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Pancreatic Neoplasms: HELP
Articles by Mario Plebani
Based on 13 articles published since 2010
(Why 13 articles?)
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Between 2010 and 2020, Mario Plebani wrote the following 13 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Review Inflammation and Pancreatic Cancer: Focus on Metabolism, Cytokines, and Immunity. 2019

Padoan, Andrea / Plebani, Mario / Basso, Daniela. ·Department of Medicine ⁻ DIMED, University of Padova, Via Giustiniani 2, 35128 Padova, Italy. andrea.padoan@unipd.it. · Department of Medicine ⁻ DIMED, University of Padova, Via Giustiniani 2, 35128 Padova, Italy. mario.plebani@unipd.it. · Department of Medicine ⁻ DIMED, University of Padova, Via Giustiniani 2, 35128 Padova, Italy. daniela.basso@unipd.it. ·Int J Mol Sci · Pubmed #30764482.

ABSTRACT: Systemic and local chronic inflammation might enhance the risk of pancreatic ductal adenocarcinoma (PDAC), and PDAC-associated inflammatory infiltrate in the tumor microenvironment concurs in enhancing tumor growth and metastasis. Inflammation is closely correlated with immunity, the same immune cell populations contributing to both inflammation and immune response. In the PDAC microenvironment, the inflammatory cell infiltrate is unbalanced towards an immunosuppressive phenotype, with a prevalence of myeloid derived suppressor cells (MDSC), M2 polarized macrophages, and T

2 Review CA 19-9: handle with care. 2013

Galli, Claudio / Basso, Daniela / Plebani, Mario. ·Scientific Affairs, Abbott Diagnostics Division, Rome, Italy. ·Clin Chem Lab Med · Pubmed #23370912.

ABSTRACT: Since its inception in the mid-1980s of the 20th century testing for carbohydrate antigen 19-9 (CA 19-9) has raised expectation for an earlier diagnosis and accurate monitoring of several malignant diseases. After almost 30 years, the available evidences have confirmed the appropriateness and usefulness of determining CA 19-9 levels as a prognostic indicator and as a reliable tool for monitoring pancreatic and gastrointestinal cancer, but concerns have been raised about its applications in screening, which is actually not recommended, and in the diagnosis of malignancies, due to several interferences that limit the specificity and to the insufficient sensitivity of this marker. In this paper we aimed to review the basic concepts of CA 19-9 testing and its current applications, with a major focus on the most recent evidences dealing with assay interference, methods comparison and monitoring of malignant diseases. The prognostic value and monitoring recommendations for pancreatic, gastric and colorectal cancers are described in depth.

3 Article PDAC-derived exosomes enrich the microenvironment in MDSCs in a 2017

Basso, Daniela / Gnatta, Elisa / Padoan, Andrea / Fogar, Paola / Furlanello, Sara / Aita, Ada / Bozzato, Dania / Zambon, Carlo-Federico / Arrigoni, Giorgio / Frasson, Chiara / Franchin, Cinzia / Moz, Stefania / Brefort, Thomas / Laufer, Thomas / Navaglia, Filippo / Pedrazzoli, Sergio / Basso, Giuseppe / Plebani, Mario. ·Department of Medicine - DIMED, University of Padova, Padova, Italy. · Department of Biomedical Sciences, University of Padova, Padova, Italy. · Proteomic Center, University of Padova, Padova, Italy. · Department of Woman and Child Health, Oncohematology Laboratory, University of Padova, Padova, Italy. · Eurofins Medigenomix GmbH, Ebersberg, Germany. · Comprehensive Biomarker Center GmbH (Recently re-named to Hummingbird Diagnostics GmbH), Heidelberg, Germany. · Association Wirsung Onlus, Padova, Italy. ·Oncotarget · Pubmed #29156694.

