Overexpression of p73 as a Tissue Marker for High-Risk Gastritis

Carrasco, Gonzalo; Diaz, José I.; Valbuena, José R.; Ibáñez, Patricio; Rodríguez, P Luis; Araya, Gabriela; Rodríguez, Carolina; Torres, Javiera; Duarte, Ignacio; Aravena, Edmundo; Mena, Fernando; Barrientos, Carlos; Corvalán, Alejandro

doi:10.1158/1078-0432.ccr-09-2491

Cited by 24 publications

(25 citation statements)

References 37 publications

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“…Tissue microarrays. Tissue microarrays were performed using a Manual Tissue Arrayer II instrument (Beecher Instruments), as described elsewhere [32].…”

Section: Tissue Samplesmentioning

confidence: 99%

“…The presence of survivin was detected using the avidin-biotin-peroxidase complex method with a polyclonal anti-survivin antibody (R&D Systems) and a commercially available detection kit (EnVision systems, Dako Cytomation) [32]. The presence of H. pylori in samples was detected with an H. pylori-specific polyclonal antibody (Novacastra), using the same system and Warthin-Starry staining.…”

Section: Tissue Samplesmentioning

confidence: 99%

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Helicobacter pylori–Induced Loss of the Inhibitor‐of‐Apoptosis Protein Survivin Is Linked to Gastritis and Death of Human Gastric Cells

et al. 2010

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Helicobacter pylori infects the human stomach and modifies signaling pathways that affect gastric epithelial cell proliferation and viability. Chronic exposure to this pathogen contributes to the onset of gastric atrophy, an early event in the genesis of gastric cancer associated with H. pylori infection. Susceptibility to H. pylori-induced cell death ultimately depends on the presence of protective host cell factors. Although expression of the inhibitor-of-apoptosis protein survivin in adults is frequently linked to the development of cancer, evidence indicating that the protein is present in normal gastric mucosa is also available. Thus, we investigated in human gastric tissue samples and cell lines whether H. pylori infection is linked to loss of survivin and increased cell death. Our results show that infection with H. pylori decreased survivin protein levels in the mucosa of patients with gastritis. Furthermore, survivin down-regulation correlated with apoptosis and loss of cell viability in gastrointestinal cells cocultured with different H. pylori strains. Finally, overexpression of survivin in human gastric cells was sufficient to reduce cell death after infection. Taken together, these findings implicate survivin as an important survival factor in the gastric mucosa of humans.

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“…Tissue microarrays. Tissue microarrays were performed using a Manual Tissue Arrayer II instrument (Beecher Instruments), as described elsewhere [32].…”

Section: Tissue Samplesmentioning

confidence: 99%

Section: Tissue Samplesmentioning

confidence: 99%

Helicobacter pylori–Induced Loss of the Inhibitor‐of‐Apoptosis Protein Survivin Is Linked to Gastritis and Death of Human Gastric Cells

et al. 2010

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“…10 In humans, several recent reports have linked p73 expression to inflammatory diseases such as otitis media, gastritis and chronic rhinosinusitis. 35,36 However, definitive evidence as to which p73 isoforms are involved and their specific roles has been lacking.…”

Section: Discussionmentioning

confidence: 99%

TAp73 is required for macrophage-mediated innate immunity and the resolution of inflammatory responses

et al. 2012

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The multiple isoforms of p73, a member of the p53 family, share the ability to modulate p53 activities but also have unique properties, leading to a complex and poorly understood functional network. In vivo, p73 isoforms have been implicated in tumor suppression (TAp73 À / À mice), DNA damage (DNp73 À / À mice) and development (p73 À / À mice). In this study, we investigated whether TAp73 contributes to innate immunity and septic shock. In response to a lethal lipopolysaccharide (LPS) challenge, TAp73À / À mice showed higher blood levels of proinflammatory cytokines and greater mortality than their wild-type littermates. In vitro, TAp73À / À macrophages exhibited elevated production of tumor necrosis factor alpha , interleukin-6 and macrophage inflammatory protein-2 as well as prolonged survival, decreased phagocytosis and increased major histocompatibility complex class II expression. Mice depleted of endogenous macrophages and reconstituted with TAp73 À / À macrophages showed increased sensitivity to LPS challenge. These results suggest that macrophage polarization is altered in the absence of TAp73 such that maintenance of the M1 effector phenotype is prolonged at the expense of the M2 phenotype, thus impairing resolution of the inflammatory response. Our data indicate that TAp73 has a role in macrophage polarization and innate immunity, enhancing the action field of this important regulatory molecule.

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“…Posteriormente, un número creciente de genes han sido identificados 22,23 y algunos de ellos han sido descritos en las lesiones precancerosas ya mencionadas previamente 24 . Sin embargo, la frecuencia de alteraciones genéticas de cada uno de estos genes es muy baja y no permite construir un modelo molecular del cáncer gástrico.…”

Section: Bases Moleculares Del Cáncer Gástricounclassified

Bases epigenéticas del cáncer gástrico: oportunidades para la búsqueda de nuevos biomarcadores

2013

Rev. méd. Chile

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Epigenetics in the pathogenesis and early detection of gastric cancerpuc.cl E l cáncer gástrico es la primera causa de muerte por enfermedades neoplásicas en Chile y la segunda en el mundo 1,2 . A pesar de los avances en el tratamiento y una disminución de sus lesiones precursoras 3,4 , recientes publicaciones sugieren un probable aumento de su mortalidad, particularmente en población joven 5 . Estas observaciones, en conjunto con proyecciones de la mortalidad global para los próximos 20 años, sugieren que el cáncer gástrico ocupará la décima causa global de muerte para la década del 2030 6 . El cáncer gástrico se puede clasificar según aspectos clínicos, endoscópicos o histológicos 7-13 . La clasificación más utilizada es la propuesta por Lauren 13 , la cual, según parámetros histológicos, define dos tipos de cáncer gástrico: el intestinal y el difuso. El primero se caracteriza por la formación de estructuras glandulares que semejan la mucosa colónica y que está precedida por una secuencia de lesiones muy bien caracterizadas por Correa y col. 14,15 . Por otra parte, el cáncer gástrico de tipo difuso, no forma estructuras histológicas y en consecuencia no tiene lesiones precursoras reconocidas 16 . Una particularidad importante de la clasificación de Lauren es que ha sido muy útil para estudiar el rol del ambiente, en particular en la variante intestinal 15 . En este sentido, las lesiones precancerosas han demostrado progresar de forma dinámica, desde la gastritis crónica superficial, gastritis crónica atrófica, metaplasia intestinal y finalmente displasia. Estos eventos constituyen las bases del "modelo humano de cáncer gástrico" postulado por Correa 17 . Una de las características fundamentales de este modelo es que junto con identificar una secuencia progresiva de lesiones, señala también la existencia de progresión/regresión de estas lesiones.

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Overexpression of p73 as a Tissue Marker for High-Risk Gastritis

Cited by 24 publications

References 37 publications

Helicobacter pylori–Induced Loss of the Inhibitor‐of‐Apoptosis Protein Survivin Is Linked to Gastritis and Death of Human Gastric Cells

Helicobacter pylori–Induced Loss of the Inhibitor‐of‐Apoptosis Protein Survivin Is Linked to Gastritis and Death of Human Gastric Cells

TAp73 is required for macrophage-mediated innate immunity and the resolution of inflammatory responses

Bases epigenéticas del cáncer gástrico: oportunidades para la búsqueda de nuevos biomarcadores

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