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| 1 | Clinical and molecular features of young-onset colorectal cancer显示文摘Colorectal cancer(CRC) is one of the leading causes of cancer related mortality worldwide. Although young-onset CRC raises the possibility of a hereditary component, hereditary CRC syndromes only explain a minority of young-onset CRC cases. There is evidence to suggest that young-onset CRC have a different molecular profile than late-onset CRC. While the pathogenesis of young-onset CRC is well characterized in individuals with an inherited CRC syndrome, knowledge regarding the molecular features of sporadic young-onset CRC is limited. Understanding the molecular mechanisms of young-onset CRC can help us tailor specific screening and management strategies. While the incidence of late-onset CRC has been decreasing, mainly attributed to an increase in CRC screening, the incidence of young-onset CRC is increasing. Differences in the molecular biology of these tumors and low suspicion of CRC in young symptomatic individuals, may be possible explanations. Currently there is no evidence that supports that screening of average risk individuals less than 50 years of age will translate into early detection or increased survival. However, increasing understanding of the underlying molecular mechanisms of young-onset CRC could help us tailor specific screening and management strategies. The purpose of this review is to evaluate the current knowledge about young-onset CRC, its clinicopathologic features, and the newly recognized molecular alterations involved in tumor progression. | Veroushka Ballester Shahrooz Rashtak Lisa Boardman | 2016 | World Journal of Gastroenterology2016，22，5： | 9 |
| 2 | Colonoscopy surveillance for high risk polyps does not always prevent colorectal cancer显示文摘AIM To determine the frequency and risk factors for colorectal cancer(CRC) development among individuals with resected advanced adenoma(AA)/traditional serrated adenoma(TSA)/advanced sessile serrated adenoma(ASSA). METHODS Data was collected from medical records of 14663 subjects found to have AA, TSA, or ASSA at screening or surveillance colonoscopy. Patients with inflammatory bowel disease or known genetic predisposition for CRC were excluded from the study. Factors associated with CRC developing after endoscopic management of high risk polyps were calculated in 4610 such patients who had at least one surveillance colonoscopy within 10 years following the original polypectomy of the incident advanced polyp. RESULTS84/4610(1.8%) patients developed CRC at the polypectomy site within a median of 4.2 years(mean 4.89 years), and 1.2%(54/4610) developed CRC in a region distinct from the AA/TSA/ASSA resection site within a median of 5.1 years(mean 6.67 years). Approximately, 30%(25/84) of patients who developed CRC at the AA/TSA/ASSA site and 27.8%(15/54) of patients who developed CRC at another site had colonoscopy at recommended surveillance intervals. Increasing age; polyp size; male sex; right-sided location; high degree of dysplasia; higher number of polyps resected; and piecemeal removal were associated with an increased risk for CRC developmentat the same site as the index polyp. Increasing age; right-sided location; higher number of polyps resected and sessile endoscopic appearance of the index AA/TSA/ASSA were significantly associated with an increased risk for CRC development at a different site. CONCLUSION Recognition that CRC may develop following AA/TSA/ASSA removal is one step toward improving our practice efficiency and preventing a portion of CRC related morbidity and mortality. | Mohamad A Mouchli Lidia Ouk Marianne R Scheitel Alisha P Chaudhry Donna Felmlee-Devine Diane E Grill Shahrooz Rashtak Panwen Wang Junwen Wang Rajeev Chaudhry Thomas C Smyrk Ann L Oberg Brooke R Druliner Lisa A Boardman | 2018 | World Journal of Gastroenterology2018，24，8： | 5 |
| 3 | Spontaneous lupus-like syn- drome in HLA-DQ2 transgenic mice with a mixed genetic background 显示文摘 | Rashtak S Marietta E Cheng S | 2010 | Lupus2010，19，7： | 1 |
| 4 | From fu- runcle to axillary web syndrome:shedding light on histopathology and pathogenesis 显示文摘 | Rashtak S Gamble G L Gibson L E | 2012 | Dermatology2012，224，2： | 1 |
| 5 | Skin involvement in systemic autoimmune diseases显示文摘 | Rashtak S Pittelkow MR | 2008 | Curr Dir Autoimmun2008，10，： | 1 |
| 6 | Comparative Usefulness of Deamidated Gliadin Antibodies in the Diagnosis of Celiac Disease显示文摘 | Shadi Rashtak Michael W. Ettore Henry A. Homburger Joseph A. Murray | 2008 | Clinical Gastroenterology and Hepatology2008，，： | 1 |
| 7 | Skin involvement in systemic autoimmune diseases显示文摘 | RASHTAK S PITFELKOW M R | 2008 | Curr Dir Autoimmun2008，10，： | 1 |
| 8 | From furuncle to axillary web syndrome:shedding light on histopathology and pathogenesis显示文摘 | Rashtak S Gamble GL Gibson LE | | 0，，02： | 1 |
| 9 | Skin involvement in systemic autoimmune diseases显示文摘 | Rashtak S Pittelkow MR | | 0，，： | 1 |
| 10 | Correlation analysis of celiac sprue tissue transglutaminase and deamidated gliadin IgG/IgA显示文摘AIM:To indirectly determine if tissue transglutaminase(tTG)-specific T cells play a crucial role in the propagation of celiac disease.METHODS:Anti-deamidated gliadin peptide(DGP) and anti-tTG IgA and IgG were measured in the sera of celiac patients(both untreated and treated).The correlations were determined by Spearman's rank correlation test.RESULTS:In celiac patients,we found a very significant correlation between the production of DGP IgA and IgG(r = 0.75),indicating a simultaneous and ongoing production of these two isotypes reminiscent of oral vaccination studies.However,there was far less association between the production of tTG IgA and tTG IgG in celiac patients(r = 0.52).While tTG IgA was significantly correlated with DGP IgA(r = 0.80) and DGP IgG(r = 0.67),there was a weak correlation between production of anti-tTG IgG and the production of anti-DGP IgA(r = 0.38) and anti-DGP IgG(r = 0.43).CONCLUSION:These data demonstrate that the production of anti-tTG IgA is directly correlated to the production of anti-DGP IgG and IgA,whereas anti-tTG IgG is only weakly correlated.This result therefore supports the hapten-carrier theory that in well-established celiac patients anti-tTG IgA is produced by a set of B cells that are reacting against the complex of tTG-DGP in the absence of a tTG-specific T cell. | Eric V Marietta Shadi Rashtak Joseph A Murray | 2009 | World Journal of Gastroenterology2009，15，7： | 0 |
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