ABSTRACT: Tumor genetics and escape from immune surveillance concur in the poor prognosis of PDAC. In this study an experimental model was set up to verify whether CONCLUSION: PDAC-derived Exo from cells with

4 Article SMAD4 loss enables EGF, TGFβ1 and S100A8/A9 induced activation of critical pathways to invasion in human pancreatic adenocarcinoma cells. 2016

Moz, Stefania / Basso, Daniela / Bozzato, Dania / Galozzi, Paola / Navaglia, Filippo / Negm, Ola H / Arrigoni, Giorgio / Zambon, Carlo-Federico / Padoan, Andrea / Tighe, Paddy / Todd, Ian / Franchin, Cinzia / Pedrazzoli, Sergio / Punzi, Leonardo / Plebani, Mario. ·University of Padova, Laboratory Medicine, Department of Medicine - DIMED, Padova, Italy. · University of Padova, Rheumatology Unit, Department of Medicine - DIMED, Padova, Italy. · University of Nottingham, School of Life Sciences, Queen's Medical Centre, Nottingham, UK. · Mansoura University, Medical Microbiology and Immunology Department, Faculty of Medicine, Mansoura City, Egypt. · University of Padova, Department of Biomedical Sciences, Padova, Italy. · Proteomics Center, University of Padova and Azienda Ospedaliera di Padova, Padova, Italy. · Associazione Wirsung-onlus, Padova, Italy. ·Oncotarget · Pubmed #27655713.

ABSTRACT: Epidermal Growth Factor (EGF) receptor overexpression, KRAS, TP53, CDKN2A and SMAD4 mutations characterize pancreatic ductal adenocarcinoma. This mutational landscape might influence cancer cells response to EGF, Transforming Growth Factor β1 (TGFβ1) and stromal inflammatory calcium binding proteins S100A8/A9. We investigated whether chronic exposure to EGF modifies in a SMAD4-dependent manner pancreatic cancer cell signalling, proliferation and invasion in response to EGF, TGFβ1 and S100A8/A9. BxPC3, homozigously deleted (HD) for SMAD4, and BxPC3-SMAD4+ cells were or not stimulated with EGF (100 ng/mL) for three days. EGF pre-treated and non pretreated cells were stimulated with a single dose of EGF (100 ng/mL), TGFβ1 (0,02 ng/mL), S100A8/A9 (10 nM). Signalling pathways (Reverse Phase Protein Array and western blot), cell migration (Matrigel) and cell proliferation (XTT) were evaluated. SMAD4 HD constitutively activated ERK and Wnt/β-catenin, while inhibiting PI3K/AKT pathways. These effects were antagonized by chronic EGF, which increased p-BAD (anti-apoptotic) in response to combined TGFβ1 and S100A8/A9 stimulation. SMAD4 HD underlied the inhibition of NF-κB and PI3K/AKT in response to TGFβ1 and S100A8/A9, which also induced cell migration. Chronic EGF exposure enhanced cell migration of both BxPC3 and BxPC3-SMAD4+, rendering the cells less sensitive to the other inflammatory stimuli. In conclusion, SMAD4 HD is associated with the constitutive activation of the ERK and Wnt/β-catenin signalling pathways, and favors the EGF-induced activation of multiple signalling pathways critical to cancer proliferation and invasion. TGFβ1 and S100A8/A9 mainly inhibit NF-κB and PI3K/AKT pathways and, when combined, sinergize with EGF in enhancing anti-apoptotic p-BAD in a SMAD4-dependent manner.

5 Article Blood expression of matrix metalloproteinases 8 and 9 and of their inducers S100A8 and S100A9 supports diagnosis and prognosis of PDAC-associated diabetes mellitus. 2016

