Stelow EB, Shaco-Levy R, Bao F, et al..Pancreatic acinar cell carcinomas with prominent ductal differentiation: mixed acinar ductal carcinoma and mixed acinar endocrine ductal carcinoma
ABSTRACT Pancreatic acinar cell carcinomas (ACCs) are clinically and pathologically distinct from pancreatic ductal adenocarcinomas (PDAs). Whereas endocrine differentiation has been well shown in ACCs, significant ductal components are rare. This paper reviews the clinicopathologic features of a series of ACCs with prominent ductal differentiation.
Cases of pancreatic ACCs with significant ductal differentiation were identified in the surgical pathology databases of 2 academic centers. Patient clinical information, gross and histologic features, and histochemical and immunohistochemical (IHC) results were recorded. Cases were tested for KRAS2 mutations.
Eleven cases were identified (10 men and 1 woman; age range 52 to 79 y). Four patients presented with jaundice. At last follow-up, 7 patients died of disease and 2 others had recurrences. Tumors measured between 2 and 5.5 cm and were ill-defined, nodular, and multilobulated. Ten were located in the head of the pancreas. All but 2 exhibited extrapancreatic invasion. All cases showed significant evidence of both acinar and ductal differentiation, estimated to be at least 25% of the neoplastic cells, and 3 cases in addition had endocrine differentiation in more than 25% of cells. Five cases were predominately acinar with intracellular and sometimes extracellular mucin ("mucinous acinar cell carcinoma" pattern). Six cases seemed more mixed with areas recapitulating typical PDAs whereas the other portions of the tumors seemed akin to typical acinar cell carcinomas ("combined acinar and ductal" pattern). IHC positive staining results were as: trypsin (92%), chymotrypsin (92%), monoclonal carcinoembryonic antigen (100%), CK19 (100%), B72.3 (73%), CA19.9 (73%), CD56 (18%), synaptophysin (36%), and chromogranin (36%). One case showed p53 over-expression aznd none showed DPC4/Smad4 loss. Two cases had KRAS2 mutations.
Despite the early embryologic divergence of acinar and ductal cell lineages, rare pancreatic tumors have both acinar and ductal differentiation, usually predominantly the former. The clinical course is highly aggressive.
Conference Paper: Text chunking for intonational phrase prediction in Chinese[Show abstract] [Hide abstract]
ABSTRACT: Two methods for intonational phrase (INP) prediction in Chinese TTS (text to speech) system are proposed, both of which exploit the information of base phrase (BP). Method 1 is called BP-based INP boundary prediction, in which, BPs in a sentence are recognized at first, then INP boundaries are predicted on the basis of words and recognized BPs. Method 2 is called BP-filtering INP boundary prediction, in which, recognized BPs are used to filter out some impossible boundaries. Decision tree (DT) was used as learning method for both BP recognition and INP boundary prediction. Comparing to the conventional method without BP recognition, the two methods proposed here achieved 3.6% and 5.6% reduction in the measure of unacceptability separately. More analysis shows that, by improving the performance of BP recognition, there is maximally 36.9% reduction in unacceptability.Natural Language Processing and Knowledge Engineering, 2003. Proceedings. 2003 International Conference on; 11/2003
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ABSTRACT: In magnetic resonance imaging (MRI), surface coils have the advantage of higher signal to noise ratio (SNR) but suffer from image inhomogeneity due to the non-uniform sensitivity profile. To remove bright spots caused by non-uniform sensitivity profiles, a gradient weighted smoothing method is discussed in this work. A partial differential equations (PDE) based model is applied for this locally adaptive smoothing. The filtered gradient of the corrupted image is used as the weight for smoothing. For accuracy evaluation, the energy of the histogram spectrum difference and the correlation of the intensity corrected image with the image acquired using the body coil are used as quantitative criteria. Clinical data collected on various MRI systems are used for evaluation of stability. The experimental results show that the proposed method is accurate and robust for intensity correction, and outperforms non-adaptive methods.Conference proceedings: ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Conference 02/2005; 3:3016-9. DOI:10.1109/IEMBS.2005.1617109
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ABSTRACT: Alterations in the p16/cyclinD1/Rb and ARF/Mdm2/p53 pathways are frequent events in the pathogenesis of squamous cell carcinomas. Different mechanisms of p16 regulation have been described for penile carcinomas so far. Therefore, expression of p16 and p53 was immunohistochemically detected with monoclonal antibodies in 52 primary invasive penile squamous cell carcinomas. The carcinomas were analyzed for allelic loss (LOH) in p16(INK4A) and p53, as well as for mutations in the p16(INK4A) and the p53 gene. In addition, we examined the promoter status of p16(INK4A) by methylation-specific PCR. The presence of human papilloma virus (HPV) 6/11, HPV 16 and HPV 18 DNA was analyzed by PCR. Data were compared to clinical data. Concerning p16, 26 (50%) tumors showed positive immunohistochemistry, 32 (62%) tumors showed allelic loss and 22 tumors (42%) showed promoter hypermethylation. All tumors with negative p16 immunohistochemistry showed LOH near the p16(INK4A) locus and/or hypermethylation of the p16(INK4A) promoter. HPV 16 DNA was detected in 17 tumors, ten of them with positive p16 immunostaining. The remaining seven tumors with negative p16 staining showed allelic loss and/or promoter hypermethylation. Evidence of lymph node metastasis was significantly associated with negative p16 immunohistochemistry as well as with combined LOH and promoter hypermethylation (p = 0.003 and p = 0.018, respectively). Allelic loss around p53 was found in 22 tumors (42%), and seven mutations of the p53 gene could be demonstrated in our tumors. No correlations could be found between any p53 alteration and clinical parameters.Archiv für Pathologische Anatomie und Physiologie und für Klinische Medicin 11/2010; 458(2):221-9. DOI:10.1007/s00428-010-1007-4 · 2.56 Impact Factor