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Pancreatic Neoplasms: HELP
Articles by Carlo M. Croce
Based on 6 articles published since 2009
(Why 6 articles?)

Between 2009 and 2019, Carlo M. Croce wrote the following 6 articles about Pancreatic Neoplasms.
+ Citations + Abstracts
1 Editorial Will detection of microRNA biomarkers in blood improve the diagnosis and survival of patients with pancreatic cancer? 2014

Buchsbaum, Donald J / Croce, Carlo M. ·Division of Radiation Biology, Department of Radiation Oncology, University of Alabama, Birmingham. · Comprehensive Cancer Center, Department of Molecular Virology, Immunology and Medical Genetics, Ohio State University, Columbus. ·JAMA · Pubmed #24449314.

ABSTRACT: -- No abstract --

2 Article A differential microRNA profile distinguishes cholangiocarcinoma from pancreatic adenocarcinoma. 2014

Collins, Amy L / Wojcik, Sylwia / Liu, James / Frankel, Wendy L / Alder, Hansjuerg / Yu, Lianbo / Schmittgen, Thomas D / Croce, Carlo M / Bloomston, Mark. ·Department of Surgery, The Ohio State University, Columbus, OH, USA. ·Ann Surg Oncol · Pubmed #24046106.

ABSTRACT: BACKGROUND: Cancers of the bile duct and the pancreas are virtually indistinguishable using conventional histopathological and clinical characteristics. We sought to use microRNA (miR) profiling to differentiate these two cancers. METHODS: RNA was harvested from the tumors of patients undergoing curative resection for cholangiocarcinoma or pancreatic adenocarcinoma and compared with adjacent normal bile duct or pancreas, respectively. There were 31 pairs of cholangiocarcinoma with matched tumor and adjacent bile duct and nine pairs of pancreatic cancer with matched tumor and adjacent uninvolved pancreas that had sufficient quantity of RNA that were included in the final analysis. Differential microRNA expression profiles were determined using the nCounter System from nanoString Technologies (Seattle, WA,USA). RESULTS: A total of 41 differentially expressed miRs were identified in cholangiocarcinoma (25 overexpressed, 16 underexpressed) and 52 differentially expressed miRs were found in pancreatic adenocarcinoma (30 overexpressed, 22 underexpressed) relative to adjacent normal tissue. Of these two profiles, 15 miRs were commonly dysregulated between tumor types. Also, eight miRs were similarly overexpressed or underexpressed in cholangiocarcinoma and pancreatic adenocarcinoma, whereas the other seven miRs had inverse expression levels. CONCLUSIONS: Cholangiocarcinoma has a distinct miR profile from pancreatic adenocarcinoma. Discrimination between these two tumor types may be possible with as few as seven miRs.

3 Article Hypoxia induces the overexpression of microRNA-21 in pancreatic cancer cells. 2013

Mace, Thomas A / Collins, Amy L / Wojcik, Sylwia E / Croce, Carlo M / Lesinski, Gregory B / Bloomston, Mark. ·Department of Internal Medicine, The Ohio State University, Columbus, Ohio. ·J Surg Res · Pubmed #23726431.

ABSTRACT: BACKGROUND: Pancreatic cancer cells exist in a hypoxic microenvironment containing numerous factors that impact tumor survival, proliferation, and metastasis. MicroRNAs (miRs) are differentially expressed in cancer but also altered by hypoxia. We hypothesized that hypoxia could induce expression of miR-21, an oncomir in pancreatic cancer cells. MATERIALS AND METHODS: We examined how hypoxia regulates miR-21 expression in pancreatic cancer cell lines (BxPC-3, AsPC-1) by stem-loop RT-PCR. Chromatin immunoprecipitation assays were used to study how hypoxia alters hypoxia-inducible factor (HIF)-1α binding to the hypoxia response element of miR-21. BxPC-3 and AsPC-1 cells were transfected with a constitutively stable HIF-1α subunit or vector control (pcDNA3.1) to determine the influence of miR-21 in normoxia. The effect of mature miR-21 sense and antisense oligonucleotides on proliferation and apoptosis in hypoxic and normoxic conditions was assessed via WST-1 assay and flow cytometry. RESULTS: MiR-21 levels increased in all cell lines grown in hypoxic conditions versus normoxia, whereas siRNA targeting HIF-1α reduced miR-21 expression. Hypoxic conditions resulted in direct binding of HIF-1α to the predicted binding site in miR-21. Transfection with a constitutively stable HIF-1α expression plasmid in normoxia resulted in upregulated miR-21, similar to that seen in hypoxia. Cells transfected with antisense constructs targeting miR-21 had reduced proliferation and increased apoptosis in normoxia, whereas miR-21 overexpression abrogated hypoxia-associated reductions in proliferation. CONCLUSIONS: MiR-21 is induced by hypoxia in pancreatic cancer cells via HIF-1α upregulation. MiR-21 overexpression allows cells to avoid apoptosis in a hypoxic microenvironment. Inhibition of miR-21 expression may increase cellular susceptibility to hypoxia in pancreatic cancer.

4 Article MicroRNAs in cancer: personalizing diagnosis and therapy. 2010

Nana-Sinkam, S Patrick / Fabbri, Muller / Croce, Carlo M. ·Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, The Ohio State University, Columbus, Ohio 43210, USA. ·Ann N Y Acad Sci · Pubmed #20973796.