Moz, Stefania / Basso, Daniela / Padoan, Andrea / Bozzato, Dania / Fogar, Paola / Zambon, Carlo-Federico / Pelloso, Michela / Sperti, Cosimo / Vigili de Kreutzenberg, Saula / Pasquali, Claudio / Pedrazzoli, Sergio / Avogaro, Angelo / Plebani, Mario. ·Department of Medicine - DIMED, University of Padova, via Giustiniani 2, 35128 Padova, Italy. · Department of Laboratory Medicine, University Hospital of Padova, via Giustiniani 2, 35128 Padova, Italy. Electronic address: daniela.basso@sanita.padova.it. · Department of Laboratory Medicine, University Hospital of Padova, via Giustiniani 2, 35128 Padova, Italy. · Department of Surgical, Oncological and GastroenterologicalSciences - DISCOG, University of Padova, via Giustiniani 2, 35128 Padova, Italy. · Associazione Wirsung-onlus, via Giustiniani 2, 35128 Padova, Italy. · Department of Medicine - DIMED, University of Padova, via Giustiniani 2, 35128 Padova, Italy; Department of Laboratory Medicine, University Hospital of Padova, via Giustiniani 2, 35128 Padova, Italy. ·Clin Chim Acta · Pubmed #26923392.

ABSTRACT: BACKGROUND: Based on the knowledge that matrix metalloproteinases (MMPs) and S100A8/A9 synergistically work in causing PDAC-associated type 2 diabetes mellitus (T2DM), we verified whether tissue and blood MMP8, MMP9, S100A8 and S100A9 expression might help in distinguishing PDAC among diabetics. METHODS: Relative quantification of MMP8, MMP9, S100A8 and S100A9 mRNA was performed in tissues obtained from 8 PDAC, 4 chronic pancreatitis (ChrPa), 4 non-PDAC tumors and in PBMCs obtained from 30 controls, 43 T2DM, 41 ChrPa, 91 PDAC and 33 pancreatic-biliary tract tumors. RESULTS: T2DM was observed in PDAC (66%), in pancreatic-biliary tract tumors (64%) and in ChrPa (70%). In diabetics, with or without PDAC, MMP9 tissue expression was increased (p<0.05). Both MMPs increased in PDAC and MMP9 increased also in pancreatic-biliary tract tumors PBMCs. In diabetics, MMP9 was independently associated with PDAC (p=0.025), but failed to enhance CA 19-9 discriminant efficacy. A highly reduced S100A9 expression, found in 7 PDAC, was significantly correlated with a reduced overall survival (p=0.015). CONCLUSIONS: An increased expression of tissue and blood MMP9 reflects the presence of PDAC-associated diabetes mellitus. This finding fits with the hypothesized role of MMPs as part of the complex network linking cancer to diabetes.

6 Article Inflammation and pancreatic cancer: molecular and functional interactions between S100A8, S100A9, NT-S100A8 and TGFβ1. 2014

Basso, Daniela / Bozzato, Dania / Padoan, Andrea / Moz, Stefania / Zambon, Carlo-Federico / Fogar, Paola / Greco, Eliana / Scorzeto, Michele / Simonato, Francesca / Navaglia, Filippo / Fassan, Matteo / Pelloso, Michela / Dupont, Sirio / Pedrazzoli, Sergio / Fassina, Ambrogio / Plebani, Mario. ·Department of Laboratory Medicine, University-Hospital of Padova, Via Giustiniani 2, 35128 Padova, Italy. daniela.basso@sanita.padova.it. ·Cell Commun Signal · Pubmed #24670043.

ABSTRACT: BACKGROUND: In order to gain further insight on the crosstalk between pancreatic cancer (PDAC) and stromal cells, we investigated interactions occurring between TGFβ1 and the inflammatory proteins S100A8, S100A9 and NT-S100A8, a PDAC-associated S100A8 derived peptide, in cell signaling, intracellular calcium (Cai2+) and epithelial to mesenchymal transition (EMT). NF-κB, Akt and mTOR pathways, Cai2+ and EMT were studied in well (Capan1 and BxPC3) and poorly differentiated (Panc1 and MiaPaCa2) cell lines. RESULTS: NT-S100A8, one of the low molecular weight N-terminal peptides from S100A8 to be released by PDAC-derived proteases, shared many effects on NF-κB, Akt and mTOR signaling with S100A8, but mainly with TGFβ1. The chief effects of S100A8, S100A9 and NT-S100A8 were to inhibit NF-κB and stimulate mTOR; the molecules inhibited Akt in Smad4-expressing, while stimulated Akt in Smad4 negative cells. By restoring Smad4 expression in BxPC3 and silencing it in MiaPaCa2, S100A8 and NT-S100A8 were shown to inhibit NF-κB and Akt in the presence of an intact TGFβ1 canonical signaling pathway. TGFβ1 counteracted S100A8, S100A9 and NT-S100A8 effects in Smad4 expressing, not in Smad4 negative cells, while it synergized with NT-S100A8 in altering Cai2+ and stimulating PDAC cell growth. The effects of TGFβ1 on both EMT (increased Twist and decreased N-Cadherin expression) and Cai2+ were antagonized by S100A9, which formed heterodimers with TGFβ1 (MALDI-TOF/MS and co-immuno-precipitation). CONCLUSIONS: The effects of S100A8 and S100A9 on PDAC cell signaling appear to be cell-type and context dependent. NT-S100A8 mimics the effects of TGFβ1 on cell signaling, and the formation of complexes between TGFβ1 with S100A9 appears to be the molecular mechanism underlying the reciprocal antagonism of these molecules on cell signaling, Cai2+ and EMT.

