scholarly journals Sessile serrated adenomas: prevalence of dysplasia and carcinoma in 2139 patients

2010 ◽  
Vol 63 (8) ◽  
pp. 681-686 ◽  
Author(s):  
Richard H Lash ◽  
Robert M Genta ◽  
Christopher M Schuler

Background and aimsSessile serrated adenomas (SSAs) are recognised as precursors to microsatellite unstable adenocarcinomas. This study attempts to estimate the progression rate of SSAs based upon the epidemiology of a large cohort as well as identify relationships to other colorectal polyps.MethodsPathological reports generated at Caris Diagnostics from 290 810 colonoscopic specimens on 179 111 patients were analysed using computerised algorithms.ResultsSSAs with or without dysplasia/carcinoma (SSA+/–) were identified in 2416 specimens from 2139 patients (54% women). The distribution of SSA+/– was: right-sided (81.2%); left-sided (11.2%); both right- and left-sided (3.2%); not specified (4.3%). There were 1816 (85%) patients without dysplasia (SSA–), 257 (12%) with low-grade dysplasia (SSA-LD), 45 (2%) with high-grade dysplasia (SSA-HD) and 21 (1%) with adenocarcinoma (SSA-CA). The difference in median age between almost all groups was significant (SSA–=61 years versus SSA-LD=66 years (p<0.001) vs SSA-HD=72 years (p=0.002) vs SSA-CA=76 years (p=0.07, NS)). Women comprised 53% of the SSA– group (968/1816), 57% of the SSA-LD group (147/257), 69% of the SSA-HD group (31/45) and 76% of the SSA-CA group (16/21), being more likely to have high-grade dysplasia (OR 1.94, 95% CI 1.03 to 3.67) and adenocarcinoma (OR 2.80, 95% CI 1.02 to 7.68).Conclusions1.7% of patients with mucosal polyps had SSAs (with and without dysplasia), more commonly in women and primarily in the right colon. Dysplasia or carcinoma was identified in 15% of patients and significantly disproportionately among women. Based on significant age differences between groups, there appears to be a stepwise progression of dysplasia and carcinoma in SSAs over 10 to 15 years, a period two to three times longer than that for conventional adenomas.

2007 ◽  
Vol 64 (11) ◽  
pp. 753-758
Author(s):  
Vesna Zivkovic ◽  
Aleksandar Petrovic ◽  
Biljana Djordjevic ◽  
Vuka Katic ◽  
Jasmina Gligorijevic ◽  
...  

Background/Aim. The aim of this study was to apply computer- assisted methodology in assessment of Ki-67 positivity in "adenoma-like" dysplasia associated lesions or masses (DALMs), and carcinoma in ulcerative colitis (UC), and to determine a new approach to grading of Ki-67 staining intensity. Methods. Immunohistochemical slides were quantitatively analyzed for estimation of proportion and intensity of Ki-67 positive-stained cells in a total of 50 "adenoma-like" DALMs (27 with low-grade dysplasia and 23 with high-grade dysplasia), and 17 adenocarcinomas associated with UC. The four grades of immunohistochemical staining intensity were established by an automated classification of nuclear optical densities. Results. The Ki-67 labeling index (LI) in low-grade dysplasia was significantly lower than in high-grade dysplasia, and carcinoma (p < 0.001). The Ki-67 LI of carcinomas was not significantly different from the value obtained in highgrade dysplasia (p > 0.05), however having the difference in percentage values of the moderate stained nuclei (p < 0.05). The overall average values of chromogene nuclear optical density, showed statistically significant differences between DALMs and carcinoma (p < 0.05), although not between normal mucosa and low-grade dysplasia (p > 0.05). Conclusion. The obtained results imply, according to the overall percentage of labeled nuclei, that high-grade dysplasia is very close to carcinoma, while there is the difference in the percentage of moderately stained nuclei. We showed that Ki-67 positivity have a different internal distribution which could be useful in analysing these lesions. These findings also, indicate the important biological differences between low-grade dysplasia and carcinoma in UC, and a low proliferative potential of the former. Automated image analysis permits an objective estimation of Ki-67 immunohistochemical staining in UCassociated dysplasia and carcinoma.


2012 ◽  
Vol 30 (4_suppl) ◽  
pp. 468-468
Author(s):  
Chara Papadaki ◽  
Maria Sfakianaki ◽  
Zacharenia Saridaki ◽  
Georgios Giagas ◽  
Kyriakos Mpananis ◽  
...  

