29 research outputs found
The cadherinâcatenin complex in nasopharyngeal carcinoma
Abnormal Wnt signaling and impaired cellâcell
adhesion due to abnormal E-cadherin and b-catenin func tion have been implicated in many cancers, but have not
been fully explored in nasopharyngeal carcinoma. The aim
of this study was to analyze b-Catenin cellular location and
E-cadherin expression levels in nasopharyngeal carcinoma.
E-cadherin expression levels were also correlated with
clinical data and underlying pathology. b-Catenin and
E-cadherin expression were examined in 18 nasopharyn geal carcinoma and 7 non-tumoral inflammatory pharynx
tissues using immunohistochemical methods. Patient clin ical data were collected, and histological evaluation was
performed by hematoxylin/eosin staining. b-catenin was
detected in membrane and cytoplasm in all cases of naso pharyngeal carcinoma, regardless of histological type; in
non-tumoral tissues, however, b-catenin was observed only
in the membrane. As for E-cadherin expression levels,
strong staining was observed in most non-tumoral tissues,
but staining was only moderate in nasopharyngeal carci noma tissues. E-cadherin expression was associated with
b-catenin localization, study group, metastatic disease, and
patient outcomes. Reduced levels of E-cadherin protein
observed in nasopharyngeal carinoma may play an
important role in invasion and metastasis. Cytoplasmic
b-catenin in nasopharyngeal carcinoma may impair cellâ
cell adhesion, promoting invasive behavior and a metastatic
tumor phenotype
R-Allyl Nickel(II) Complexes with Chelating N-Heterocyclic Carbenes: Synthesis, Structural Characterization, and Catalytic Activity
The N-heterocyclic carbene (NHC) nickel complexes [(L)Ni(NHC)][BArF4] (ArF = 3,5-bis(trifluoromethyl)-
phenyl; L = allyl (1), methylallyl (2); NHC = 1-(2-picolyl)-3-methylimidazol-2-ylidene (a), 1-(2-picolyl)-3-isopropylimidazol-2-ylidene (b), 1-(2-picolyl)-3-n-butylimidazol-2-ylidene (c), 1-(2-picolyl)-3-phenylimidazol-2-ylidene (d), 1-(2-picolyl)-3- methylbenzoimidazol-2-ylidene (e), 1-(2-picolyl)-4,5-dichloro-3-methylimidazol-2-ylidene (f)) have been obtained in high yields and characterized by NMR spectroscopy. Furthermore, 1d was unambiguously characterized by single-crystal X-ray crystallography. Complexes 1aâf/2aâf have shown catalytic activity toward dimerization and hydrosilylation of styrenes. In particular, 1a proved to be the most efficient catalyst in the dimerization of styrene derivatives in the absence of cocatalyst. Also, complexes 1a,d showed high selectivity and moderate to good yields in hydrosilylation reactions
The cadherinâcatenin complex in laryngeal squamous cell carcinoma
Abnormal Wnt signaling and impaired cellâcell adhesion due to abnormal E-cadherin and ÎČ-catenin function have been implicated in many cancers, but have not been fully explored in laryngeal squamous cell carcinoma. In this study, ÎČ-catenin cellular location and E-cadherin expression levels were analyzed in 16 laryngeal squamous cell carcinomas (LSCCs) (9 glottic and 7 supraglottic) and 11 samples of non-tumoral inflammatory larynx tissue, using immunohistochemical methods. All non-tumoral tissues showed equally strong membranous expression of ÎČ-catenin, while cytoplasmic expression was found in only 3 of the 11 samples. By contrast, whereas 8/9 glottic LSCCs exhibited only membranous expression of ÎČ-catenin, 6/7 supraglottic LSCCs displayed both membranous and cytoplasmic expression (p = 0.003). Strong E-cadherin staining was observed in 9/11 non-tumoral tissues and 7/9 glottic LSCCs, whereas 4/7 supraglottic LSCCs exhibited weak expression. Reduced membrane expression of E-cadherin and cytoplasmic retention of ÎČ-catenin in supraglottic LSCC seems to be related with more aggressive biological behavior which has been described in clinical studies. Further research is required to clarify the involvement of ÎČ-catenin in the mechanism associated with malignant transformation in laryngeal tissues
The cadherinâcatenin complex in nasopharyngeal carcinoma
