Asunto(s)
Carcinoma de Células Escamosas/diagnóstico , Reservorios Cólicos/patología , Neoplasias del Íleon/diagnóstico , Carcinoma de Células Escamosas/complicaciones , Carcinoma de Células Escamosas/cirugía , Femenino , Humanos , Histerectomía , Neoplasias del Íleon/complicaciones , Neoplasias del Íleon/cirugía , Persona de Mediana Edad , Invasividad Neoplásica/diagnóstico , Ovariectomía , Reservoritis/etiología , Reservoritis/patología , SalpingectomíaRESUMEN
We report an unusual presentation of acute pancreatitis as a tender, irreducible, inguinoscrotal swelling mimicking a strangulated hernia. Lack of abdominal symptoms or signs can lead to misdiagnosis and unnecessary surgery.
Asunto(s)
Hernia Inguinal/diagnóstico por imagen , Pancreatitis Aguda Necrotizante/diagnóstico por imagen , Celulitis (Flemón)/diagnóstico por imagen , Diagnóstico Diferencial , Humanos , Masculino , Persona de Mediana Edad , Músculos Psoas/diagnóstico por imagen , Espacio Retroperitoneal/diagnóstico por imagen , Tomografía Computarizada por Rayos XRESUMEN
BACKGROUND AND AIMS: Characterisation of the underlying molecular mechanisms that promote Barrett's progression may ultimately lead to identification of potential predictive genetic markers that classify patients' malignant risk. In an attempt to understand these causative pathways, fluorescence in situ hybridisation (FISH) was used in this study to determine when specific genetic alterations arise during Barrett's associated neoplastic progression. METHODS: Endoscopic cytology brushings were obtained from 28 patients with Barrett's metaplasia, 28 with dysplasia (20 low grade dysplasia (LGD) and eight with high grade dysplasia (HGD)), and seven with adenocarcinoma, together with paired control brushings from regions of normal proximal squamous cell epithelium. The exfoliated epithelial cells were washed and deposited onto slides. Probes specific for the centromeres of chromosomes 4, 8, 20, and Y, and locus specific probes for the tumour suppressor genes p16, p53, and Rb were subsequently hybridised. RESULTS: Aneuploidy was found early in progression, with metaplastic tissues displaying increased copy numbers of chromosomes 4 and 8. Chromosome 4 hyperploidy was found in 89%, 90%, 88%, and 100% of metaplasias, LGD, HGD, adenocarcinomas, respectively, while chromosome 8 hyperploidy occurred in 71%, 75%, 100%, and 100% of patients with the respective staging. Loss of the p16 tumour suppressor gene also presented in metaplastic epithelium (7%) but most other genetic aberrations were only seen in HGD. CONCLUSIONS: Genetic instability arises well before dysplasia in Barrett's oesophagus, with chromosome 4 and 8 hyperploidy representing the earliest and most common alterations identified. As these aberrations are widespread at all the premalignant stages, there may be genes on chromosomes 4 and 8 that are involved in both the initiation and progression of Barrett's oesophagus.
Asunto(s)
Adenocarcinoma/genética , Esófago de Barrett/genética , Aberraciones Cromosómicas , Cromosomas Humanos Par 4/genética , Neoplasias Esofágicas/genética , Lesiones Precancerosas/genética , Adenocarcinoma/patología , Adulto , Anciano , Anciano de 80 o más Años , Aneuploidia , Cromosomas Humanos Par 20/genética , Cromosomas Humanos Par 8/genética , Cromosomas Humanos Y/genética , Neoplasias Esofágicas/patología , Femenino , Genes Supresores de Tumor/fisiología , Humanos , Masculino , Persona de Mediana Edad , Lesiones Precancerosas/patologíaRESUMEN
BACKGROUND: The prediction of which patients with Barrett's metaplasia will develop cancer is difficult. Better genetic characterization of the condition may aid clinicians in devising more effective management and follow-up strategies. METHODS: A review was undertaken of the accumulated genetic data relating to the progression of squamous epithelium to adenocarcinoma. The normal functions of a number of cancer-related genes are described and an explanation is given of how alterations in these genes interfere with normal cell processes and lead to cancer. RESULTS AND CONCLUSION: The main genetic alterations accompanying the progression through dysplasia to adenocarcinoma were collated from 135 papers. The principal genetic changes implicated are the loss of p16 gene expression (by deletion or hypermethylation), the loss of p53 expression (by mutation and deletion), the increase in cyclin D1 expression, the induction of aneuploidy and the losses of the Rb, DCC and APC chromosomal loci.
Asunto(s)
Adenocarcinoma/genética , Esófago de Barrett/genética , Neoplasias Esofágicas/genética , Adhesión Celular/genética , Comunicación Celular/genética , Ciclo Celular/genética , Cromosomas Humanos/genética , Progresión de la Enfermedad , Eliminación de Gen , Humanos , Mutación/genética , Oncogenes/genéticaRESUMEN
An anterior neopharyngeal diverticulum is a recognized cause of dysphagia following laryngectomy. It is easily treated by endoscopic stapling.