468 Background: Tumor cells have been shown to express exclusively the embryonic M2 isoform of pyruvate kinase (PKM2), which is a key enzyme that regulates aerobic glycolysis in tumor cells. Use of RNA interfering (RNAi) targeting PKM2 significantly inhibits tumor growth when combined with cisplatin in xenograft models. We evaluated the predictive significance of PKM2 in patients with “high” risk stage II or stage III colon cancer treated with oxaliplatin-fluoropyrimidines chemotherapy adjuvant treatment. Methods: FFPE primary tumours from 261 patients with stage II or III colon cancer with colon cancer were analyzed for PKM2 mRNA expression by RT-qPCR. All patients had received adjuvant treatment with an oxaliplatin and fluoropyrimidine combination. Also, match normal mucosas from 50 of these patients have been analyzed. Finally, 50 polyps (20 with low grade dysplasia, 20 high grade dysplasia and 10 serrated adenomas) from non-colon cancer patients were included in the for PKM2 mRNA expression by RT-qPCR. The analysis was performed with a set of primers and probes which amplify only the M2 isoform. Results: PKM2 mRNA expression was significantly higher in tumor areas in comparison with normal mucosa (p=0.001) and low-grade adenomas (p=0.001) as well as in tumors with BRAF mutations (p=0.001). Adenomas with high-grade dysplasia (p=0.002) and serrated adenomas (p=0.001) presented significantly higher PKM2 mRNA expression. Overexpression of PKM2 was associated with significantly lower Disease Free (p=0.018) and Overall Survival (p=0.031). Multivariate analysis revealed PKM2 high mRNA expression as independent prognostic factors for decreased DFS (HR: 2.1, p=0.003) and OS (HR: 1.8, p=0.019). Conclusions: These results provide evidence that the PKM2 mRNA expression could be used as prognostic/predictive marker for disease recurrence in patients with operable colon cancer. Analysis of the PKM2 mRNA expression in patients treated with non-oxaliplatin containing adjuvant treatment is currently performed.


Author(s):  
Amy L Lightner ◽  
Sarah Vogler ◽  
John McMichael ◽  
Xue Jia ◽  
Miguel Regueiro ◽  
...  

Abstract Background We sought to determine the rate of progression from dysplasia to adenocarcinoma in ulcerative colitis [UC] vs Crohn’s diseases [CD] and describe the risk factors unique to each. Methods All adult patients [≥18 years] with a known diagnosis of either UC or CD who underwent a surveillance colonoscopy between January 1, 2010 and January 1, 2020 were included. Results A total of 23 751 surveillance colonoscopies were performed among 12 289 patients between January 1, 2010 and January 1, 2020; 6909 [56.2%] had a diagnosis of CD and 5380 [43.8%] had a diagnosis of UC. There were a total of 668 patients [5.4%] with low-grade dysplasia [LGD], 76 patients [0.62%] with high-grade dysplasia [HGD], and 68 patients [0.55%] with adenocarcinoma in the series; the majority of the dysplastic events were located in the right colon. Significantly more UC patients had a dysplastic event, but the rate of LGD and HGD dysplasia progression to adenocarcinoma was not significantly different in CD or UC [p = 0.682 and p = 1.0, respectively]. There was no significant difference in the rate of progression from LGD/HGD to adenocarcinoma based on random biopsies vs targeted biopsies of visible lesions [p = 0.37]. However, the rate of progression from LGD vs HGD to adenocarcinoma was significantly greater for HGD [p &lt; 0.001]. Conclusion While more UC patients were found to have neoplasia on colonoscopy, the rate of progression from LGD and HGD to adenocarcinoma was equivalent in UC and CD, suggesting that endoscopic surveillance strategies can remain consistent for all IBD patients.


2019 ◽  
Vol 152 (Supplement_1) ◽  
pp. S75-S75
Author(s):  
Adebayo Adedotun ◽  
Lateef Odukoya ◽  
Kabir Badmos

Abstract Introduction Death from colorectal cancer is still a major concern in low- and middle-income countries. According to GLOBOCAN 2018 report, 1,096,601 new cases of colorectal cancer were reported worldwide and about 551,269 would die from the disease process. Colorectal cancer is the fifth most common cancer and accounts for 5.8% of all new cases seen annually in Nigeria. It has been shown incontrovertibly that neoplastic polyps are precursors to adenocarcinomas, even though the rate is lower among blacks. The increasing awareness and availability of colonoscopy in Nigeria have resulted in an increased volume of colonic biopsy for histopathologic examination. This has resulted in increased frequency of detection of colorectal neoplastic polyps. Aim This study aims at auditing colorectal neoplastic polyps histopathologic reporting in Lagos University Teaching Hospital over a 10-year period (2009-2018). Methods All reports of colorectal polyps within the study period (2008-2018) were retrieved from the departmental database. The histologic type, microscopic dimensions, and anatomic locations of these polyps were documented and analyzed. Results Seventy-two colorectal neoplastic polyps were reported with an M:F ratio of 2:1. The peak incidence was in the fifth decade, with 98% of the polyps in the colon. A breakdown of the adenomatous polyps showed that most (66.7%) were tubular, and 33.2% were tubulovillous adenoma and a case of villous adenoma. Majority of the lesions had low-grade dysplasia while 30% had high-grade dysplasia. There was no mention of excision margins, and in some cases, the biopsy site was not stated. Conclusion Some of these polyps, particularly those with high-grade dysplasia, may likely progress to colorectal carcinoma following the adenoma-carcinoma sequence. Epidemiological data of precursor lesions are relevant as an accurate predictor of colorectal cancer incidence in the coming decade and as a determinant in the evaluation of screening and surveillance practices.