7 Article Pancreatic tumors and immature immunosuppressive myeloid cells in blood and spleen: role of inhibitory co-stimulatory molecules PDL1 and CTLA4. An in vivo and in vitro study. 2013

Basso, Daniela / Fogar, Paola / Falconi, Massimo / Fadi, Elisa / Sperti, Cosimo / Frasson, Chiara / Greco, Eliana / Tamburrino, Domenico / Teolato, Sara / Moz, Stefania / Bozzato, Dania / Pelloso, Michela / Padoan, Andrea / De Franchis, Giuseppe / Gnatta, Elisa / Facco, Monica / Zambon, Carlo-Federico / Navaglia, Filippo / Pasquali, Claudio / Basso, Giuseppe / Semenzato, Gianpietro / Pedrazzoli, Sergio / Pederzoli, Paolo / Plebani, Mario. ·Department of Medicine, University of Padova, Padova, Italy. daniela.basso@sanita.padova.it ·PLoS One · Pubmed #23359812.

ABSTRACT: BACKGROUND: Blood and spleen expansion of immature myeloid cells (IMCs) might compromise the immune response to cancer. We studied in vivo circulating and splenic T lymphocyte and IMC subsets in patients with benign and malignant pancreatic diseases. We ascertained in vitro whether pancreatic adenocarcinoma (PDAC)-associated IMC subsets are induced by tumor-derived soluble factors and whether they are immunosuppressive focusing on the inhibitory co-stimulatory molecules PDL1 and CTLA4. METHODOLOGY AND PRINCIPAL FINDINGS: 103 pancreatic and/or splenic surgical patients were enrolled including 52 PDAC, 10 borderline and 10 neuroendocrine tumors (NETs). Lymphocytes and IMCs were analysed by flow cytometry in blood, in spleen and in three PDAC cell conditioned (CM) or non conditioned PBMC. PDL1 and CTLA4 were studied in 30 splenic samples, in control and conditioned PBMC. IMCs were FACS sorted and co-coltured with allogenic T lymphocytes. In PDAC a reduction was found in circulating CD8(+) lymphocytes (p = 0.004) and dendritic cells (p = 0.01), which were reduced in vitro by one PDAC CM (Capan1; p = 0.03). Blood myeloid derived suppressive cells (MDSCs) CD33(+)CD14(-)HLA-DR(-) were increased in PDAC (p = 0.022) and were induced in vitro by BxPC3 CM. Splenic dendritic cells had a higher PDL1 expression (p = 0.007), while CD33(+)CD14(+)HLA-DR(-) IMCs had a lower CTLA4 expression (p = 0.029) in PDAC patients. In vitro S100A8/A9 complex, one of the possible inflammatory mediators of immune suppression in PDAC, induced PDL1 (p = 0.018) and reduced CTLA4 expression (p = 0.028) among IMCs. IMCs not expressing CTLA4 were demonstrated to be immune suppressive. CONCLUSION: In PDAC circulating dendritic and cytotoxic T cells are reduced, while MDSCs are increased and this might favour tumoral growth and progression. The reduced CTLA4 expression found among splenic IMCs of PDAC patients was demonstrated to characterize an immune suppressive phenotype and to be consequent to the direct exposure of myeloid cells to pancreatic cancer derived products, S100A8/A9 complex in particular.

