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Pancreatic Neoplasms: HELP
Articles by Ana Paula Santos
Based on 5 articles published since 2010
(Why 5 articles?)
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Between 2010 and 2020, Ana Santos wrote the following 5 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article [Errata to the article "Treatment of Gastroenteropancreatic Neuroendocrine Tumors with 177Lu-DOTA-TATE: Experience of the Portuguese Institute of Oncology in Porto" by Inês Lucena Sampaio, Henrique Vara Luiz, Liliana Sobral Violante, Ana Paula Santos, Luís Antunes, Isabel Torres, Cristina Sanches, Isabel Azevedo, Hugo Duarte published on Acta Med Port 2016 Nov;29(11):726-733]. 2020

Sampaio, Inês Lucena / Luíz, Henrique Vara / Violante, Liliana Sobral / Santos, Ana Paula / Antunes, Luis / Torres, Isabel / Sanches, Cristina / Azevedo, Isabel / Duarte, Hugo. ·Serviço de Medicina Nuclear. Instituto Português de Oncologia. Porto. Portugal. · Serviço de Endocrinologia. Hospital Garcia de Orta. Almada. Portugal. · Serviço de Endocrinologia. Instituto Português de Oncologia. Porto. Portugal. · Serviço de Epidemiologia. Instituto Português de Oncologia. Porto. Portugal. · Serviço de Cirurgia Geral. Instituto Português de Oncologia do Porto. Portugal. · Serviço de Oncologia. Instituto Português de Oncologia. Porto. Portugal. ·Acta Med Port · Pubmed #31928610.

ABSTRACT: -- No abstract --

2 Article Higher IL-6 peri-tumoural expression is associated with gastro-intestinal neuroendocrine tumour progression. 2019

Pereira, Sofia S / Pereira, Rúben / Santos, Ana P / Costa, Madalena M / Morais, Tiago / Sampaio, Paula / Machado, Bianca / Afonso, Luís Pedro / Henrique, Rui / Monteiro, Mariana P. ·Endocrine, Cardiovascular and Metabolic Research, Multidisciplinary Unit for Biomedical Research (UMIB), Department of Anatomy of Instituto de Ciências Biomédicas Abel Salazar, University of Porto (ICBAS/UP), Porto, Portugal; Institute for Research and Innovation in Health (I3S), University of Porto, Portugal; Institute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Porto, Portugal. · Endocrine, Cardiovascular and Metabolic Research, Multidisciplinary Unit for Biomedical Research (UMIB), Department of Anatomy of Instituto de Ciências Biomédicas Abel Salazar, University of Porto (ICBAS/UP), Porto, Portugal. · Endocrinology Service/Clinical Research Unit, Portuguese Institute of Oncology of Porto Research Center (CI-IPOP), Portuguese Institute of Oncology of Porto (IPO-Porto), Portugal. · Institute for Research and Innovation in Health (I3S), University of Porto, Portugal; Institute for Molecular and Cellular Biology (IBMC), University of Porto, Portugal. · Department of Pathology, Portuguese Oncology Institute of Porto (IPO Porto), Portugal. · Department of Pathology, Portuguese Oncology Institute of Porto (IPO Porto), Portugal; Cancer Biology and Epigenetics Group, Research Center of Portuguese Oncology Institute of Porto (CI-IPOP), Portuguese Oncology Institute of Porto (IPO Porto), Portugal; Department of Pathology and Molecular Immunology, ICBAS, University of Porto, Portugal. · Endocrine, Cardiovascular and Metabolic Research, Multidisciplinary Unit for Biomedical Research (UMIB), Department of Anatomy of Instituto de Ciências Biomédicas Abel Salazar, University of Porto (ICBAS/UP), Porto, Portugal. Electronic address: mpmonteiro@icbas.up.pt. ·Pathology · Pubmed #31466863.

