RESUMEN
We describe a case of lymphoepithelial lesion of the parotid gland, also known as salivary lymphoepithelial lesion. Lymphoepithelial lesions are usually seen in conjunction with autoimmune disease of the salivary glands and these lesions do not always remain benign. Our case consisted of two masses that had different imaging features. Moreover, we could investigate the changes of the size and internal architecture on imaging due to the postponement of surgical intervention on the masses. At review 6 months later, the size of the masses had increased. The aims of this paper were to: (1) investigate the contribution of gray-scale sonography, power Doppler sonography, magnetic resonance imaging, and computed tomography to the diagnosis; and (2) consider the appropriate imaging modality to follow-up this case to monitor for recurrence or malignant transformation.
Asunto(s)
Enfermedades Linfáticas/diagnóstico , Enfermedades de las Parótidas/diagnóstico , Diagnóstico Diferencial , Células Epiteliales/patología , Femenino , Estudios de Seguimiento , Humanos , Hialina , Enfermedades Linfáticas/diagnóstico por imagen , Enfermedades Linfáticas/patología , Linfocitos/patología , Imagen por Resonancia Magnética , Persona de Mediana Edad , Enfermedades de las Parótidas/diagnóstico por imagen , Enfermedades de las Parótidas/patología , Tomografía Computarizada por Rayos X , UltrasonografíaRESUMEN
We have synthesized a recombinant gene encoding a single-chain HLA-A2/beta 2-microglobulin (beta 2m) molecule by linking beta 2m through its carboxyl terminus via a short peptide spacer to HLA-A2 (A*0201). This gene has been expressed in the beta 2m-deficient colorectal tumor cell line DLD-1. Transfection of this cell with the single-chain construct was associated with conformationally correct cell surface expression of a class I molecule of appropriate molecular mass. The single-chain HLA class I molecule presented either exogenously added peptide or (after interferon-gamma treatment) endogenously processed antigen to an influenza A matrix-specific, HLA-A2-restricted cytotoxic T-lymphocyte line. The need for interferon gamma for the processing and presentation of endogenous antigen suggests that DLD-1 has an antigen-processing defect that can be up-regulated, a feature that may be found in other carcinomas. Our data indicate that single-chain HLA class I constructs can form functional class I molecules capable of presenting endogenously processed antigens. Such molecules should be of use for functional studies, as well as providing potential anticancer immunotherapeutic agents or vaccines.
Asunto(s)
Células Presentadoras de Antígenos/fisiología , Antígeno HLA-A2/química , Linfocitos T Citotóxicos/inmunología , Microglobulina beta-2/química , Secuencia de Aminoácidos , Secuencia de Bases , Línea Celular , Cartilla de ADN/química , Humanos , Cooperación Linfocítica , Datos de Secuencia Molecular , Oligopéptidos/química , Oligopéptidos/inmunología , Proteínas Recombinantes de Fusión , Transducción de Señal , TransfecciónRESUMEN
Adenomatous polyposis coli (APC) is a genetic disorder transmitted as an autosomal dominant trait. This syndrome is characterized by the development of numerous polyps during the first 20-30 years of life and classified into two phenotypes according to the number of polyps: the profuse and sparse types. If left untreated, most or all affected individuals are at a high risk of developing adenocarcinoma by as early as 40 years of age. Therefore, comparison of APC adenocarcinomas with non-polyposis colorectal carcinomas (NPCC) was thought to be useful for understanding genetically determined carcinogenesis. I investigated gene alterations in specimens obtained from 53 APC patients, of which 16 represented the profuse type and the others the sparse type, and from 15 NPCC patients. The results are summarized as follows: 1) K-ras gene mutations were detected more frequently in the profuse-type adenomas (43%) than in the sparse ones (14%) (p less than 0.05). 2) Loss of heterozygosity on the long arm of chromosome 5(5q), 18(18q) and the short arm of chromosome 17(17p) in the profuse-type adenomas was observed more frequently (22%) than in the sparse ones (7.3%) (p less than 0.05). 3) No significant differences were observed between APC adenocarcinomas and NPCCs regarding the allelic deletions on 5q, 17p and 18q in these tumors. 4) The alteration of the DCC gene, which is known to be involved in the formation of NPCC, was frequently detected in the APC adenocarcinomas, suggesting that similar genetic events are involved in the oncogenesis of adenocarcinomas from APC and NPCC.
Asunto(s)
Poliposis Adenomatosa del Colon/genética , Genes DCC/genética , Genes p53/genética , Genes ras/genética , Alelos , Animales , Secuencia de Bases , Cromosomas Humanos Par 18 , Cromosomas Humanos Par 5 , Amplificación de Genes , Heterocigoto , Humanos , Ratones , Datos de Secuencia Molecular , MutaciónAsunto(s)
Cromosomas , Pólipos del Colon/diagnóstico , Deleción Cromosómica , Pólipos del Colon/genética , Genes DCC/genética , Genes Supresores de Tumor , Genes p53/genética , Heterocigoto , Humanos , Fusión Nuclear , Hibridación de Ácido Nucleico , Oncogenes/genética , Polimorfismo de Longitud del Fragmento de RestricciónRESUMEN
The p53 gene has been elucidated as a tumor suppressor gene, and inactivation of this gene caused by deletion or point mutations may play a crucial role in the development of human malignancies. In colorectal carcinomas with an allelic deletion of the p53 gene, the remaining p53 gene was mutated with considerable frequency. It is most difficult to detect point mutations or small deletions of the gene because the mutations occur in diverse regions, although four hot spots have been observed [J.M. Nigro et al., Nature (Lond.), 342: 705-708, 1989]. The polymerase chain reaction and denaturing gradient gel electrophoresis facilitate detection of mutations in the hot spots of the p53 gene. Using these methods, we detected mutations in three adenomatous polyps and one carcinoma from familial polyposis coli patients and three carcinomas of sporadic cases. The DNA sequence analysis confirmed mutations of the p53 gene in 2 adenomas (13 base-pair deletions in one and a point mutation in the other) and 1 carcinoma (point mutation) from familial polyposis coli patients. These results suggest that the p53 gene mutations may be involved in the formation not only of carcinomas but also of adenomas which occur in familial polyposis coli patients.