8 Article Usefulness of MALDI-TOF/MS identification of low-MW fragments in sera for the differential diagnosis of pancreatic cancer. 2013

Padoan, Andrea / Seraglia, Roberta / Basso, Daniela / Fogar, Paola / Sperti, Cosimo / Moz, Stefania / Greco, Eliana / Marchet, Alberto / de Manzoni, Giovanni / Zambon, Carlo-Federico / Navaglia, Filippo / Cristadoro, Luigi / Di Chiara, Alda / Nitti, Donato / Pedrazzoli, Sergio / Pavanello, Girolamo / Plebani, Mario. ·Department of Laboratory Medicine, University of Padova, Italy. ·Pancreas · Pubmed #23271396.

ABSTRACT: OBJECTIVES: To identify new biomarkers of pancreatic cancer (PaCa), we performed MALDI-TOF/MS analysis of sera from 22 controls, 51 PaCa, 37 chronic pancreatitis, 24 type II diabetes mellitus (DM), 29 gastric cancer (GC), and 24 chronic gastritis (CG). METHODS: Sera were purified by Sep-Pak C18 before MALDI-TOF/MS Anchorchip analysis. RESULTS: Features present in at least 5% of all spectra were selected (n = 160, m/z range, 1200-5000). At univariate analysis, 2 features (m/z 2049 and 2305) correlated with PaCa, 3 (m/z 1449, 1605, and 2006) with DM. No feature characterized gastric cancer or chronic gastritis. Ten-fold cross-validation binary recursive partitioning trees were obtained for patients' classification. The tree (CA 19-9, age, m/z 2006, 2599, 2753, and 4997), built considering only patients with diabetes, allowed a distinction between DM [area under the receiver operating characteristic curve (AUC), 0.997], chronic pancreatitis (AUC, 0.968), and PaCa (AUC, 0.980), with an overall correct classification rate of 89%. The tree including CA 19-9, 1550, and 2937 m/z features, achieved an AUC of 0.970 in distinguishing localized from advanced PaCa. MALDI-TOF-TOF analysis revealed the 1550 feature as a fragment of Apo-A1, which was determined as whole protein and demonstrated to be closely correlated with PaCa. CONCLUSIONS: The findings made demonstrate a role for serum peptides identified using MALDI-TOF/MS for addressing PaCa diagnosis.

9 Article Genetic susceptibility to pancreatic cancer and its functional characterisation: the PANcreatic Disease ReseArch (PANDoRA) consortium. 2013

Campa, Daniele / Rizzato, Cosmeri / Capurso, Gabriele / Giese, Nathalia / Funel, Niccola / Greenhalf, William / Soucek, Pavel / Gazouli, Maria / Pezzilli, Raffaele / Pasquali, Claudio / Talar-Wojnarowska, Renata / Cantore, Maurizio / Andriulli, Angelo / Scarpa, Aldo / Jamroziak, Krzysztof / Delle Fave, Gianfranco / Costello, Eithne / Khaw, Kay-Tee / Heller, Anette / Key, Tim J / Theodoropoulos, George / Malecka-Panas, Ewa / Mambrini, Andrea / Bambi, Franco / Landi, Stefano / Pedrazzoli, Sergio / Bassi, Claudio / Pacetti, Paola / Piepoli, Ada / Tavano, Francesca / di Sebastiano, Pierluigi / Vodickova, Ludmila / Basso, Daniela / Plebani, Mario / Fogar, Paola / Büchler, Markus W / Bugert, Peter / Vodicka, Pavel / Boggi, Ugo / Neoptolemos, John P / Werner, Jens / Canzian, Federico. ·German Cancer Research Center (DKFZ), Heidelberg, Germany. d.campa@dkfz.de ·Dig Liver Dis · Pubmed #23206934.

