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MUTYH-associated polyposis: Is it time to change upper gastrointestinal surveillance? A single-center case series and a literature overview

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World Journal of Gastrointestinal Oncology 2023年第11期15卷 1891-1899页

作者： Lupe Sanchez-Mete Lorenzo Mosciatti Marco Casadio Luigi vittori aline Martayan vittoria Stigliano Gastroenterology and Digestive Endoscopy Regina Elena National Cancer InstituteIRCCSRome 00144Italy Department of Radiological Oncological and Pathological SciencesRegina Elena National Cancer InstituteIRCCSRome 00144Italy

BACKGROUND The presence of Spigelman stage(SS)Iv duodenal polyposis is considered the most significant risk factor for duodenal cancer in patients with MUTYH-associated polyposis(MAP).However,advanced SS disease is rarely reported in MAP patients,and no clear recommendations on small bowel(SB)surveillance have been proposed in this patient *** To research more because that case reports of duodenal cancers in MAP suggest that they may develop in the absence of advanced benign SS disease and often involve the distal portion of the *** We describe a series of MAP patients followed up at the Regina Elena National Cancer Institute of Rome(Italy).A literature overview on previously reported SB cancers in MAP is also *** We identified two(6%)SB adenocarcinomas with no previous history of duodenal *** observations,supported by literature evidence,suggest that the formula for staging duodenal polyposis and predicting risk factors for distal duodenum and jejunal cancer may need to be adjusted to take this into account rather than focusing solely on the presence or absence of SS Iv *** Tip:Case reports of duodenal cancers in MUTYH-associated polyposis suggest that they may develop in the absence of advanced Spigelman stage(SS)benign disease and often involve the distal portion of the *** our case series,we identified two(6%)small-bowel adenocarcinomas with no previous history of duodenal *** observations,supported by literature evidence,suggest that the formula for staging duodenal polyposis and predicting risk factors for distal duodenum and jejunal cancer should be adjusted to take into consideration the presence of SS Iv disease,rather than focusing only on this *** of invasive adenocarcinoma.

关键词： MUTYH-associated polyposis Duodenal adenomatosis Duodenal cancer Endoscopic management Case report

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Glycine-extended gastrin activates two independent tyrosine-kinases in upstream of p85/p110 phosphatidylinositol 3-kinase in human colonic tumour cells

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World Journal of Gastroenterology 2006年第12期12卷 1859-1864页

作者： Audrey Ferrand aline Kowalski-Chauvel Claudine Bertrand Daniel Fourmy Marlene Dufresne Catherine Seva Julie Pannequin INSERM U.531 Groupe de Recherche de Biologie et Pathologie DigestivesIFR31Institut Louis BugnardBP 8422531432 toulouse Cedex 4France University of Melbourne Department of Surgery Austin CampusARMCHeidelbergVictoria 3084Australia

AIM： To investigate whether Src, JAK2 and phosphatidylinositol 3-kinase （PI3K） pathways are involved in the proliferation of human colonic tumour cells induced by glycine-extended gastrin （G-gly）, the precursor of the mature amidated gastrin and to elucidate the molecular interaction between these three kinases in response to this peptide. METHODS： Using the human colonic tumour cell line HCT116 as a model, we first measured the activation of PI3K, p60-Src and JAK2 in response to G-gly by in vitro kinase assays. Then we investigated the involvement of these kinases in G-gly-induced cell proliferation by MTT test. RESULTS： G-gly stimulation induced p60-Src, JAK2 and PI3K activation in HCT116. The different pathways were involved in proliferation of human colon cancer cells induced by G-gly. Furthermore, we found that both Src and JAK2 were necessary to PI3K regulation by this peptide. However, we did not find any cross-talk between the two tyrosine kinases. CONCLUSION： Our results suggest that the p60-Src/ PI3K and JAK2/PI3K pathways act independently to mediate G-gly proliferative effect on human colonic tumour cells.

关键词： Colon cancer Src JAK2 Phosphatidylinositol 3-kinase Glycine-extended gastrin

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Ipilimumab associated colitis: An Ipi Colitis case series at Med Star Georgetown University Hospital

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World Journal of Gastroenterology 2015年第14期21卷 4373-4378页

作者： Pawan Rastogi Mohamed Sultan aline J Charabaty Michael B Atkins Mark C Mattar Department of Medicine MedS tar Georgetown University Hospital Department of Gastroenterology MedS tar Georgetown University Hospital Department of Oncology Georgetown Lombardi Comprehensive Cancer Center

Although ipilimumab has been shown to improve survival in patients with metastatic melanoma and cause regression of metastatic renal cell carcinoma, the associated immune-related toxicities are of *** resultant T cell activation by this monoclonal antibody causes an increased immune response, which has been associated with many immune-regulated adverse *** of the most concerning effects is the development of *** to 8% of patients have been reported to develop colitis, with 5% being severe(Grades 3-4).While initial treatment of such adverse effects is generally comprised of supportive and symptomatic treatment, more severe cases warrant the use of high dose ***, use of anti-TNF agents is usually reserved for those cases that prove to be refractory to *** describe a systematic case review of seven patients who developed gastrointestinal symptoms following initiation of ipilimumab immunotherapy, and present the steps in their evaluation, treatment and outcomes at our institution.

