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Pathological Marker (pathological + marker)
Selected AbstractsTumor budding as a useful prognostic marker in esophageal squamous cell carcinomaDISEASES OF THE ESOPHAGUS, Issue 4 2004M. S. Roh SUMMARY, We examined the prognostic significance of tumor budding in patients with esophageal squamous cell carcinoma, particularly in comparison to other routine pathological findings. Fifty-six cases who underwent an esophagectomy were reviewed. We defined tumor budding as an isolated single cancer cell or a cluster composed of fewer than five cancer cells and divided these into two grades; low-grade (< 5 budding foci) and high-grade (, 5 budding foci) within a microscopic field of ×200. There were 22 (39.3%) and 34 (60.7%) cases with low- and high-grade budding, respectively. There were significant differences in the patients with low- and high-grade budding in relation to tumor size, pT stage, lymphovascular invasion, perineural invasion, circumferential resection margin involvement, and AJCC stage (P < 0.05). The 3-year survival rates of the patients with low- and high-grade budding were 72.3% and 30.7%, respectively (P = 0.04). We propose that tumor budding may be a pathological marker suggesting high malignancy potential and decreased postoperative survival in patients with esophageal squamous cell carcinoma. [source] Are giant axons a pathological marker of charcot-marie-tooth neuropathy type 2E?JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 2 2004T Cavallaro Background: According to electrophysiological and pathological criteria Charcot Marie Tooth (CMT) disease includes primary demyelinating forms (CMT1) and neuropathies with primary axonal loss (CMT2). In CMT1, genetic analysis provided some associations between characteristic lesions and different proteins. In CMT2, four genes were identified recently (CMT2A, B, D, E); the molecular diagnosis is complex and phenotypical hallmarks are lacking. Objectives: To describe the nerve biopsy in three pedigrees with CMT2E caused by mutations of the neurofilament-light chain gene (NF-L): two pedigrees from Campania sharing a Pro22Ser substitution in the head domain of protein and one pedigree from Apulia with a novel Leu268Prol substitution in the central rod domain. In all three pedigrees electrophysiology was consistent with a mixed, demyelinating and axonal neuropathy. Results: The three patients analysed revealed a primary axonopathy characterized by giant axonal swelling filled with densely packed neurofilaments and some atrophic axons. Conclusions: We propose that, in the diagnostic work up of CMT2, giant axons may orientate towards CMT2E. The pathological alterations detected correlate intuitively with an altered function of the neurofilaments which constitute the axonal cytoskeleton and are critical for radial growth and for axonal transport. [source] Absence of neuronal nitric oxide synthase (nNOS) as a pathological marker for the diagnosis of Becker muscular dystrophy with rod domain deletionsNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 5 2004S. Torelli Immunohistochemistry using antibodies to dystrophin is the pathological basis for the diagnosis of Duchenne and Becker muscular dystrophy (DMD and BMD). While the sarcolemma of DMD muscle is negative, BMD muscle generally shows variable labelling because of the translation of a partially functional dystrophin that is localized to the sarcolemma. In rare cases, however, this labelling is equivocal and similar to that observed in controls making diagnosis difficult. We report here that in such instances immunolabelling with antibodies to the neuronal form of nitric oxide synthase (nNOS) can be useful in suspecting a dystrophinopathy with a mutation in the ,hot-spot' rod domain and help to direct molecular analysis. nNOS localizes to the sarcolemma of mature muscle fibres via several components of the dystrophin-associated protein complex (DAPC) including dystrophin but sarcolemmal nNOS is lost when dystrophin levels are very low or absent because of deletions in critical regions of the rod domain. We report three cases who presented with only mild or no muscle weakness but had elevated serum creatine kinase activity and dystrophin immunolabelling indistinguishable from normal, making a pathological diagnosis difficult. All three cases had a complete absence of sarcolemmal nNOS and were subsequently found to have an in-frame deletion in the common rod domain exons (in these cases 48, 45,51, 47,53) compatible with a BMD. In addition, we observed that nNOS appears to be developmentally regulated with the antibody used and was often absent from the sarcolemma of immature fibres. These findings demonstrate the value of including antibodies to nNOS in routine immunohistochemical studies and that absence of nNOS can be a more sensitive marker than up-regulation of utrophin for diagnosis of BMD. Immaturity of fibres, however, needs to be taken into account, especially in neonates. [source] Influence of glutathione- S -transferase theta (GSTT1) and mu (GSTM1) gene polymorphisms on the susceptibility of hepatocellular carcinoma in Taiwan,JOURNAL OF SURGICAL ONCOLOGY, Issue 4 2010Chia-Chun Kao MD Abstract Background and Objectives Hepatocellular carcinoma (HCC) is one of the most frequent malignant neoplasms worldwide and is the second leading cause of cancer death in Taiwan. Genetic polymorphism has been reported as a factor for increased susceptibility of HCC. Glutathione- S -transferases theta (GSTT1) and mu (GSTM1) play essential roles in detoxification of ingested xenobiotics and modulation of the susceptibility of gene-related cancer. The aim of this study was to estimate the relationships between these two gene polymorphisms and HCC risk and clinicopathological status in Taiwanese. Methods Polymerase chain reaction (PCR) was used to determine gene polymorphisms of 102 patients with HCC and 386 healthy controls. Results Both gene polymorphisms were not associated with the clinical pathological status of HCC and serum levels of liver-related clinical pathological markers. While no relationship between GSTM1 gene polymorphism and HCC susceptibility was found, individuals of age <56 years old with GSTT1 present genotype have a risk of 2.77-fold (95% CI: 1.09,7.09) for HCC compared to that with null variant, after adjustment for other confounders. Conclusions GSTT1 and GSTM1 null genotypes do not associate with increased risk of HCC. J. Surg. Oncol. 2010;102:301,307. © 2010 Wiley-Liss, Inc. [source] Specialized intestinal metaplasia in patients with gastro-oesophageal reflux diseaseBRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 1 2000E. Carton Background: There is an increasing awareness that short (less than 3 cm) segments of Barrett's epithelium and macroscopically normal cardia epithelium may harbour specialized intestinal metaplasia (SIM), a premalignant phenotype. The prevalence of SIM was studied prospectively in an unselected population of patients attending for endoscopy, and the association of SIM with symptoms, lifestyle, medication, endoscopic oesophagitis and carditis was investigated. Methods: Two hundred consecutive patients underwent endoscopy. Biopsies taken from just below the squamocolumnar junction were stained for SIM, and were analysed for carditis and Helicobacter pylori infection. A detailed questionnaire of symptoms, tobacco consumption and the use of proton pump inhibitors was completed. Results: Forty-two patients (21 per cent) had SIM: 19 (15 per cent) of 126 in an endoscopically normal oesophagus, 15 (24 per cent) of 63 in a short segment of Barrett's epithelium and eight of 11 in classical Barrett's oesophagus. There was a significant association between SIM and carditis (P < 0·0001) and endoscopic oesophagitis (P = 0·03). Conclusion: SIM is prevalent in patients undergoing endoscopy, does not correlate with symptoms or H. pylori infection, but is significantly associated with endoscopic and pathological markers of gastro-oesophageal reflux. © 2000 British Journal of Surgery Society Ltd [source] | ||||||||||