Browsing by Author "Valbuena Mora, José Rafael"

Now showing 1 - 9 of 9
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    Anatomic hepatectomy as a definitive treatment for hepatolithiasis: a cohort study
    (2012) Jarufe Cassis, Nicolás; Figueroa, Eduardo; Muñoz Castro, César; Moisan Paravic, Fabricio Robertino; Varas Cohen, Julián; Valbuena Mora, José Rafael; Bambs S., Claudia; Martínez Castillo, Jorge; Pimentel Müller, Fernando
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    Early-Onset EBV-Positive Post-transplant Plasmablastic Lymphoma Arising in a Liver Allograft : A Case Report and Literature Review
    (2013) Benítez, Carlos; Rey Gnecco, Paula; Zoroquiain Vélez, José Pablo; Martínez Castillo, Jorge; Ramírez Villanueva, Pablo Antonio; Arrese Jiménez, Marco; Pérez Ayuso, Rosa María; Valbuena Mora, José Rafael
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    Linfoma anaplásico de células grandes asociado a implantes mamarios diagnosticado mediante punción por aguja fina : caso clínico
    (2020) Carlos Misad, S.; Kenneth Walker, B.; Valbuena Mora, José Rafael; Guerra Sánchez, Claudio Alejandro; Camus, Mauricio; Ocqueteau Tachini, Mauricio; Loyola Zunino, Sandra; Zoroquiain Vélez, José Pablo
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    Loss of Expression of Reprimo, a p53-induced Cell Cycle Arrest Gene, Correlates with Invasive Stage of Tumor Progression and p73 Expression in Gastric Cancer
    (2015) Saavedra, K.; Valbuena Mora, José Rafael; Olivares, W.; Marchant, M.; Rodríguez, A.; Torres, V.; Carrasco, G.; Gúzman, L.; Aguayo González, Francisco; Roa Strauch, Juan Carlos Enrique; Corvalán R., Alejandro
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    Lymphoma-like lesion of the cervix with monoclonal immunoglobulin heavy chain gene rearrangement in PCR analysis. A case report
    (2012) Zoroquiain Vélez, José Pablo; Vidal, M.; Valbuena Mora, José Rafael
    Resumen La lesión del cérvix es una proliferación linfoide benigna que simula un linfoma B difuso de células grandes, por ello es causa de potencial error diagnóstico. Presentamos el caso de una mujer de 24 años con PAP atípico y conización subsecuente, identificándose una proliferación linfoide atípica. El infiltrado linfoide era polimórfico, con numerosas células grandes entremezcladas, sin necrosis ni esclerosis. El epitelio presentó displasia epitelial moderada. Las células grandes fueron inmunorreactivas para CD20, sin expresión de cadenas ligeras de inmunoglobulinas. La hibridación in situ para el virus de Epstein-Barr resultó positiva en escasas células grandes aisladas. Mediante técnica de PCR, para amplificación de la región FR3 de la cadena pesada de la IgH, se observaron 2 bandas monoclonales. Hasta el último seguimiento (24 meses), no se encontró evidencia de enfermedad sistémica/progresión.
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    Metastatic neuroendocrine carcinoma of the colon: response to standard colorectal therapy
    (2013) Acevedo Claros, Francisco Nicolás; Otarola, C.; Valbuena Mora, José Rafael; Garrido, M.
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    Primary leiomyosarcoma of the greater omentum: a case report
    (2016) Brañes, A.; Bustamante, C.; Valbuena Mora, José Rafael; Pimentel Muller, Fernando; Quezada Sanhueza, Nicolás
    Introduction Greater omentum leiomyosarcomas are rare tumors with only a few cases reported in literature. Presentation of case We report the case of a 68-year-old man who consulted complaining of diffuse abdominal pain without a palpable mass at physical examination. Imaging studies revealed a solid-cystic lesion in the right lower quadrant. Surgical resection was performed and the tumor was diagnosed as a leiomyoscarcoma by histological and immunohistochemical examinations. Discussion Surgical resection of all lesions seems to be a reasonable therapeutic approach if resection is feasible. Chemotherapy may be used in selected cases. Conclusion More cases are needed to define the best treatment approach of this disease.
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    Small molecule inhibitor screening identifified HSP90 inhibitor 17-AAG as potential therapeutic agent for gallbladder cancer
    (2017) Weber, Helga; Valbuena Mora, José Rafael; Barbhuiya, Mustafa A.; Stein, Stefan; Kunkel, Hana; García Muñoz, Patricia; Bizama, Carolina; Riquelme, Ismael; Espinoza, Jaime A.; Kurtz, Stephen E.; Tyner, Jeffrey W.; Calderon, Juan Francisco; Corvalán R., Alejandro; Grez, Manuel; Pandey, Akhilesh; Leal Rojas, Pamela; Roa Strauch, Juan Carlos Enrique
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    Transcriptomic profiles reveal differences in zinc metabolism, inflammation, and tight junction proteins in duodenum from cholesterol gallstone subjects
    (2020) Riveras Hernández, Eleodoro Javier; Azócar, Lorena; Moyano, Tomás C.; Ocares, Marcia; Molina, Héctor; Romero, Diego; Roa Strauch, Juan Carlos Enrique; Valbuena Mora, José Rafael; Gutiérrez, Rodrigo A.; Miquel P., Juan Francisco
    Cholesterol Gallstone Disease (GSD) is a common multifactorial disorder characterized by crystallization and aggregation of biliary cholesterol in the gallbladder. The global prevalence of GSD is similar to 10-20% in the adult population but rises to 28% in Chile (17% among men and 30% among women). The small intestine may play a role in GSD pathogenesis, but the molecular mechanisms have not been clarified. Our aim was to identify the role of the small intestine in GSD pathogenesis. Duodenal biopsy samples were obtained from patients with GSD and healthy volunteers. GSD status was defined by abdominal ultrasonography. We performed a transcriptome study in a discovery cohort using Illumina HiSeq. 2500, and qPCR, immunohistochemistry and immunofluorescence were used to validate differentially expressed genes among additional case-control cohorts. 548 differentially expressed genes between GSD and control subjects were identified. Enriched biological processes related to cellular response to zinc, and immune and antimicrobial responses were observed in GSD patients. We validated lower transcript levels of metallothionein, NPC1L1 and tight junction genes and higher transcript levels of genes involved in immune and antimicrobial pathways in GSD patients. Interestingly, serum zinc and phytosterol to cholesterol precursor ratios were lower in GSD patients. A significant association was observed between serum zinc and phytosterol levels. Our results support a model where proximal small intestine plays a key role in GSD pathogenesis. Zinc supplementation, modulation of proximal microbiota and/or intestinal barrier may be novel targets for strategies to prevent GSD.