ABSTRACT: Pancreatic cancer is the fourth leading cause of cancer deaths in the European Union and in the USA, but little is known about its genetic susceptibility. The PANcreatic Disease ReseArch (PANDoRA) consortium was established to unite the efforts of different research groups; its aim is to create a large bio-database to uncover new genetic factors for pancreatic cancer risk, response to treatment, and patient survival. So far 2220 cases of pancreatic adenocarcinoma, a smaller number of cases of endocrine pancreatic tumours (n=86), chronic pancreatitis (n=272) and 3847 healthy controls have been collected. As a collective effort of the consortium, SNPs associated with pancreatic adenocarcinoma risk from a genome-wide association study performed in Caucasians were replicated. The possibility that the same genetic polymorphisms may influence patient survival as well was also addressed. This collective effort is particularly important for pancreatic cancer because it is a relatively rare disease for which little is known about aetiopathogenesis and risk factors. The recruitment of additional collaborators and partner institutions is continuously on-going.

10 Article Pancreatic cancer alters human CD4+ T lymphocyte function: a piece in the immune evasion puzzle. 2011

Fogar, Paola / Basso, Daniela / Fadi, Elisa / Greco, Eliana / Pantano, Giorgia / Padoan, Andrea / Bozzato, Dania / Facco, Monica / Sanzari, Maria Colomba / Teolato, Sara / Zambon, Carlo-Federico / Navaglia, Filippo / Semenzato, Gianpietro / Pedrazzoli, Sergio / Plebani, Mario. ·Department of Laboratory Medicine, University of Padova, Padova, Italy. ·Pancreas · Pubmed #21792088.

ABSTRACT: OBJECTIVES: To verify whether the dysregulation of CD4 T cells concurs in worsening the outcome of pancreatic cancer, we compared the effects of pancreatic cancer and other gastrointestinal cancer cell-conditioned media on the (1) proliferation, migration, and differentiation of CD4 T cells and (2) expansion of CD4 memory (CD45RO), naive (CD45RA), activated (CD69), and regulatory (CD25) subsets. METHODS: After culture of CD4 T cells in control, pancreatic (BxPC3, Capan1, MiaPaCa2), or gastrointestinal cancer (AGS, HepG2, HT29) cell-conditioned media, we evaluated proliferation, migration, interferon γ (IFNγ) production, and CD45RA, CD45RO, CD69, and CD25 membrane expression in control and conditioned CD4 T cells. RESULTS: Only pancreatic cancer-conditioned media (1) inhibited CD4 T-cell proliferation (P < 0.001) and migration under human stromal cell-derived factor-α chemotaxis (P < 0.001) and (2) induced CD4 T-cell IFNγ production (P < 0.05) and the expansion of the CD69-positive subset (P < 0.001) with respect to the control, with no changes being found in the CD45RA, CD45RO, and CD25 subsets. CONCLUSIONS: The in vitro findings achieved in the present study demonstrate that pancreatic cancer cells inhibit CD4 T-cell proliferation and migration, induce IFNγ production, and favor a CD69 subset expansion, suggesting that CD4 T cells play an important role in pancreatic cancer immune evasion.

11 Article Altered intracellular calcium fluxes in pancreatic cancer induced diabetes mellitus: Relevance of the S100A8 N-terminal peptide (NT-S100A8). 2011

Basso, Daniela / Greco, Eliana / Padoan, Andrea / Fogar, Paola / Scorzeto, Michele / Fadi, Elisa / Bozzato, Dania / Moz, Stefania / Navaglia, Filippo / Zambon, Carlo-Federico / Seraglia, Roberta / De Carlo, Eugenio / Valerio, Anna / Reggiani, Carlo / Pedrazzoli, Sergio / Plebani, Mario. ·Department of Laboratory Medicine, University of Padua, Padua, Italy. ·J Cell Physiol · Pubmed #20717964.

