34 IPMNs and 5/17 IPMN-associated carcinomas. In contrast to IPMNs, only one of four ITPNs had detectable driver gene (GNAS and NRAS) mutations. Deep sequencing DNA from seven cyst fluid aspirates identified 10 of the 13 mutations detected in their associated IPMN. Using next-generation sequencing to detect cyst fluid mutations has the potential to improve the diagnostic and prognostic stratification of pancreatic cystic neoplasms.

5 Article Clinicopathological correlates of activating GNAS mutations in intraductal papillary mucinous neoplasm (IPMN) of the pancreas. 2013

Molin, Marco Dal / Matthaei, Hanno / Wu, Jian / Blackford, Amanda / Debeljak, Marija / Rezaee, Neda / Wolfgang, Christopher L / Butturini, Giovanni / Salvia, Roberto / Bassi, Claudio / Goggins, Michael G / Kinzler, Kenneth W / Vogelstein, Bert / Eshleman, James R / Hruban, Ralph H / Maitra, Anirban. ·Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD. · Unit of General Surgery B, Pancreas Institute, Department of Surgery, "G.B. Rossi" Hospital, University of Verona Hospital Trust, Verona, Italy. · Department of General, Visceral, Thoracic and Vascular Surgery, University of Bonn, Bonn, Germany. · Ludwig Center for Cancer Genetics, Johns Hopkins University School of Medicine, Baltimore, MD. · Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, MD. · Department of Surgery, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD. · Department of Oncology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD. ·Ann Surg Oncol · Pubmed #23846778.

ABSTRACT: BACKGROUND: Intraductal papillary mucinous neoplasms (IPMNs) are the most common cystic precursor lesions of invasive pancreatic cancer. The recent identification of activating GNAS mutations at codon 201 in IPMNs is a promising target for early detection and therapy. The purpose of this study was to explore clinicopathological correlates of GNAS mutational status in resected IPMNs. METHODS: Clinical and pathologic characteristics were retrieved on 54 patients in whom GNAS codon 201 mutational status was previously reported ("historical group", Wu et al. Sci Transl Med 3:92ra66, 2011). In addition, a separate cohort of 32 patients (validation group) was included. After microdissection and DNA extraction, GNAS status was determined in the validation group by pyrosequencing. RESULTS: GNAS activating mutations were found in 64% of the 32 IPMNs included in the validation group, compared with a previously reported prevalence of 57% in the historical group. Overall, 52 of 86 (61%) of IPMNs demonstrated GNAS mutations in the two studies combined. Analysis of both groups confirmed that demographic characteristics, tumor location, ductal system involvement, focality, size, grade of dysplasia, presence of an associated cancer, and overall survival were not correlated with GNAS mutational status. Stratified by histological subtype, 100% of intestinal type IPMNs demonstrated GNAS mutations compared to 51% of gastric IPMN, 71% of pancreatobiliary IPMNs, and 0% of oncocytic IPMNs. CONCLUSIONS: GNAS activating mutations can be reliably detected in IPMNs by pyrosequencing. In terms of clinicopathological parameters, only histological subtype was correlated with mutational frequency, with the intestinal phenotype always associated with GNAS mutations.