Clas Une

Universidad de Costa Rica

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Vanessa Ramírez

Universidad de Costa Rica

Wendy Malespín-Bendaña

Universidad de Costa Rica

Warner Alpízar‐Alpízar

Copenhagen University Hospital

Silvia Molina‐Castro

Universidad de Costa Rica

Ericka Méndez Chacón

Universidad de Costa Rica

Rafaela Sierra

Universidad de Costa Rica

AÖ

Anders Örn

Karolinska Institutet

Guillermo I. Pérez‐Pérez

NYU Langone Health

Rafael Fernandez-Botrán

University of Louisville

Patricia Cuenca

Universidad de Costa Rica

Cooperative Institutions

Universidad de Costa Rica

Karolinska Institutet

Karolinska University Hospital

Inserm

Instituto Costarricense de Investigación y Enseñanza en Nutrición y Salud

NYU Langone Health

University of San Carlos of Guatemala

Instituto de Investigaciones en Ciencias de la Salud

Memorial Sloan Kettering Cancer Center

Université de Bordeaux

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Valor diagnóstico de las proteínas uPAR en sangre para el cáncer gástrico en Guatemala

Ciencia Tecnología y Salud (2018)

Irmgardt A. Wellmann Castellanos Carmen I. Villagrán Rafael Fernandez-Botrán Elisa Hernández Ericka Méndez Chacón

El cáncer gástrico es la neoplasia más frecuente del tubo digestivo, Guatemala posee altas tasas de incidencia y mortalidad. Helicobacter pylori se ha identificado como un carcinógeno gástrico, especialmente si la infección es por cepas que expresen factor de virulencia CagA, asociado a lesiones atróficas y precancerosas. Reportes previos indican que el análisis de biopsias gástricas en pacientes positivos para H. pylori, muestran un incremento de la expresión del activador del plasminógeno uroquinasa (uPA) y su receptor (uPAR). El presente estudio tuvo como objetivo determinar el valor diagnóstico de uPAR en sangre como marcador de cáncer gástrico en Guatemala y la asociación de uPAR con la infección por de H. pylori. Se tomaron muestras sanguíneas de pacientes diagnosticados con cáncer gástrico (n = 68) y controles sanos apareados por edad y sexo (n = 136) en cuatro instituciones de la ciudad de Guatemala, se determinó uPAR e IgG anti H. pylori por metodología Elisa. Los niveles de uPAR en pacientes con cáncer estaban significativamente elevados (p < .001), no se encontró diferencia por edad, sexo, apariencia macroscópica o microscópica del tumor. El cáncer gástrico se asoció significativamente a H. pylori (p = .03). El coeficiente de correlación biserial indica una relación negativa débil (rb = -0.01, p = .443) entre uPAR y H. pylori. Las curvas ROC en uPAR reportaron alta precisión (área bajo la curva = .80) para identificar cáncer gástrico. Estos resultados sugieren que los niveles séricos de uPAR pueden tener valor en el diagnóstico cáncer gástrico.

10.36829/63cts.v5i1.478

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Citations (3)

Pepsinógenos séricos para detectar cáncer gástrico en Costa Rica

Acta bioquímica clínica latinoamericana/Acta bioquímica clínica latinoamericana (2003)

Rafaela Sierra Ramos Fernando Carrión Mena Vanessa Ramírez Ericka Méndez Chacón Maritza R. Salazar

Articulo cientifico -- Universidad de Costa Rica, Instituto de Investigaciones en Salud. 2003

Pepsin

Source

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Citations (3)

The geographic origin ofHelicobacter pyloriisolated from Costa Rican patients

Gut Microbes (2014)

Silvia Molina‐Castro Dayana Herrera Wendy Malespín-Bendaña Vanessa Ramírez Clas Une

