Objectives: This study aimed to clarify the validity and long-term outcomes of colorectal endoscopic submucosal dissection (ESD) of visible lesions (≥20 mm) in patients with ulcerative colitis (UC) and investigate the incidence of undetected lesions in surgical specimens.Methods: This single-center retrospective study included 11 lesions from nine patients with UC who underwent ESD and 19 lesions from nine patients with UC who underwent colectomy between March 2001 and January 2019. We evaluated the endoscopic findings of scarring, atrophy, and loss of haustra in the ESD group, and we determined the lesion visibility in the colectomy group. We investigated the clinicopathological features of all lesions and examined the follow-up evaluations in the ESD group. Results:The en bloc and curative resection rates of ESDs were 91% and 82%, respectively. Endoscopic findings of scarring, atrophic colitis, and loss of haustra were observed in two (18%), seven (64%), and one (9%) lesions, respectively. The two lesions with scarring showed severe submucosal fibrosis. Mortality and recurrence were not observed during the median follow-up of 25 months. Metachronous lesions ≥20 mm were detected in two patients, which were successfully treated with ESDs. In the colectomy specimens, 21% of the lesions were undetected, 67% had multiple neoplasms, and 33% had multiple invasive cancers.Conclusions: ESD is feasible and valid for large visible lesions in patients with UC; however, for lesions with endoscopic findings of scarring, technical difficulties in endoscopic resection must be considered. In addition, intensive surveillance colonoscopy is necessary to detect undetected lesions.This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
BackgroundColorectal adenoma develops into cancer with the accumulation of genetic and epigenetic changes. We studied the underlying molecular and clinicopathological features to better understand the heterogeneity of colorectal neoplasms (CRNs).MethodsWe evaluated both genetic (mutations of KRAS, BRAF, TP53, and PIK3CA, and microsatellite instability [MSI]) and epigenetic (methylation status of nine genes or sequences, including the CpG island methylator phenotype [CIMP] markers) alterations in 158 CRNs including 56 polypoid neoplasms (PNs), 25 granular type laterally spreading tumors (LST-Gs), 48 non-granular type LSTs (LST-NGs), 19 depressed neoplasms (DNs) and 10 small flat-elevated neoplasms (S-FNs) on the basis of macroscopic appearance.ResultsS-FNs showed few molecular changes except SFRP1 methylation. Significant differences in the frequency of KRAS mutations were observed among subtypes (68% for LST-Gs, 36% for PNs, 16% for DNs and 6% for LST-NGs) (P<0.001). By contrast, the frequency of TP53 mutation was higher in DNs than PNs or LST-Gs (32% vs. 5% or 0%, respectively) (P<0.007). We also observed significant differences in the frequency of CIMP between LST-Gs and LST-NGs or PNs (32% vs. 6% or 5%, respectively) (P<0.005). Moreover, the methylation level of LINE-1 was significantly lower in DNs or LST-Gs than in PNs (58.3% or 60.5% vs. 63.2%, P<0.05). PIK3CA mutations were detected only in LSTs. Finally, multivariate analyses showed that macroscopic morphologies were significantly associated with an increased risk of molecular changes (PN or LST-G for KRAS mutation, odds ratio [OR] 9.11; LST-NG or DN for TP53 mutation, OR 5.30; LST-G for PIK3CA mutation, OR 26.53; LST-G or DN for LINE-1 hypomethylation, OR 3.41).ConclusionWe demonstrated that CRNs could be classified into five macroscopic subtypes according to clinicopathological and molecular differences, suggesting that different mechanisms are involved in the pathogenesis of colorectal tumorigenesis.
There are several reports on the correlation between early tumor shrinkage (ETS) or depth of response (DpR) and survival in chemotherapies for colorectal cancer; however, few studies have investigated it in pancreatic cancer. We therefore investigated whether the ETS will predict outcomes in 59 patients with advanced pancreatic cancer treated with FOLFIRINOX therapy. The association of ETS with progression-free survival (PFS) and overall survival (OS) was evaluated but also we addressed to the correlation between outcomes and DpR. ETS was defined as a reduction ≥ 20% of target lesions' diameters measured at 6 to 8 weeks from treatment start. DpR was percentage of maximal tumor shrinkage observed at the nadir diameter compared with baseline. Among 47 evaluable patients for the ETS, 12 (25.5%) patients experienced ETS. The ETS was significantly associated with better PFS (9.0 vs. 4.2 months) as well as OS (24.0 vs. 9.1 months); moreover, the association had a statistically significance for PFS but a strong trend for OS in multivariate analysis. The DpR was statistically significantly but weakly associated with OS. In conclusion, this is the first report that the early response to chemotherapy may predict favorable outcomes in patients with advanced pancreatic cancer treated with FOLFIRINOX therapy.
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