RESUMO
Pre-operative radiotherapy may induce radiation colitis and tumour regression. Histological evaluation of radiation colitis needs to be reproducible to assess disease progression. The severity of radiation colitis can be assessed and graded according to its histological features. Increased severity of disease appears to be associated with a higher degree of cellular atypia and a lesser eosinophilic infiltrate. The severity of histological changes does not appear to be associated with post-operative complications. Tumour regression is an interesting phenomenon, the histological grading of which is of prognostic importance. Patients treated with long course radiotherapoy appear to have more incidences of postoperative complications. However, these are though to be related to the degree of tumour regression rather than to the type of radiotherapy.
Assuntos
Colite/etiologia , Lesões por Radiação , Colite/patologia , Colite/fisiopatologia , Humanos , Neoplasias Intestinais/radioterapia , Neoplasias Intestinais/cirurgia , Terapia Neoadjuvante , Lesões por Radiação/patologia , Lesões por Radiação/fisiopatologiaRESUMO
The antiangiogenic factor METH-2 (ADAMTS-8) was identified in a previous dual-channel cDNA microarray analysis to be at least two-fold under-represented in 85% (28 out of 33) of primary non-small-cell lung carcinomas (NSCLCs). This observation has been validated in an independent series of NSCLCs and adjacent normal tissues by comparative multiplex RT-PCR, and METH-2 mRNA expression was dramatically reduced in all 23 tumour samples analysed. Immunohistochemical analysis of the same sample set demonstrated that METH-2 was strongly expressed in 14 out of 19 normal epithelial sites examined but only one out of 20 NSCLCs. DNA methylation analysis of the proximal promoter region of this gene revealed abnormal hypermethylation in 67% of the adenocarcinomas and 50% of squamous cell carcinomas, indicating that epigenetic mechanisms are involved in silencing this gene in NSCLC. No homozygous deletions of METH-2 were found in lung cancer cell lines. Allelic imbalance in METH-2 was assessed by an intronic single nucleotide polymorphism (SNP) assay and observed in 44% of informative primary samples. In conclusion, the downregulation of METH-2 expression in primary NSCLC, often associated with promoter hypermethylation, is a frequent event, which may be related to the development of the disease.
Assuntos
Carcinoma Pulmonar de Células não Pequenas/genética , Inativação Gênica , Neoplasias Pulmonares/genética , Metaloendopeptidases/genética , Regiões Promotoras Genéticas/genética , Proteínas ADAM , Proteínas ADAMTS , Adenocarcinoma/genética , Idoso , Carcinoma de Células Escamosas/genética , Metilação de DNA , DNA de Neoplasias/genética , Regulação Neoplásica da Expressão Gênica/genética , Humanos , Pessoa de Meia-Idade , RNA Mensageiro/genética , Reação em Cadeia da Polimerase Via Transcriptase ReversaRESUMO
BACKGROUND: Sudden and unexpected death is not an uncommon event in otherwise healthy epileptics. AIMS: To study the autopsied cases of sudden death in known epileptic patients in the West of Ireland. METHODS: A retrospective study was carried out which involved the review of 3,103 autopsy reports over a 10-year period in Galway University Hospital. RESULTS: Twenty-two cases were classified as sudden, unexpected death in epilepsy (SUDEP). Forty-five per cent had been found dead in bed. The mean age was 38 years and 68% were males. Of 16 cases with data about antiepileptic drug (AED) levels, 68% had absent or low levels at postmortem. Eighty-eight per cent of the cases had a past history of a generalised seizure. Pulmonary oedema was present in 86% of cases at postmortem. CONCLUSIONS: Compliance with treatment and frequent nightly observations to those at high risk of sudden death may help to minimise its incidence. The patients and their families should be aware of this potential outcome.