关键词： Colitis Ipilimumab Immunology Infliximab Immune-re

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Innate lymphoid cells in tissue homeostasis and diseases

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World Journal of Hepatology 2017年第23期9卷 979-989页

作者： aline Ignacio Cristiane Naffah Souza Breda Niels Olsen Saraiva Camara Laboratory of Transplantation Immunobiology Institute of Biomedical SciencesDepartment of ImmunologyUniversity of Sao PauloSP 05508-900Brazil

Innate lymphoid cells(ILCs) are the most recently discovered family of innate immune cells. They are a part of the innate immune system, but develop from the lymphoid lineage. They lack pattern-recognition receptors and rearranged receptors, and therefore cannot directly mediate antigen specific responses. The progenitors specifically associated with the ILCs lineage have been uncovered, enabling the distinction between ILCs and natural killer cells. Based on the requirement of specific transcription factors and their patterns of cytokine production, ILCs are categorized into three subsets(ILC1, ILC2 and ILC3). First observed in mucosal surfaces, these cell populations interact with hematopoietic and non-hematopoietic cells throughout the body during homeostasis and diseases, promoting immunity, commensal microbiota tolerance, tissue repair and inflammation. Over the last 8 years, ILCs came into the spotlight as an essential cell type able to integrate diverse host immune responses. Recently, it became known that ILC subsets play a key role in immune responses at barrier surfaces, interacting with the microbiota, nutrients and metabolites. Since the liver receives the venous blood directly from the intestinal vein, the intestine and liver are essential to maintain tolerance and can rapidly respond to infections or tissue damage. Therefore, in this review, we discuss recent findings regarding ILC functions in homeostasis and disease, with a focus on the intestine and liver.

关键词： Innate lymphoid cells Intestine Liver Homeostasis Inflammatory diseases

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Mechanism for Src activation by the CCK2 receptor:Patho-physiological functions of this receptor in pancreas

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World Journal of Gastroenterology 2006年第28期12卷 4498-4503页

作者： Audrey Ferrand Sebastien vatinel aline Kowalski-Chauvel Claudine Bertrand Chantal Escrieut Daniel Fourmy Marlene Dufresne Catherine Seva Dufresne Catherine SevaINSERM U 531IFR 31Institut Louis BugnardBP 8422531432 Toulouse cedex 4France

AIM： TO investigate in vivo, whether CCK2 receptors （CCK2R） regulate proteins known to play a crucial role in cell proliferation and cancer development and analyse in vitro the molecular mechanisms that lead to Src activation; in particular, to identify the domains within the CCK2R sequence that are implicated in this activation. METHODS： The expression and activation of Src and ERK were studied in vivo using immunofluorescence and western-blot techniques. We used pancreatic tissues derived from wild type or Elas-CCK2 mice that expressed the CCK2R in pancreatic acini, displayed an increased pancreatic growth and developed preneoplastic lesions. The pancreatic tumor cell line AR4-2J expressing the endogenous CCK2R or COS-7 cells transiently transfected with wild type or mutant CCK2R were used as in vitro models to study the mechanism of Src activation. Src activation was measured by in vitro kinase assays, ERK activation by western blot using antiphospho-ERK antibodies and the involvement of Src in gastrin-induced cell proliferation by MTT test. RESULTS： We showed in vivo that the targeted CCK2R expression in the pancreas of Elas-CCK2 mice, led to the activation of Src and the ERK pathway. Src was activated upstream of the ERK pathway by the CCK2R in pancreatic tumoral cells and contributed to the proliferative effects mediated by this receptor. In vitro results demonstrated that activation of the Src/ERK pathway by the CCK2R required the NPXXY motif, located within the CCK2R sequence at the end of the 7^th transmembrane domain, and suggested the putative role of Gq in this mechanism. CONCLUSION： Deregulation of the Src/ERK pathway by the CCK2R might represent an early step that contributes to cell proliferation, formation of preneoplastic lesions and pancreatic tumor development.