ABSTRACT: MicroRNAs (miRNAs) are 19-24nt noncoding RNAs that have been implicated in the pathogenesis of both solid and hematological malignancies. Frequently located in fragile chromosomal regions, miRNAs are essential to key biological functions, such as cellular differentiation, apoptosis, and growth. miRNAs may serve as either tumor suppressors or oncogenes. As a result, they have the potential to serve as both biomarkers and therapeutic agents in cancer. Based on our presentation at the recent Towards Personalized Cancer Medicine conference held in Barcelona, Spain, May 19-21, 2010, we provide an overview of the current knowledge of miRNA deregulation in solid and hematological malignancies and their application as biomarkers of disease.

5 Article Pancreatic endocrine tumors: expression profiling evidences a role for AKT-mTOR pathway. 2010

Missiaglia, Edoardo / Dalai, Irene / Barbi, Stefano / Beghelli, Stefania / Falconi, Massimo / della Peruta, Marco / Piemonti, Lorenzo / Capurso, Gabriele / Di Florio, Alessia / delle Fave, Gianfranco / Pederzoli, Paolo / Croce, Carlo M / Scarpa, Aldo. ·Departments of Pathology and Surgical and Gastroenterological Sciences, University of Verona, Verona, Italy. ·J Clin Oncol · Pubmed #19917848.

ABSTRACT: PURPOSE: We investigated the global gene expression in a large panel of pancreatic endocrine tumors (PETs) aimed at identifying new potential targets for therapy and biomarkers to predict patient outcome. PATIENTS AND METHODS: Using a custom microarray, we analyzed 72 primary PETs, seven matched metastases, and 10 normal pancreatic samples. Relevant differentially expressed genes were validated by either quantitative real-time polymerase chain reaction or immunohistochemistry on tissue microarrays. RESULTS: Our data showed that: tuberous sclerosis 2 (TSC2) and phosphatase and tensin homolog (PTEN) were downregulated in most of the primary tumors, and their low expression was significantly associated with shorter disease-free and overall survival; somatostatin receptor 2 (SSTR2) was absent or very low in insulinomas compared with nonfunctioning tumors; and expression of fibroblast growth factor 13 (FGF13) gene was significantly associated with the occurrence of liver metastasis and shorter disease-free survival. TSC2 and PTEN are two key inhibitors of the Akt/mammalian target of rapamycin (mTOR) pathway and the specific inhibition of mTOR with rapamycin or RAD001 inhibited cell proliferation of PET cell lines. CONCLUSION: Our results strongly support a role for PI3K/Akt/mTOR pathway in PET, which ties in with the fact that mTOR inhibitors have reached phase III trials in neuroendocrine tumors. The finding of differential SSTR expression raises the potential for SSTR expression to be evaluated as a marker of response to somatostatin analogs. Finally, we identified FGF13 as a new prognostic marker that predicted poorer outcome in patients who were clinically considered free from disease.

6 Article Coordinate loss of fragile gene expression in pancreatobiliary cancers: correlations among markers and clinical features. 2009

Bloomston, Mark / Kneile, Jeffrey / Butterfield, Matthew / Dillhoff, Mary / Muscarella, Peter / Ellison, E Christopher / Melvin, W Scott / Croce, Carlo M / Pichiorri, Flavia / Huebner, Kay / Frankel, Wendy L. ·Department of Surgery, The Ohio State University, Columbus, OH, USA. mark.bloomston@osumc.edu ·Ann Surg Oncol · Pubmed #19434452.

ABSTRACT: BACKGROUND: Loss of expression of fragile gene products, Fhit and Wwox, occurs in many cancer types, with loss exhibited early in the neoplastic process in some. Wwox has been understudied in pancreatobiliary cancers, especially in relation to other involved tumor suppressors. We have assessed the status of the Fhit and Wwox proteins encoded by DNA damage susceptible chromosome fragile sites encompassed by FHIT and WWOX tumor suppressor genes. METHODS: Pancreatic, gallbladder and ampullary cancers, normal pancreas, chronic pancreatitis, and benign gallbladder specimens were stained for expression of Fhit, Fhit effector protein Fdxr, Wwox, and other tumor suppressors by immunohistochemistry, and comparisons were made between benign and malignant tissue. Correlations of expression among proteins and clinicopathologic features were sought using Spearman's rank order. Survival curves were created using the Kaplan-Meier method and compared by log-rank analysis. Predictors of survival were determined using multivariate Cox proportional hazards analysis. RESULTS: Fhit and Wwox were ubiquitously expressed in benign samples and significantly and coordinately reduced in pancreatic, gallbladder, and ampullary cancers. In pancreatic cancers, Fdxr expression was positively correlated with Fhit and Wwox expression. Neither Fhit nor Wwox expression correlated with expression of other tumor suppressors or with clinicopathologic characteristics measured. CONCLUSION: Loss of Fhit and Wwox expression does not predict tumor progression or patient survival, suggesting that loss of expression of genes at the exquisitely replication stress sensitive chromosome fragile regions is an early event in the pathogenesis of cancers of the gallbladder, pancreas, and ampulla.