2014 ◽  
Vol 23 (2) ◽  
pp. 161-170 ◽  
Author(s):  
Claudiu Margaritescu ◽  
Daniel Pirici ◽  
Irina Cherciu ◽  
Alexandru Barbalan ◽  
Tatiana Cârtâna ◽  
...  

Background & Aims: Colorectal cancer represents the third most common malignancy and the fourth most common cause of cancer death worldwide. The existence of drug-resistant colon cancer stem cells is thought to be one of the most important reasons behind treatment failure in colon cancer, their existence putatively leading to metastasis and recurrences. The aim of our study was to investigate the immunoexpression patterns of CD133 and CD166 in colon carcinoma, both individually and in combination, assessing their significance as prognostic markers.Methods. A total of 45 retrospective colon adenocarcinoma cases were investigated by enzymatic and multiple fluorescence immunohistochemistry for their CD133 and CD166 expression and colocalization.Results. Both CD133 and CD166 were expressed to different extents in all cancer specimens, with apredominant cytoplasmic pattern for CD133 and a more obvious membranous-like pattern for CD166.Overall, when comparing their reactivity for the tumoral tissue, CD166 expression areas seemed to be smaller than those of CD133. However, there was a direct correlation between CD133 and CD166 expression levels throughout the entire spectrum of lesions, with higher values for dysplastic lesions. Colocalization of CD133/ CD166 was obvious at the level of cells membranes, with higher coeficients in high grade dysplasia, followed by well and moderate differentiated tumours.Conclusions. CD133/CD166 colocalization is an early event occurring in colon tumorigenesis, with thehighest coeficients recorded for patients with high grade dysplasia, followed by well differentiated tumours. Thus, we consider that the coexpression of these two markers could be useful for further prognostic andtherapeutically stratification of patients with colon cancer.Abbreviations: AJCC - American Joint Committee on Cancer; CCD - charge-coupled device camera sensor; CD133 - prominin-1 (PROM1); CD166 - Activated Leukocyte Cell Adhesion Molecule (ALCAM); CRC - colorectal cancer; CSC - cancer stem cells; DAB - 3,3'-diaminobenzidine chromogen; DAPI - 4',6-diamidino- 2-phenylindole; HE - Hematoxylin and eosin staining; HGD - high grade dysplasia; HRP - horseradish peroxidase; LGD - low grade dysplasia; SDS - sodium dodecyl sulfate*Part of this work has been accepted as a poster presentation at the Digestive Disease Week (DDW) meeting, Chicago, IL, USA May 3-6, 2014


2021 ◽  
Vol 4 (Supplement_1) ◽  
pp. 117-118
Author(s):  
D Maillet ◽  
E Desilets ◽  
T Maniere

Abstract Background Endoscopic submucosal dissection (ESD) is an endoscopic procedure developed in Asian countries to treat early gastric cancer (EGC). Western countries have less experience with this challenging technique. Aims The goal of this study is to evaluate the effectiveness of ESD as a preliminary experience. Methods This is an unicentric retrospective study of all consecutive gastric ESD for adenomas or EGC from 07/2017 to 08/2020. The primary endpoints were en bloc and R0 resection rates. Results Nineteen patients (mean age 74.2 (54–88), sex ratio 3F/16M) and 23 lesions were included. Mean diameter was 25 mm (10–90). Treatment was previously performed in 7 cases (30.4%), by ESD (5) or EMR (2). The procedure, performed under general anaesthesia, lasted on average 148 minutes (45–412). En bloc resections were performed in 16 cases (69.6%); 5 cases (21.7%) were converted to P-EMR and there was a failure to resect the lesion because of deep invasion or perforation in 2 cases (8.7%). Pathologic examination demonstrated 2 low-grade dysplasia, 4 high-grade dysplasia and 15 adenocarcinomas: intramucosal (8), sm1 (2), sm2 (2), sm3 (1) or sm deep (2). R0 and curative resection rates were 43.5% and 39.1% respectively. The complication rate related to the procedure was 30.4% including 5 perforations and 2 delayed bleeding: all were managed endoscopically. Five patients (21.7%) underwent subsequent gastrectomy for non-curative resection (4) or failed resection (1); 3 had no residual disease on final pathology, 1 had high grade dysplasia and 1 had intramucosal adenocarcinoma. One patient went to palliative care because he was unfit for surgery. Follow-up endoscopy was completed in all 17 patients who underwent endoscopic resection (mean 10 months (2–24)). Recurrence occurred in 23.5% (4/17); all were successfully treated by another ESD. Conclusions In our preliminary experience, the rate of en bloc and R0 resection were 70% and 44%. Compared to other studies, these low en bloc and curative resection rates may be explained by technically difficult lesions during the learning curve and might improve with experience. Nevertheless, surgery has been avoided in 13/19 patients (68%) with endoscopic intervention. Funding Agencies None


