Maria Simona Pino

ORCID: 0000-0001-5248-392X
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About
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Research Areas
  • Colorectal Cancer Treatments and Studies
  • Genetic factors in colorectal cancer
  • Pancreatic and Hepatic Oncology Research
  • Lung Cancer Treatments and Mutations
  • Cancer Treatment and Pharmacology
  • Melanoma and MAPK Pathways
  • Cancer, Hypoxia, and Metabolism
  • Cancer-related Molecular Pathways
  • Cancer Research and Treatments
  • Cancer Genomics and Diagnostics
  • Palliative Care and End-of-Life Issues
  • Cancer survivorship and care
  • HER2/EGFR in Cancer Research
  • Ubiquitin and proteasome pathways
  • Childhood Cancer Survivors' Quality of Life
  • Cutaneous Melanoma Detection and Management
  • Health Systems, Economic Evaluations, Quality of Life
  • Lung Cancer Research Studies
  • Cancer Cells and Metastasis
  • Colorectal Cancer Screening and Detection
  • Gastric Cancer Management and Outcomes
  • Systemic Sclerosis and Related Diseases
  • COVID-19 and healthcare impacts
  • Estrogen and related hormone effects
  • SARS-CoV-2 and COVID-19 Research

Hospital de Clínicas "José de San Martín"
2018-2024

University of Buenos Aires
2021-2023

Azienda Usl Toscana Centro
2016-2022

Ospedale Santa Maria Annunziata
2016-2021

Tumour Institute of Tuscany
2021

University of Messina
2017

Universidad de Cádiz
2016

Florence (Netherlands)
2015

Massachusetts General Hospital
2009-2014

Harvard University
2009-2013

Bortezomib (PS-341, Velcade) is a potent and selective inhibitor of the proteasome that currently under investigation for treatment solid malignancies. We have shown previously bortezomib has activity in pancreatic cancer models drug induces endoplasmic reticulum (ER) stress but also suppresses unfolded protein response (UPR). Because UPR an important cytoprotective mechanism, we hypothesized would sensitize cells to ER stress-mediated apoptosis. Here, show promotes apoptosis triggered by...

10.1158/0008-5472.can-05-2370 article EN Cancer Research 2005-12-15

Abstract The proteasome inhibitor bortezomib (formerly known as PS-341) recently received Food and Drug Administration approval for the treatment of multiple myeloma, its activity is currently being evaluated in solid tumors. Bortezomib triggers apoptosis pancreatic cancer cells, but mechanisms involved have not been fully elucidated. Here, we show that cells exposed to formed aggregates ubiquitin-conjugated proteins (“aggresomes”) vitro vivo. Bortezomib-induced aggresome formation was...

10.1158/0008-5472.can-05-2961 article EN Cancer Research 2006-04-01

Abstract Purpose: BRAF mutations are grouped in activating RAS-independent signaling as monomers (class 1–V600E) or dimers 2–codons 597/601), and RAS-dependent with impaired kinase activity 3–codons 594/596). Although clinical, pathologic, molecular features of V600EBRAF-mutated metastatic colorectal cancer (mCRC) well known, limited data available from the two other classes. Experimental Design: Data 117 patients (92 class 1, 12 2, 13 3)-mutated mCRC were collected. A total 540 wt mCRCs...

10.1158/1078-0432.ccr-19-0311 article EN Clinical Cancer Research 2019-04-09

Abstract Although it displays promising activity in other tumor models, the effects of necrosis factor–related apoptosis-inducing ligand (TRAIL) on human pancreatic cancer cells have not been comprehensively explored. We report that a majority cell lines (seven nine) underwent apoptosis when they were exposed to recombinant TRAIL vitro. Characterization surface receptors by fluorescence-activated sorting showed TRAIL-resistant (Panc-1 and HS766T) expressed lower levels DR4 DR5 than did...

10.1158/1535-7163.mct-06-0075 article EN Molecular Cancer Therapeutics 2006-09-01

Abstract KRAS and BRAF mutations are frequently observed in human colon cancers. These occur a mutually exclusive manner, each is associated with distinctive biological features. We showed previously that K-ras can interact hypoxia to activate multiple signaling pathways. Many hypoxic responses mediated by hypoxia-inducible factor (HIF)-1α HIF-2α, we sought define the roles of mutant induction HIF-1α HIF-2α cancer cells. Ectopic expression Caco2 cells enhanced only HIF-1α, whereas both...