Abnormal Wnt signaling and impaired cellâcell adhesion due to abnormal E-cadherin and ÎČ-catenin function have been implicated in many cancers, but have not been fully explored in nasopharyngeal carcinoma. The aim of this study was to analyze ÎČ-Catenin cellular location and E-cadherin expression levels in nasopharyngeal carcinoma. E-cadherin expression levels were also correlated with clinical data and underlying pathology. ÎČ-Catenin and E-cadherin expression were examined in 18 nasopharyngeal carcinoma and 7 non-tumoral inflammatory pharynx tissues using immunohistochemical methods. Patient clinical data were collected, and histological evaluation was performed by hematoxylin/eosin staining. ÎČ-catenin was detected in membrane and cytoplasm in all cases of nasopharyngeal carcinoma, regardless of histological type; in non-tumoral tissues, however, ÎČ-catenin was observed only in the membrane. As for E-cadherin expression levels, strong staining was observed in most non-tumoral tissues, but staining was only moderate in nasopharyngeal carcinoma tissues. E-cadherin expression was associated with ÎČ-catenin localization, study group, metastatic disease, and patient outcomes. Reduced levels of E-cadherin protein observed in nasopharyngeal carinoma may play an important role in invasion and metastasis. Cytoplasmic ÎČ-catenin in nasopharyngeal carcinoma may impair cellâcell adhesion, promoting invasive behavior and a metastatic tumor phenotype
Cerebral infarction secondary to internal carotid thrombosis following cervical trauma
ComunicaciĂłn presentada a la ReuniĂłn del Club de Autopsias. XXV Congreso de la SEAP, XX Congreso de la SEC, I Congreso de la SEPAF. Zaragoza 18-21 de Mayo de 2011.In this paper, a case of post-traumatic thrombosis in the internal carotid artery after a blow with a ball in the neck of
a 33-year-old male is presented. The death came 10 days after the coup as a result of intracranial hypertension and
cerebral herniation secondary to ischemic infarction affecting the entire territory of the middle right cerebral artery, both
superficial and profound. Macroscopic and microscopic findings that largely explain the mechanism of vascular injury
with intimal dissection in the proximity of an atheroma plaque located above the carotid bifurcation are discussed.YesSe presenta el caso de una trombosis postraumåtica de la arteria carótida interna en un varón de 33 años, tras recibir
un golpe con un balĂłn en el cuello. La muerte se produjo 10 dĂas despuĂ©s del golpe como consecuencia de un cuadro
de hipertensión intracraneal y herniación cerebral secundaria a infarto isquémico extenso que afectaba a todo el territorio
de la arteria cerebral media derecha, tanto superficial como profundo
Tres casos de malformaciĂłn adenomatoidea quĂstica en el adulto tratados por cirugĂa videotoracoscĂłpica
Multiple non-metastatic gastrointestinal stromal tumors: Differential features Tumores del estroma gastrointestinal mĂșltiples no metastĂĄsicos: Aspectos diferenciales
Introduction: gastrointestinal stromal tumors (GISTs) are specific, generally KIT (CD117)-positive, mesenchymal tumors of the digestive tract displaying KIT or PDGFRA gene mutations. Clinically, they tend to present as solitary tumors of the intestinal wall; more rarely, multiple tumors may occur in one or more organs. Objective: to review the morphological, immunohistochemical and molecular features of multiple, non-metastatic forms of GIST. Sources: review of the literature on Medline, and authors' own experience. Conclusions: multiples GISTs may occur in three different contexts: as spontaneous lesions (in both adults and children); due to familial GIST syndrome (autosomal dominant inheritance); or in association with specific syndromes (e.g. Carney's triad, Carney-Stratakis syndrome, type I neurofibromatosis). Outside these contexts, the existence of multiple GISTs is deemed to be the result of tumor metastasis, and therefore indicative of advanced-stage disease. Clinicians need to be aware of these variants, whose prognosis and treatment differ.IntroducciĂłn: los tumores del estroma gastrointestinal (GIST) son neoplasias mesenquimales del tubo digestivo que generalmente expresan el receptor KIT (CD117) y muestran mutaciones en los genes KIT o PDGFRA. Aunque la forma de presentaciĂłn clĂnica habitual es como una neoplasia mural solitaria, excepcionalmente pueden presentarse formas mĂșltiples en el mismo o diferente Ăłrgano. Objetivo: revisar las caracterĂsticas morfolĂłgicas, inmunohistoquĂmicas y moleculares de las formas de GIST mĂșltiples no metastĂĄsicos. Fuentes: revisiĂłn de la literatura en Medline y la propia experiencia. Conclusiones: los GIST mĂșltiples pueden presentarse en tres contextos diferentes: lesiones espontĂĄneas (del adulto o de la edad infantil); sĂndrome familiar propio (transmitido con herencia autosĂłmica dominante); y lesiones asociadas a sĂndromes especĂficos (trĂada de Carney, sĂndrome de Carney-Stratakis, y neurofibromatosis tipo I). Fuera de estos ĂĄmbitos, se interpreta que todo GIST mĂșltiple es el resultado de siembras tumorales metastĂĄsicas y, por tanto, corresponde a enfermedad avanzada. Estas variantes deben ser conocidas por el clĂnico dado las connotaciones pronĂłsticas y terapĂ©uticas que ello conlleva