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M Stolte - One of the best experts on this subject based on the ideXlab platform.
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why is the hyperplastic polyp a marker for the Precancerous Condition of the gastric mucosa
Virchows Archiv, 2006Co-Authors: Klaus Dirschmid, Claudia Platzbaudin, M StolteAbstract:It is well known from the older literature that gastric carcinomas are more likely to develop in a stomach containing hyperplastic polyps. The reason why such a stomach should represent a Precancerous Condition is, however, largely unexplained. The aim of this study was to determine the disorders of the gastric mucosa in which hyperplastic polyps occur. In 244 patients with hyperplastic polyp, in whom at least two additional biopsies each from the antrum and corpus were available, gastritis was classified on the basis of the updated Sydney System. In none of the 244 patients was the gastric mucosa found to be normal. The most common disorder, at 51.3%, was autoimmune gastritis of the corpus mucosa, while chronic active Helicobacter pylori (Hp) gastritis was seen in 37.3% of the patients. Of the patients with Hp gastritis, 56.1% had corpus-dominant Hp gastritis. Other forms were relatively rare: when A-gastritis, corpus-dominant Hp gastritis and any other form of Hp gastritis were lumped together as a Precancerous Condition, these changes were found in 88.6% of the patients with hyperplastic polyps of the stomach. In the presence of hyperplastic polyps of the gastric mucosa, additional biopsies obtained from the antrum and corpus should always be performed to obtain a basis for deciding whether to apply Hp eradication treatment as potential carcinoma prophylaxis.
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the syndrome of juvenile polyposis
Leber Magen Darm, 1993Co-Authors: I Hofting, G Pott, M StolteAbstract:Juvenile polyposis (JP) was first distinguished from other gastrointestinal polyposis syndromes in 1964. Since then, some 272 cases of this entity have been reported in the literature. The underlying polyps found in JP are of the hamartomatous type, but it is known that juvenile polyps may contain adenomatous tissue, or may be accompanied by adenomas. For the most part, juvenile polyps are found in the colon, but may also develop in the stomach, duodenum, jejunum or ileum. In 20 to 50% of the cases, juvenile polyposis occurs as a familial Condition. Extra-intestinal anomalies are found in approximately 11% of JP patients. A particular clinical feature is anaemia caused by chronic gastrointestinal bleeding. In infants and young children, however, massive diarrhoea may become life-threatening. A reported malignant degeneration rate of 17.6% (among known cases) justifies the classification of JP as a Precancerous Condition, and has both therapeutic and, in particular, prophylactic consequences. These include the need to carry out regular follow-up examinations of the entire gastrointestinal tract, and also screening examinations in other members of the family.
B C Morson - One of the best experts on this subject based on the ideXlab platform.
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Juvenile polyposis--a Precancerous Condition.
Histopathology, 2007Co-Authors: Jeremy R. Jass, H. J. R. Bussey, C. B. Williams, B C MorsonAbstract:Clinical and pathological findings in 87 patients with juvenile polyposis have been reviewed; 1032 polyps were available from 80 of these patients; 840 were typical spherical juvenile polyps whereas 169 differed in being multilobulated or showing a villous configuration; 79 (46.7%) of the latter contained foci of epithelial dysplasia whereas only 76 (9.0%) of the typical juvenile polyps were dysplastic. The series also included 21 adenomas and two hyperplastic (metaplastic) polyps. The demonstration of dysplasia provides a histogenetic mechanism for the evolution of colorectal cancer from hamartomatous polyps; 18 juvenile polyposis patients have developed colorectal cancer at a mean age of 34 years (range 15-59). The clinical outcome was generally poor. No clinical or pathological distinction could be made between polyposis patients with and without colorectal cancer. Thus, the development of cancer in juvenile polyposis appears to be a random event. A working definition of juvenile polyposis is provided: (1) more than five juvenile polyps of the colorectum; and/or (2) juvenile polyps throughout the gastrointestinal tract; and/or (3) any number of juvenile polyps with a family history of juvenile polyposis. It is suggested that the Condition should be treated as seriously as familial adenomatous polyposis except that regular colonoscopic surveillance may obviate the need for prophylactic colectomy.
Senqing Chen - One of the best experts on this subject based on the ideXlab platform.