10.1158/0008-5472.can-09-2213 article EN Cancer Research 2009-10-21

Abstract In a previous study, we found that the small-molecule epidermal growth factor receptor (EGFR) inhibitor gefitinib (ZD1839, Iressa) blocked cell proliferation at biologically relevant concentrations in approximately one third (6 of 17) human bladder cancer lines examined. Here, studied effects on apoptosis representative subset same panel cells. The drug had modest DNA fragmentation as single agent produced strong inhibition (≤1 μmol/L) and also failed to promote induced by...

10.1158/0008-5472.can-06-1224 article EN Cancer Research 2007-02-15

Suicidal behavior, especially in young populations such as university students, is currently one of the most concerning health problems worldwide, suicide being second leading cause death among students. Although literature still scarce, risk factors that correlates with suicidal behavior people appears to be problematic internet use (PIU). The aim this study was investigate relationship between PIU and a Spanish population.An ex post facto prospective design used sample 1,386 students...

10.7334/psicothema2022.153 article EN publisher-specific-oa Psicothema 2023-02-01

Abstract Purpose: hMena, member of the enabled/vasodilator-stimulated phosphoprotein family, is a cytoskeletal protein that involved in regulation cell motility and adhesion. The aim this study was to determine whether or not expression hMena isoforms correlated with sensitivity EGFR tyrosine kinase inhibitors could serve as markers potential clinical use. Experimental Design: Human pancreatic ductal adenocarcinoma lines were characterized for vitro erlotinib, HER family receptors,...

10.1158/1078-0432.ccr-08-0436 article EN Clinical Cancer Research 2008-08-01

Abstract We characterized the effects of small molecule epidermal growth factor receptor (EGFR) inhibitor gefitinib (ZD1839, Iressa) on cell proliferation in a panel 17 human bladder cancer lines. Gefitinib inhibited DNA synthesis concentration-dependent fashion 6 Growth inhibition was associated with p27Kip1 accumulation and decreased cyclin-dependent kinase 2 activity. also baseline EGFR, AKT, extracellular signal-regulated (ERK) phosphorylation EGFR-dependent cells maintained serum-free...

10.1158/1535-7163.mct-06-0513 article EN Molecular Cancer Therapeutics 2007-01-01

The KRAS proto-oncogene plays a key role in the development of many human tumors and is commonly activated by somatic mutation or signaling through specific growth factor receptors. However, interaction between micro-environment K-ras activity has not been defined. Hypoxia invariably develops as outgrow their supply oxygen. A series well-orchestrated cellular adaptations occur that stimulate angiogenesis enhance survival tumor hypoxic conditions. Our previous studies demonstrated mutant...

10.1371/journal.pone.0010966 article EN cc-by PLoS ONE 2010-06-04

BackgroundCapecitabine and oxaliplatin are both active anticancer agents in the treatment of patients with advanced colorectal cancer. The aim this phase II study is to determine efficacy tolerability combining capecitabine non-pretreated cancer.Patients methodsForty-three chemotherapy-naïve were enrolled. Capecitabine 2500 mg/m2/day was administered orally twice a day continuously for 14 days 120 mg/m2 as 2-h infusion on 1, repeated every 3 weeks.ResultsForty-three assessable toxicity 39...

10.1093/annonc/mdg360 article EN publisher-specific-oa Annals of Oncology 2003-09-01

Abstract The epidermal growth factor receptor (EGFR) is considered an important therapeutic target in pancreatic cancer, but it currently impossible to identify those patients who are most likely benefit from EGFR-directed therapy. We examined the biological effects of EGFR tyrosine kinase inhibitor gefitinib (ZD1839, Iressa) a panel nine human cancer cell lines. drug strongly inhibited DNA synthesis and induced low levels apoptosis at clinically relevant concentrations subset three lines...

10.1158/0008-5472.can-05-3753 article EN Cancer Research 2006-04-01

<i>Objective:</i> An increasing number of patients with advanced pancreatic or biliary tract cancer who progress after a gemcitabine-containing regimen are candidates for further chemotherapy. We therefore evaluated fully oral capecitabine and celecoxib (CapCel) as second-line treatment in these patients. <i>Methods:</i> Thirty-five documented progressive disease first-line were enrolled. Capecitabine was administered at dose 1,000 mg/m<sup>2</sup> b.i.d....

10.1159/000205388 article EN Oncology 2009-01-01
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