2010 ◽  
Vol 134 (10) ◽  
pp. 1479-1484 ◽  
Author(s):  
John R. Goldblum

Abstract Context.—Pathologists frequently assess esophageal biopsy specimens to “rule out Barrett esophagus,” as well as to assess for the presence or absence of dysplasia. Objective.—To review some of the recent controversies in the diagnosis of Barrett esophagus and Barrett-related dysplasia. Data Sources.—Sources were the author's experience and review of the English literature from 1978 to 2009. Conclusions.—Although goblet cells are required by the American College of Gastroenterology to confirm a diagnosis of Barrett esophagus, this definition might expand to include columnar-lined esophagus without goblet cells. The recognition of dysplasia in Barrett esophagus remains a difficult task for the surgical pathologist, with difficulties in distinguishing reactive epithelium from dysplasia, low-grade dysplasia from high-grade dysplasia, and even high-grade dysplasia from intramucosal adenocarcinoma.


2003 ◽  
Vol 48 (2) ◽  
pp. 43-45 ◽  
Author(s):  
E F Shen ◽  
S Gladstone ◽  
G Milne ◽  
S Paterson-Brown ◽  
I D Penman

Management of columnar lined oesophagus (CLO; Barrett s oesophagus) is controversial. We prospectively audited surveillance practices in Scotland and prospectively assessed the impact of introducing local guidelines for Barrett s surveillance in Edinburgh. Most respondents were gastroenterologists. The majority take random, not four quadrant, biopsies from the CLO. In Edinburgh during 2000, 80 patients underwent surveillance. The guideline protocol was not followed in 30 (37.5%) patients. Follow up of patients without dysplasia generally conformed to the guidelines. Follow up of patients with low grade dysplasia was highly variable while management of those with high grade dysplasia followed the guidelines. Overall we found a wide variability in the management and surveillance of CLO. Early experience suggests that implementation of guidelines is helpful but there is still variation in practice.


Author(s):  
K Y Song ◽  
A J Henn ◽  
A A Gravely ◽  
H Mesa ◽  
S Sultan ◽  
...  

SUMMARY Patients with Barrett's esophagus (BE) and low-grade dysplasia (LGD) are at increased risk of esophageal adenocarcinoma (EAC), although many regress to nondysplastic BE. This has significant clinical importance for patients being considered for endoscopic eradication therapy. Our aim is to determine the risk for progression in patients with confirmed persistent LGD. We performed a single-center retrospective cohort study of patients with BE and confirmed LGD between 2006 and 2016. Confirmed LGD was defined as LGD diagnosed by consensus conference with an expert GI pathologist or review by an expert GI pathologist and persistence as LGD present on subsequent endoscopic biopsy. The primary outcome was the incidence rate of HGD (high-grade dysplasia)/EAC. Secondary outcomes included risk factors for dysplastic progression. Risk factors for progression were assessed using univariate and multivariate analysis with logistic regression. Of 69 patients (mean age 65.2 years) with confirmed LGD were included. In total, 16 of 69 patients (23.2%) with LGD developed HGD/EAC during a median follow-up of 3.74 years (IQR, 1.24–5.45). For persistent confirmed LGD, the rate was 6.44 (95% confidence interval (CI), 2.61–13.40) compared to 2.61 cases per 100 patient-years (95% CI, 0.83–6.30) for nonpersistent LGD. Persistent LGD was found in only 29% of patients. Persistent LGD was an independent risk factor for the development of HGD/EAC (OR 4.18; [95% CI, 1.03–17.1]). Persistent confirmed LGD, present in only 1/3 of patients, was an independent risk factor for the development of HGD/EAC. Persistence LGD may be useful in decision making regarding the management of BE.


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