关键词： Gastrin, Src Pancreas CCK2 receptor

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αv integrin:A new gastrin target in human pancreatic cancer cells

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World Journal of Gastroenterology 2011年第40期17卷 4488-4495页

作者： Celine Cayrol Claudine Bertrand aline Kowalski-Chauvel Laurence Daulhac Elizabeth Cohen-Jonathan-Moyal Audrey Ferrand Catherine Seva INSERM UMR1037-Cancer Research Center of Toulouse Paul Sabatier University Toulouse Ⅲ 31432 Toulouse cedex 4 France INSERM U766 Department of pharma-cology Clermont 1 University of Pharmacy 63001 Clermont-Ferrand France

AIM： To analyse αv integrin expression induced by gas- trin in pancreatic cancer ***： αv integrin mRNA expression in human pan- creatic cancer cells was analysed using a ＂cancer genes＂ array and confirmed by real-time reverse transcription- polymerase chain reaction （PCR）. Western blotting and semi-quantitative immunohistochemistry were used to examine protein levels in human pancreatic cancer cell lines and pancreatic tissues, respectively, The role of αv integrin on gastrin-induced cell adhesion was examined using blocking anti-αv integrin monoclonal antibodies. Adherent cells were quantified by staining with crystal ***： Using a ＂cancer genes＂ array we identi- fied c^v integrin as a new gastrin target gene in human pancreatic cancer cells. A quantitative real-time PCR approach was used to confirm αv integrin gene expression. We also demonstrate that Src family kinases and the PI 3-kinase, two signalling pathways specifically activated by the CCK-2 receptor （CCK2R）, are involved in gastrin-mediated αv integrin expression. In contrast, inhibition of the ERK pathway was without any effect on αv integrin expression induced by gastrin. Our results also show that gastrin modulates cell adhesion via αv integrins. Indeed, in vitro adhesion assays performed on fibronectin show that gastrin significantly increases adhesion of pancreatic cancer cells. The use of blocking anti-αv integrin monoclonal antibodies completely reversed the increase in cell-substrate adhesion induced by gastrin. In addition, we showed in vivo that the targeted CCK2R expression in the pancreas of Elas-CCK2 mice, leads to the overexpression of αv integrin. This process may contribute to pancreatic turnout development observed in these transgenic ***： αv integrin is a new gastrin target in pancreatic cancer models and contributes to gastrin effects on cell adhesion.

关键词： v integrin Cell adhesion CCK-2 receptor Gastrin Pancreatic cancer

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Renin angiotensin system in liver diseases: Friend or foe?

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World Journal of Gastroenterology 2017年第19期23卷 3396-3406页

作者： Ana Cristina Simoes e Silva aline S Miranda Natália P Rocha Antonio L Teixeira Department of Pediatrics Faculty of MedicineFederal University of Minas Gerais Interdisciplinary Laboratory of Medical Investigation Faculty of MedicineUFMG Laboratory of Neurobiology Department of MorphologyInstitute of Biological SciencesUFMG Neuropsychiatry Program Department of Psychiatry and Behavioral SciencesMcGovern Medical SchoolUniversity of Texas Health Science Center at Houston

In the last three decades,the understanding of the renin angiotensin system(RAS)has been changed by the discoveries of functional local systems,novel biologically active peptides,additional specific receptors,alternative pathways of angiotensin(Ang)?Ⅱ?generation,and new roles for enzymes and precursor components other than those in Ang?Ⅱ?*** this regard,the discovery that Ang-(1-7)opposes the pressor,proliferative,pro-fibrotic,and pro-inflammatory effects mediated by Ang?Ⅱ?has contributed to the realization that the RAS is composed of two *** first axis consists of the angiotensin-converting enzyme(ACE),with Ang?Ⅱ?as the end product,and the angiotensin type 1(AT1)receptor as the main effector mediating the biological actions of Ang?Ⅱ.The second axis results from ACE2-mediated hydrolysis of Ang?Ⅱ,leading to the production of Ang-(1-7),with the Mas receptor as the main effector conveying the vasodilatory,antiproliferative,anti-fibrotic,and anti-inflammatory effects of Ang-(1-7).Experimental and clinical studies have shown that both axes of the RAS may take part in the pathogenesis of liver *** this manuscript,we summarize the current evidence regarding the role of RAS in hepatic cirrhosis and its complications,including hemodynamic changes and hepatorenal *** therapeutic potential of the modulation of RAS molecules in liver diseases is also discussed.

