scholarly journals PTH-015 Inflammatory reaction patterns and molecular genetics in high-grade colorectal adenomas

Author(s):  
Andrew Emmanuel ◽  
Salvador Diaz-Cano ◽  
Shraddha Gulati ◽  
Savvas Papagrigoriadis ◽  
Bu Hayee ◽  
...  
2019 ◽  
Vol 156 (6) ◽  
pp. S-838
Author(s):  
Andrew Emmanuel ◽  
Salvador Diaz-Cano ◽  
Shraddha Gulati ◽  
Margaret Burt ◽  
Savvas Papagrigoriadis ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-9
Author(s):  
Jakub Karczmarski ◽  
Krzysztof Goryca ◽  
Jacek Pachlewski ◽  
Michalina Dabrowska ◽  
Kazimiera Pysniak ◽  
...  

Accumulation of allelic variants in genes that regulate cellular proliferation, differentiation, and apoptosis may result in expansion of the aberrant intestinal epithelium, generating adenomas. Herein, we compared the mutation profiles of conventional colorectal adenomas (CNADs) across stages of progression towards early carcinoma. DNA was isolated from 17 invasive adenocarcinomas (ACs) and 58 large CNADs, including 19 with low-grade dysplasia (LGD), 21 with LGD adjacent to areas of high-grade dysplasia and/or carcinoma (LGD-H), and 28 with high-grade dysplasia (HGD). Ion AmpliSeq Comprehensive Cancer Panel libraries were prepared and sequenced on the Ion Proton. We identified 956 unique allelic variants; of these, 499 were considered nonsynonymous variants. Eleven genes (APC, KRAS, SYNE1, NOTCH4, BLNK, FBXW7, GNAS, KMT2D, TAF1L, TCF7L2, and TP53) were mutated in at least 15% of all samples. Out of frequently mutated genes, TP53 and BCL2 had a consistent trend in mutation prevalence towards malignancy, while two other genes (HNF1A and FBXW7) exhibited the opposite trend. HGD adenomas had significantly higher mutation rates than LGD adenomas, while LGD-H adenomas exhibited mutation frequencies similar to those of LGD adenomas. A significant increase in copy number variant frequency was observed from LGD through HGD to malignant samples. The profiling of advanced CNADs demonstrated variations in mutation patterns among colorectal premalignancies. Only limited numbers of genes were repeatedly mutated while the majority were altered in single cases. Most genetic alterations in adenomas can be considered early contributors to colorectal carcinogenesis.


2014 ◽  
Vol 146 (5) ◽  
pp. S-405
Author(s):  
Jianhua A. Tau ◽  
Joseph J. Cano ◽  
Yasser H. Shaib ◽  
Michael M. Pan

2011 ◽  
Vol 13 (4) ◽  
pp. 370-373 ◽  
Author(s):  
A. D. Toll ◽  
D. Fabius ◽  
T. Hyslop ◽  
E. Pequignot ◽  
A. J. DiMarino ◽  
...  

Author(s):  
Andrew Emmanuel ◽  
Salvador Diaz-Cano ◽  
Shraddha Gulati ◽  
Savvas Papagrigoriadis ◽  
Bu Hayee ◽  
...  

2008 ◽  
Vol 23 (2) ◽  
pp. 89-95 ◽  
Author(s):  
R. Vernillo ◽  
B. Lorenzi ◽  
T. Banducci ◽  
C. Minacci ◽  
C. Vindigni ◽  
...  

The aim of this study was to investigate the immunohistochemical expression of p53 and Ki67 in colorectal adenomas in order to clarify their significance as indicators of malignancy and development of new polyps. Seventy-eight polyps were removed from 51 patients and examined. Twenty-nine patients (56.9%) had adenomas with low-grade atypia (13 of them developed new polyps at 3-year follow-up) and 22 (43.1%) had adenomas with high-grade atypia (6 of them developed new polyps at 3-year follow-up). We tested the association between p53 and Ki67 expression and various clinicopathological variables, and regression analysis was performed to identify the risk factors for malignancy and development of new adenomas. A significant correlation between the grade of atypia and p53 immunoreactivity was observed. Ki67 expression was not related to atypia and no correlation was found between p53 and Ki67 immunoreactivity. Regression analysis showed that size (p=0.0002) and p53 staining (p=0.0111) were the selected factors related to malignant transformation, whereas the number of synchronous primary polyps emerged as the only predictive factor of development of new adenomas, although without statistical significance. The expression of biological markers may be in future added to the currently examined features of polyps; however, further studies are needed to better define their predictive value.


2005 ◽  
Vol 129 (11) ◽  
pp. 1398-1400 ◽  
Author(s):  
Chakshu Gupta ◽  
Paul F. Mazzara

Abstract Familial adenomatous polyposis (FAP) is caused by mutation of the adenomatous polyposis coli (APC) gene and is characterized by multiple colorectal adenomas and tumors of other organs and sites. A 58-year-old woman with FAP syndrome and previous total colectomy presented for routine follow-up examination. Abdominal ultrasound and subsequent endoscopic evaluation revealed ampullary and duodenal polyps, as well as inhomogeneity of the pancreatic head. A pancreaticoduodenectomy confirmed multiple duodenal adenomas. In addition, high-grade pancreatic intraepithelial neoplasia (PanIN-3) was found in the smaller pancreatic ducts. Pancreatic precancerous lesions have only rarely been described in FAP, including 2 pancreatic duct adenomas and 2 intraductal papillary mucinous neoplasms. A review of the world English literature revealed no reports of PanIN-3 in association with FAP. Further studies are required to determine if patients with FAP are at increased risk for pancreatic premalignant lesions.


1994 ◽  
Vol 103 (11) ◽  
pp. 911-914 ◽  
Author(s):  
Karen R. Cleary ◽  
John G. Batsakis

Advances in immunocytochemical phenotyping and molecular genetics have nearly resolved the histopathologic and therapeutic quandaries brought about by a diagnostic nomenclature that provided little guidance in the management of midfacial necrotizing lesions. Gone are terms like midline granuloma syndrome, lethal midline granuloma, polymorphic reticulosis, lymphomatoid granulomatosis, midline destructive granuloma, and idiopathic midline destructive disease. They have been replaced by the appreciation that the majority of the lesions are lymphomas of the sinonasal tract. The lymphomas are of B- or T-cell lineage and have a broad biologic spectrum from low to high grade. Still to be addressed are apparent geographic differences in biologic behavior, the epidemiologic significance of a preponderance of T-cell nasal lymphomas in the Orient, and optimum therapeutic regimens.


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