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analysis of small fragment deletions of the apc gene in chinese patients with familial adenomatous polyposis a Precancerous Condition
Asian Pacific Journal of Cancer Prevention, 2015Co-Authors: Qingwei Chen, Xiaomei Zhang, Jiannong Zhou, Xin Zhou, Ming Zhu, Yuanying Zhang, Jifeng Feng, Senqing ChenAbstract:Background Familial adenomatous polyposis (FAP) is an autosomal dominant inherited disease mainly caused by mutations of the adenomatous polyposis coli (APC) gene with almost complete penetrance. These colorectal polyps are Precancerous lesions that will inevitable develop into colorectal cancer at the median age of 40-year old if total proctocolectomy is not performed. So identification of APC germline mutations has great implications for genetic counseling and management of FAP patients. In this study, we screened APC germline mutations in Chinese FAP patients, in order to find novel mutations and the APC gene germline mutation characteristics of Chinese FAP patients. Materials and methods The FAP patients were diagnosed by clinical manifestations, family histories, endoscope and biopsy. Then patients peripheral blood samples were collected, afterwards, genomic DNA was extracted. The mutation analysis of the APC gene was conducted by direct polymerase chain reaction (PCR) sequencing for micromutations and multiplex ligation-dependent probe amplification (MLPA) for large duplications and/or deletions. Results We found 6 micromutations out of 14 FAP pedigrees, while there were no large duplications and/or deletions found. These germline mutations are c.5432C>T(p. Ser1811Leu), two c.3926_3930delAAAAG (p.Glu1309AspfsX4), c.3921_3924delAAAA (p.Ile1307MetfsX13), c3184_3187delCAAA(p.Gln1061AspfsX59) and c4127_4126delAT (p.Tyr1376LysfsX9), respectively, and all deletion mutations resulted in a premature stop codon. At the same time, we found c.3921_3924delAAAA and two c.3926_3930delAAAAG are located in AAAAG short tandem repeats, c3184_3187delCAAA is located in the CAAA interrupted direct repeats, and c4127_4128 del AT is located in the 5'-CCTGAACA-3' ,3'-ACAAGTCC-5 palindromes (inverted repeats) of the APC gene. Furthermore, deletion mutations are mostly located at condon 1309. Conclusions Though there were no novel mutations found as the pathogenic gene of FAP in this study, we found nucleotide sequence containing short tandem repeats and palindromes (inverted repeats), especially the 5 bp base deletion at codon 1309, are mutations in high incidence area in APC gene.
Eda Demir Onal - One of the best experts on this subject based on the ideXlab platform.
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is nodular gastritis a Precancerous Condition
Digestive Diseases and Sciences, 2012Co-Authors: Eda Demir OnalAbstract:I read with great interest the article by Hong et al. [1]. They analyzed clinico-epidemiological characteristics of 52 patients with nodular gastritis (NG) and 2,527 controls. Gastric neoplasm was detected in a single patient in the NG group (1.9 %) and in five patients in the control group (0.2 %). In this study NG was associated with increased gastric neoplasia, including gastric adenoma and adenocarcinoma based on multivariate analysis (odds ratio = 10.52, 95 % CI [1.20–92.0]). The authors stated that the clinical implication of this finding was unclear because the range of the 95 % CI was notably wide and a positive association between NG and gastric neoplasm could not be found in the subgroup analysis comparing the Helicobacter pylori (-) controls or H. pylori (?) controls [1]. The association between NG and gastric cancer have been previously suggested by various reports [2, 3]. The major limitation of these series and the present study is the small size of the study populations. It is not possible to conclude a significant relationship between NG and gastric cancer with a few malignant cases in each series. This subject necessitates a large population-based follow-up study from an epidemiological perspective. Another important point to note is that a plausible association between NG and gastric cancer should be supported by clinical and pathological evidence. We showed that the frequency of gastric ulcer (3.8 vs 7.1 %), atrophic gastritis (4.9 vs 12 %) and gastric polyp (2.2 vs 0.5 %) was not significantly more frequent in patients with NG [4]. Only 8.1 % of our patients had pangastritis and less than 5 % had nodules in other parts of the stomach. For this reason, topographically, NG cannot be regarded as a type of pangastritis (so a precursor of atrophic gastritis) as some authors suggested [3]. There was no case of gastric cancer among our 185 patients with NG [4]. In another study we examined the pathological characteristics of the cases with NG [5]. Our results showed that there was no difference between the patients with NG and the control regarding the features as presence of severe dysplasia, inflammatory activity, intestinal metaplasia and lymphoid hyperplasia. In conclusion NG cannot be accepted as a Precancerous Condition under the light of the pertinent literature.
Xi Wang - One of the best experts on this subject based on the ideXlab platform.
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expression of papillary thyroid carcinoma associated molecular markers and their significance in follicular epithelial dysplasia with papillary thyroid carcinoma like nuclear alterations in hashimoto s thyroiditis
International Journal of Clinical and Experimental Pathology, 2014Co-Authors: Jin Yan, Chao Zhang, Shenghui Qin, Lingzhi Qin, Liwei Liu, Xi WangAbstract:The aim of this study was to evaluate the expression of papillary thyroid carcinoma (PTC)-associated tumor markers in follicular epithelial dysplasia showing PTC-like nuclear alterations (FED) in Hashimoto's thyroiditis (HT) and to explore the relationship between HT and PTC. In this study, 43 PTC, 18 HT with FED and 16 peritumoral benign thyroid tissues were immunohistochemically analyzed for CK19, galectin-3, HBME-1, CD56, claudin-1 and NGAL expression. Our research revealed that in HT, the expression of CK19, galectin-3, HBME-1, claudin-1 and NGAL was focal and limited to FED, while CD56 was strongly positive in FED and most Hurthle cells. The stain intensity of CK19, claudin-1 and NGAL in FED decreased compared with PTC, but were significantly higher than that in peritumoral benign thyroid tissues (all P 0.05). In conclusion, In HT, FED might be a Precancerous Condition closely associated with PTC development as they have overlaps in cytological and immunomarker profiles, indicating that in patients with HT, under prolonged stimuli from chronic inflammation, part of follicular epithelia may show regeneration, hyperplasia, Hurthle cell metaplasia and dysplasia, eventually malignant transformation. Hence, long term follow-up and regular inspection would be necessary for Hashimoto's thyroiditis with FED.