关键词： Renin angiotensin system Angiotensin Ⅱ Angiotensin-(1-7) Hepatic cirrhosis Liver fibrosis Hepatorenal syndrome

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Haemochromatosis revisited

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World Journal of Hepatology 2022年第11期14卷 1931-1939页

作者： aline Morgan Alvarenga Pierre Brissot Paulo Caleb Junior Lima Santos Department of Pharmacology-Escola Paulista de Medicina Universidade Federal de São PauloSão Paulo 04044-020Brazil University of Rennes1 Rennes 35065France

Haemochromatosis is a genetic disease caused by hepcidin deficiency,responsible for an increase in intestinal iron *** is associated with homozygosity for the HFE ***282Tyr ***,rare cases of haemochromatosis(non-HFE haemochromatosis)can also be caused by path-ogenic variants in other genes(such as HJv,HAMP,TFR2 and SLC40A1).A working group of the International Society for the Study of Iron in Biology and Medicine(BIOIRON Society)has concluded that the classification based in different molecular subtypes is difficult to be adopted in clinical practice and has proposed a new classification approaching clinical questions and molecular *** aim of the present review is to provide an update on classification,pathophysiology and therapeutic recommendations.

关键词： Haemochromatosis Iron overload HFE Molecular diagnosis Hepcidin

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Helicobacter pylori infection: Host immune response, implications on gene expression and microRNAs

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World Journal of Gastroenterology 2014年第6期20卷 1424-1437页

作者： aline Cristina Targa Cadamuro Ana Flávia Teixeira Rossi Nathália Maciel Maniezzo Ana Elizabete Silva Department of Biology UNESP-So Paulo State University Campus So José do Rio Preto

Helicobacter pylori(H. pylori) infection is the most common bacterial infection worldwide. Persistent infection of the gastric mucosa leads to inflammatory processes and may remain silent for decades or progress causing more severe diseases, such as gastric adenocarcinoma. The clinical consequences of H. pylori infection are determined by multiple factors, including host genetic predisposition, gene regulation, environmental factors and heterogeneity of H. pylori virulence factors. After decades of studies of this successful relationship between pathogen and human host, various mechanisms have been elucidated. In this review, we have made an introduction on H. pylori infection and its virulence factors, and focused mainly on modulation of host immune response triggered by bacteria, changes in the pattern of gene expression in H. pylori-infected gastric mucosa, with activation of gene transcription involved in defense mechanisms, inflammatory and immunological response, cell proliferation and apoptosis. We also highlighted the role of bacteria eradication on gene expression levels. In addition, we addressed the recent involvement of different microRNAs in precancerous lesions, gastric cancer, and inflammatory processes induced by bacteria. New discoveries in this field may allow a better understanding of the role of major factors involved in the pathogenic mechanisms of H. pylori.

关键词： Helicobacter pylori Inflammation virulence factors Immune response Gastric lesions Gastric cancer Gene expression MicroRNAs

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Personalized medicine in gastric cancer:Where are we andwhere are we going?

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World Journal of Gastroenterology 2016年第3期22卷 1160-1171页

作者： Alexandre A Jácome Anelisa K Coutinho Enaldo M Lima aline C Andrade JoséSebastião dos Santos Department of Medical Oncology Hospital Mater DeiBelo Horizonte 30190-131Minas GeraisBrazil Department of Gastrointestinal Oncology Brazilian Gastrointestinal Tumor GroupClinica AMOSalvador 41950-640BahiaBrazil Department of Surgery and Anatomy University of São Paulo at Ribeirão PretoSchool of MedicineRibeirão Preto14049-900São PauloBrazil

Despite improvements in adjuvant therapies for gastric cancer in recent years, the disease is characterized by high recurrence rates and a dismal prognosis. The major improvement in the treatment of recurrent or metastatic gastric cancer in recent years has been the incorporation of trastuzumab, a monoclonal antibody that inhibits human epidermal growth factor receptor 2(HER2) heterodimerization, after the demonstrated predictive value of the overexpression and/or amplification of this receptor. Beyond HER2, other genetic abnormalities have been identified, and these mutations may be targetable by tyrosine kinase inhibitors or monoclonal antibodies. The demonstration of four distinct molecular subtypes of gastric cancer by the Cancer Genome Atlas study highlight the enormous heterogeneity of the disease and its complex interplay between genetic and epigenetic alterations and provide a roadmap to implement genome-guided personalized therapy in gastric cancer. In the present review, we aim to discuss, from a clinical point of view, the genomic landscape of gastric cancer described in recent studies, the therapeutic insights derived from these findings, and the clinical trials that have been conducted and those in progress that take into account tailored therapies for gastric cancer.

关键词： stomach neoplasms biological markers Molecular targeted therapy Individualized medicine Transcriptome

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