ABSTRACT: An association of well-differentiated gastroenteropancreatic neuroendocrine tumours (WD GEP NETs) with metabolic syndrome (MetS) was recently described. Yet no molecular mechanisms linking the two conditions are known. This study's aim was to identify putative molecular signatures linking WD GEP NETs and MetS to gain further insight into potential mechanisms for this association. Patients with WD GEP NETs (n=39), pancreatic (panNET) and gastro-intestinal (GI-NET), were clinically evaluated for presence of MetS. WD GEP NETs immunohistochemistry staining for Forkhead box protein M1 (FOXM1), insulin growth factor 1 receptor (IGF1R), Ki-67 and interleukin 6 (IL-6) was performed and quantified by computerised morphometric analysis. FOXM1, Ki-67, IGF1R or IL-6 expression in WD GEP NETs was not influenced by the presence of MetS. IL-6 peritumoural expression was higher in GI-NETs of patients with low HDL cholesterol (0.018±0.005% vs 0.030±0.005%, p=0.02). In GI-NETs, a higher IL-6 expression was also associated with disease progression (0.026±0.004% vs 0.016±0.002%, p=0.03). In WD GEP-NETs, MetS did not influence FOXM1, IGF1R and IL-6 expression. In GI-NETs, IL-6 expression was influenced by the MetS feature low HDL, and positively associated with disease progression. These data suggest that local and systemic inflammatory status can potentially modulate GI-NET behaviour.

3 Article [Treatment of Gastroenteropancreatic Neuroendocrine Tumors with 177Lu-DOTA-TATE: Experience of the Portuguese Institute of Oncology in Porto]. 2016

Sampaio, Inês Lucena / Luiz, Henrique Vara / Violante, Liliana Sobral / Santos, Ana Paula / Antunes, Luís / Torres, Isabel / Sanches, Cristina / Azevedo, Isabel / Duarte, Hugo. ·Serviço de Medicina Nuclear. Instituto Português de Oncologia. Porto. Portugal. · Serviço de Endocrinologia. Hospital Garcia de Orta. Almada. Portugal. · Serviço de Endocrinologia. Instituto Português de Oncologia. Porto. Portugal. · Serviço de Epidemiologia. Instituto Português de Oncologia. Porto. Portugal. · Serviço de Cirurgia Geral. Instituto Português de Oncologia do Porto. Portugal. · Serviço de Oncologia. Instituto Português de Oncologia. Porto. Portugal. ·Acta Med Port · Pubmed #28229838.

ABSTRACT: INTRODUCTION: The purpose of this article is to report the experience of the Portuguese Institute of Oncology - Porto in the treatment of gastroenteropancreatic neuroendocrine tumors with 177Lu-DOTA-TATE, regarding the safety and efficacy of this treatment modality. MATERIAL AND METHODS: A retrospective analysis of clinical reports of patients with gastroenteropancreatic neuroendocrine tumors undergoing treatment with 177Lu-DOTA-TATE between April 2011 and November 2013 was performed. RESULTS: Thirty six cases were reviewed and 30 completed all 3 cycles of 177Lu-DOTA-TATE (83.3%). In these patients it was registered: acute side effects in 8.9% of cycles; grade 3 CTCAE liver toxicity in 13.3% of patients (all with previous abnormal liver function); absence of significant renal or hematologic toxicity; symptomatic improvement in 71.4% of patients; median overall time to progression of 25.6 months; median overall survival from diagnosis of 121.7 months. Patients with higher expression of somatostatin receptors had longer progression-free survival and overall survival times (p < 0.05). DISCUSSION: Peptide receptor radionuclide therapy with 177Lu-DOTA-TATE is an effective, safe and well-tolerated treatment, as evidenced in our study by the following findings: symptomatic improvement in most patients and increased time to disease progression and survival (especially in those with higher sstr expression), with acute and significant subacute/chronic side effects reported only in a minority of cases. CONCLUSION: Peptide receptor radionuclide therapy with 177Lu-DOTA-TATE is a promising treatment for patients with gastroenteropancreatic neuroendocrine tumors, with demonstrated benefits in terms of safety and efficacy.

