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• W2977555297 abstract "Introduction: Sessile serrated adenomas/polyps (SSAs) are often right sided and are characterized by wide-bottomed crypts, disordered maturation, and dystrophic goblet cells. SSAs frequently progress to cancer via MLH1 methylation silencing and the acquisition of DNA mismatch repair deficiency. Little is known about clinical or pathogenetic differences between MLH1 intact and MLH1 deficient lesions. The aim of our study was to identify cases of either high-grade dysplasia (SSAHD) or adenocarcinoma (SSACA) that had undergone MLH1 immunohistochemical staining, and compare lesion characteristics and demographics in patients harboring MLH1 intact versus MLH1 deficient lesions. Methods: From a computerized database we extracted all cases of SSAHD (n=85) and SSACA (n=67) that had undergone immunohistochemical staining for MLH1. The cases were then categorized as MLH1 intact or deficient, and patient demographics and lesion characteristics were compared utilizing unadjusted odds ratios (ORs) and Chi-squared test. Results: Overall, loss of MLH1 expression was present in 92/152 (61%) lesions, and was significantly more frequent in SSAHD than SSACA (42/85 [49.4%] vs. 50/67 [74.6%]; p<0.01). The mean age of MLH1-intact SSAHD was significantly lower than MLH1-deficient SSAHD (67.7 years vs. 74.5 years ± 1.1; p<0.001). The mean age of MLH1-intact SSACA was lower than MLH1-deficient SSACA (70.2 years vs. 74.4 years), although not significant. There was a trend that MLH1-intact SSAHD and SSACA were more likely to be men (42% and 29% vs. 33% and 22%). Left-sided location was more frequent in MLH1-intact SSAHD (11/43; 26%) and SSACA (5/17; 29%) than in MLH1-deficient SSAHD (6/42; 15%) and SSACA (5/50; 10%; p<0.05 for combined SSAHD/SSACA). Finally, MLH1-intact SSAHD and SSACA were on average endoscopically smaller than their MLH1-deficient counterparts (6.8 mm and 6.0 mm vs. 11.0 mm and 13.4 mm). Conclusion: Loss of MLH1 is frequent in the pathogenesis of both SSAHD and SSACA, and is positively associated with increasing age, female gender, right-sided location, and increasing size. These findings indicate that there are differences in the risks and pathogenesis of MLH1 loss in the progression of SSAs in different clinical settings. The higher frequency of MLH1 loss in SSACA could be the result of MLH1 loss in the late stages of tumor progression in some cases. Alternatively, the findings could be explained by a higher risk of cancer progression or more rapid cancer progression in MLH1-deficient SSAHDs, a hypothesis that is supported by the similar average age in MLH1-deficient SSAHD and SSACA. Better understanding of the pathogenesis and associations of these different lesions could have implications for improved screening and detection of advanced lesions in patients with SSAs. Disclosure - Yes, both authors (Redston, Turner) are employees of Miraca Life Sciences." @default.
• W2977555297 created "2019-10-10" @default.
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• W2977555297 date "2014-10-01" @default.
• W2977555297 modified "2023-10-18" @default.
• W2977555297 title "Pathogenetic Differences in the Progression of MLH1 Intact and Deficient Sessile Serrated Adenomas" @default.
• W2977555297 doi "https://doi.org/10.14309/00000434-201410002-02053" @default.
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