Helicobacter pylori infects a significant proportion of the world population and it is associated with pathologies which include chronic atrophic gastritis, peptic ulcer, and gastric neoplasias such as gastric adenocarcinoma and MALT lymphoma. Costa Rica has a high prevalence of the infection and an elevated incidence of gastric cancer and its associated mortality. The global population structure for H. pylori has been established using a MLST scheme. The population structure of the strains of H. pylori circulating in Costa Rica is currently unknown. We characterized the geographical origin of 24 H. pylori isolates from Costa Rican patients. We identified 142 new alleles for the genes included in the scheme and in eight of the 24 isolates from Costa Rican patients, all seven alleles sequenced were described for the first time. Twenty-one isolates from Costa Rican patients group with hpEurope strains and the remaining three isolates grouped with hspWAfrica isolates (Bayesian posterior probability values above 0.70, P = 0.05, after 2 000 000 generations). The obtained result in the MLST analysis was not unexpected and reflects the genetic composition of the Costa Rican population.

Multilocus sequence typing

10.4161/gmic.32148

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Descriptive Epidemiology of Gastric Cancer in Costa Rica from 1990 to 2022 and Projection of Deaths to 2050

Juan Carlos Vanegas Rolando Herrero Catarina de Andrade Barboza Rebeca Ocampo Guillermo Torres

10.2139/ssrn.5061260

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Seroprevalence of Helicobacter pylori/CagA Antibodies in Guatemalan Gastric Cancer Patients: Association of Seropositivity with Increased Plasma Levels of Pepsinogens but not Soluble Urokinase Plasminogen Activator Receptor

American Journal of Tropical Medicine and Hygiene (2020)

Rafael Fernandez-Botrán Irmgardt Alicia Wellmann Clas Une Ericka Méndez Chacón Elisa Hernández de Rodas

Infection by Helicobacter pylori is a major risk factor for gastric cancer (GC), the second leading cause of cancer-related death worldwide. Although biomarkers such as pepsinogens (PGs) and soluble urokinase plasminogen activator receptor (suPAR) may have diagnostic and/or prognostic value in patients with GC, their levels may be affected by H. pylori infection. The aim of this study was to investigate the association of the presence of antibodies to H. pylori and cytotoxin-associated gene A (CagA) with plasma levels of PGs and suPAR in a cohort of Guatemalan GC patients and controls. To this end, levels of suPAR, Pepsinogens I and II (PGI and PGII), and antibodies to H. pylori and CagA toxin were determined by ELISA in plasma samples from 67 GC patients and 136 matched healthy controls. Seropositivity for CagA was significantly higher in patients with GC than in controls. Pepsinogens II and suPAR levels were higher and PGI/PGII ratios were lower in GC patients than in controls. There was a significant association of H. pylori seropositivity status with increased levels of PGII and lower PGI/PGII ratios, particularly in the control (non-GC) population. The levels of suPAR were not significantly affected by H. pylori or CagA seropositivity status. These results suggest that the seropositivity status for H. pylori and CagA need to be taken into account during the GC diagnostic process.

CagA

SuPAR

Seroprevalence

10.4269/ajtmh.19-0934

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Citations (7)

Role of IFN-α/β and IL-12 in the activation of natural killer cells and interferon-γ production during experimental infection with Trypanosoma cruzi

Clinical & Experimental Immunology (2003)

Clas Une John Andersson Anders Örn

SUMMARY Control of Trypanosoma cruzi infection depends largely upon the production of interferon (IFN)-γ. During experimental infection this cytokine is produced early, mainly by natural killer (NK) cells and later by T cells. As NK cells have been reported to participate in defence against T. cruzi, it is of importance to study the regulation of NK cell functions during infection with the parasite. Several innate cytokines regulate NK cell activity, among them being interferon (IFN)-α and IFN-β (type 1 IFNs) and interleukin (IL)-12, which have all been reported to be involved in protection against T. cruzi. The role of these cytokines in regulation of NK cell functions and disease outcome were studied by infection of mutant mice lacking the IFN-α/β receptor (IFNα/βR–/–) or IL-12 (IL-12–/–) with T. cruzi. IFNα/βR–/– mice were unable to activate the cytotoxic response but produced IFN-γ, and were not more susceptible than controls. IL-12–/– mice were extremely susceptible and failed to produce T cell-derived IFN-γ and nitric oxide (NO), although NK cytotoxicity was induced. The results indicate that IL-12 protects against T. cruzi by initiating T cell-mediated production of IFN-γ, but that endogenous IFN-α/β and NK cell cytotoxicity are not of major importance in defence.