4 Article Chemoresistance in Pancreatic Cancer Is Driven by Stroma-Derived Insulin-Like Growth Factors. 2016

Ireland, Lucy / Santos, Almudena / Ahmed, Muhammad S / Rainer, Carolyn / Nielsen, Sebastian R / Quaranta, Valeria / Weyer-Czernilofsky, Ulrike / Engle, Danielle D / Perez-Mancera, Pedro A / Coupland, Sarah E / Taktak, Azzam / Bogenrieder, Thomas / Tuveson, David A / Campbell, Fiona / Schmid, Michael C / Mielgo, Ainhoa. ·Department of Molecular and Clinical Cancer Medicine, University of Liverpool, Liverpool, United Kingdom. · Pharmacology and Translational Research, Boehringer Ingelheim RCV GmbH & Co KG, Vienna, Austria. · Cold Spring Harbor Laboratory, Cold Spring Harbor, New York. · Lustgarten Pancreatic Cancer Research Laboratory, Cold Spring Harbor, New York. · Department of Medical Physics and Clinical Engineering, Royal Liverpool University Hospital, Liverpool, United Kingdom. · Medicine and Translational Research, Boehringer Ingelheim RCV GmbH & Co KG, Vienna, Austria. · Department of Urology, University Hospital Grosshadern, Ludwig-Maximilians-University, Munich, Germany. · Rubenstein Center for Pancreatic Cancer Research, Memorial Sloan Kettering Cancer Center, New York, New York. ·Cancer Res · Pubmed #27742686.

ABSTRACT: Tumor-associated macrophages (TAM) and myofibroblasts are key drivers in cancer that are associated with drug resistance in many cancers, including pancreatic ductal adenocarcinoma (PDAC). However, our understanding of the molecular mechanisms by which TAM and fibroblasts contribute to chemoresistance is unclear. In this study, we found that TAM and myofibroblasts directly support chemoresistance of pancreatic cancer cells by secreting insulin-like growth factors (IGF) 1 and 2, which activate insulin/IGF receptors on pancreatic cancer cells. Immunohistochemical analysis of biopsies from patients with pancreatic cancer revealed that 72% of the patients expressed activated insulin/IGF receptors on tumor cells, and this positively correlates with increased CD163

5 Article Macrophage-secreted granulin supports pancreatic cancer metastasis by inducing liver fibrosis. 2016

Nielsen, Sebastian R / Quaranta, Valeria / Linford, Andrea / Emeagi, Perpetua / Rainer, Carolyn / Santos, Almudena / Ireland, Lucy / Sakai, Takao / Sakai, Keiko / Kim, Yong-Sam / Engle, Dannielle / Campbell, Fiona / Palmer, Daniel / Ko, Jeong Heon / Tuveson, David A / Hirsch, Emilio / Mielgo, Ainhoa / Schmid, Michael C. ·Department of Molecular and Clinical Cancer Medicine, University of Liverpool, Ashton Street, Liverpool L69 3GE, UK. · Department of Molecular and Clinical Pharmacology, University of Liverpool, Ashton Street, Liverpool L69 3GE, UK. · Aging Intervention Research Center, KRIBB, 125 Gwahak-ro, Yuseong-gu, Deajeon 305-806, Korea. · Korea University of Science and Technology, 217 Gajeong-ro, Yuseong-gu, Daejeon 305-350, Korea. · Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA. · Lustgarten Pancreatic Cancer Research Laboratory, Cold Spring Harbor, New York 11724, USA. · Rubenstein Center for Pancreatic Cancer Research, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. · Department of Molecular Biotechnology and Health Sciences, Center for Molecular Biotechnology, University of Torino, Via Nizza 52, 10126 Turin, Italy. ·Nat Cell Biol · Pubmed #27088855.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is a devastating metastatic disease for which better therapies are urgently needed. Macrophages enhance metastasis in many cancer types; however, the role of macrophages in PDAC liver metastasis remains poorly understood. Here we found that PDAC liver metastasis critically depends on the early recruitment of granulin-secreting inflammatory monocytes to the liver. Mechanistically, we demonstrate that granulin secretion by metastasis-associated macrophages (MAMs) activates resident hepatic stellate cells (hStCs) into myofibroblasts that secrete periostin, resulting in a fibrotic microenvironment that sustains metastatic tumour growth. Disruption of MAM recruitment or genetic depletion of granulin reduced hStC activation and liver metastasis. Interestingly, we found that circulating monocytes and hepatic MAMs in PDAC patients express high levels of granulin. These findings suggest that recruitment of granulin-expressing inflammatory monocytes plays a key role in PDAC metastasis and may serve as a potential therapeutic target for PDAC liver metastasis.