ABSTRACT: After isolating NT-S100A8 from pancreatic cancer (PC) tissue of diabetic patients, we verified whether this peptide alters PC cell growth and invasion and/or insulin release and [Ca(2+)](i) oscillations of insulin secreting cells and/or insulin signaling. BxPC3, Capan1, MiaPaCa2, Panc1 (PC cell lines) cell growth, and invasion were assessed in the absence or presence of 50, 200, and 500 nM NT-S100A8. In NT-S100A8 stimulated β-TC6 (insulinoma cell line) culture medium, insulin and [Ca(2+)] were measured at 2, 3, 5, 10, 15, 30, and 60 min, and [Ca(2+)](i) oscillations were monitored (epifluorescence) for 3 min. Five hundred nanomolars NT-S100A8 stimulated BxPC3 cell growth only and dose dependently reduced MiaPaCa2 and Panc1 invasion. Five hundred nanomolars NT-S100A8 induced a rapid insulin release and enhanced β-TC6 [Ca(2+)](i) oscillations after both one (F = 6.05, P < 0.01) and 2 min (F = 7.42, P < 0.01). In the presence of NT-S100A8, [Ca(2+)] in β-TC6 culture medium significantly decreased with respect to control cells (F = 6.3, P < 0.01). NT-S100A8 did not counteract insulin induced phosphorylation of the insulin receptor, Akt and IκB-α, but it independently activated Akt and NF-κB signaling in PC cells. In conclusion, NT-S100A8 exerts a mild effect on PC cell growth, while it reduces PC cell invasion, possibly by Akt and NF-κB signaling, NT-S100A8 enhances [Ca(2+)](i) oscillations and insulin release, probably by inducing Ca(2+) influx from the extracellular space, but it does not interfere with insulin signaling.

12 Article Analogs of vitamin E epitomized by alpha-tocopheryl succinate for pancreatic cancer treatment: in vitro results induce caution for in vivo applications. 2010

Greco, Eliana / Basso, Daniela / Fadi, Elisa / Padoan, Andrea / Fogar, Paola / Zambon, Carlo-Federico / Navaglia, Filippo / Bozzato, Dania / Moz, Stefania / Pedrazzoli, Sergio / Plebani, Mario. ·Department of Laboratory Medicine, University of Padova, Padova, Italy. ·Pancreas · Pubmed #20562578.

ABSTRACT: OBJECTIVES: alpha-Tocopheryl succinate (alpha-TOS) is thought to be toxic only for cancer cells. We ascertained in vitro alpha-TOS effects on pancreatic cancer (PC) and normal cell growth and verified whether the combination of nontoxic alpha-TOS and 5-fluorouracil (5-FU) doses causes cancer cell death and whether alpha-TOS effects are mediated by the proapoptotic proteins Bax/Bak and/or SMAD4/DPC4 status. METHODS: Five PC cell lines, myoblasts, normal monocytes, wild-type (WT) and Bax/Bak double knockout mouse embryonic fibroblast (MEF) cells, and permanently SMAD4/DPC4-transfected PSN1 cells were cultured in 1% and 10% fetal calf serums (FCSs), without or with alpha-TOS (5-500 micromol/L). Nontoxic 5-FU (0.0001 mmol/L) and alpha-TOS alone or in combination were also evaluated. RESULTS: Only PSN1 PC cell line, which had SMAD4/DPC4 homozygous deletion, was sensitive to nontoxic alpha-TOS doses (5 micromol/L in 1% FCS and 50 micromol/L in 10% FCS). A 20-micromol/L alpha-TOS inhibited MEF-WT, not MEF-double knockout growth. Only PSN1 cells were sensitive to nontoxic 5-FU and alpha-TOS combination. SMAD4/DPC4 transfection restored PSN1 resistance to the effects of combined 5-FU and alpha-TOS effects. CONCLUSIONS: Only a minority of PC cells are sensitive to the antiproliferative effects of alpha-TOS, any sensitivity appearing to be correlated with SMAD4/DPC4 homozygous deletion and Bax/Bak expression.

13 Minor Glypican-1 as a highly sensitive and specific pancreatic cancer biomarker. 2016

Diamandis, Eleftherios P / Plebani, Mario. · ·Clin Chem Lab Med · Pubmed #26389634.

ABSTRACT: -- No abstract --