10.1046/j.1365-2249.2003.02294.x

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Citations (44)

Helicobacter pylori infection induces gastric precancerous lesions and persistent expression of Angpt2, Vegf-A and Tnf-A in a mouse model

Frontiers in Oncology (2023)

Wendy Malespín-Bendaña Warner Alpízar‐Alpízar Lucía Figueroa-Protti Ledis Reyes Silvia Molina‐Castro

Helicobacter pylori colonizes the gastric mucosa and induces chronic inflammation.Using a mouse model of H. pylori-induced gastritis, we evaluated the mRNA and protein expression levels of proinflammatory and proangiogenic factors, as well as the histopathological changes in gastric mucosa in response to infection. Five- to six-week-old female C57BL/6N mice were challenged with H. pylori SS1 strain. Animals were euthanized after 5-, 10-, 20-, 30-, 40- and 50-weeks post infection. mRNA and protein expression of Angpt1, Angpt2, VegfA, Tnf-α, bacterial colonization, inflammatory response and gastric lesions were evaluated.A robust bacterial colonization was observed in 30 to 50 weeks-infected mice, which was accompanied by immune cell infiltration in the gastric mucosa. Compared to non-infected animals, H. pylori-colonized animals showed an upregulation in the expression of Tnf-A, Angpt2 and VegfA at the mRNA and protein levels. In contrast, Angpt1 mRNA and protein expression was downregulated in H. pylori-colonized mice.Our data show that H. pylori infection induces the expression of Angpt2, Tnf-A and Vegf-A in murine gastric epithelium. This may contribute to the pathogenesis of H. pylori-associated gastritis, however the significance of this should be further addressed.

Proinflammatory cytokine

Pathogenesis

10.3389/fonc.2023.1072802

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Citations (6)

Association of interleukin-1B and interleukin-1RN polymorphisms with gastric cancer in a high-risk population of Costa Rica

Clinical and Experimental Medicine (2005)

Warner Alpízar‐Alpízar Guillermo I. Pérez‐Pérez Clas Une Patricia Cuenca Rosa A. Sierra

10.1007/s10238-005-0082-3

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Citations (79)

Association of serum pepsinogen with atrophic body gastritis in Costa Rica

Clinical and Experimental Medicine (2006)

Rosa A. Sierra Clas Une Vanessa Ramírez Ma. Isabel González José Antonio Ramírez

Atrophic gastritis

CagA

10.1007/s10238-006-0098-3

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Citations (24)

La importancia del sistema activador de plasminógeno en la patogénesis y progresión del cáncer gástrico

Revista de Biología Tropical (2017)

Warner Alpízar‐Alpízar Wendy Malespín-Bendaña Clas Une Vanessa Ramírez

Gastric cancer is ranked as the third death-causing cancer and one of the most incident malignancies worldwide. Although Helicobacter pylori is the most well-established risk factor for the development of this neoplasm, most of the infected individuals do not develop gastric cancer. Two of the main challenges faced by the world’s scientific community in the combat against gastric cancer are the unraveling of its pathogenesis and the identification of novel ways to bring down the mortality. Malignant cell invasion of the non-neoplastic adjacent tissue and metastasis are pivotal events during cancer development and progression. Both processes are facilitated by proteases capable of degrading components of the extracellular matrix, some of which have been associated to clinico-pathological aspects of the disease. Recent studies have suggested the possible connection between H. pylori and the expression of some of these proteases in gastric mucosa. This review summarizes the current knowledge about epidemiological, clinical and biological aspects of gastric cancer; it also discusses the main findings about the involvement of the plasminogen activation system in the development and progression of this disease, as well as its potential repercussions in the clinical setting.

Pathogenesis

10.15517/rbt.v66i1.29014

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Citations (1)