Objective: Serrated adenoma is recognized as a precancerous lesion of colorectal cancer, and the serrated pathway is considered as an important pathway that can independently develop into colorectal cancer. However, little is known about the related risk factors of carcinogenesis of serrated adenoma. The purpose of this study was to analyze the distribution characteristics and potential malignant factors of serrated adenoma in the colon and rectum. Methods: A retrospective case-control study was conducted to collect the clinical data of patients with serrated adenoma who underwent colonoscopy and were pathologically diagnosed in the Cancer Hospital of Chinese Academy of Medical Sciences from April 2017 to July 2019, and exclude patients with two or more pathological types of lesions. The clinical characteristics of serrated adenoma were summarized, and univariate and logistic multivariate regression analysis was conducted to explore the influencing factors for serrated adenoma to develop malignant transformation. Results: Among 28 730 patients undergoing colonoscopy, 311 (1.08%) were found with 372 serrated adenomas, among which 22 (5.9%) were sessile serrated adenomas/polyps, 84 (22.6%) were traditional serrated adenomas, and 266 (71.5%) were unclassified serrated adenomas according to WHO classification. The pathological results showed that 106 (28.5%) lesions were non-dysplasia, 228 (61.3%) lesions were low grade intraepithelial neoplasia, and 38 (10.2%) lesions were high grade intraepithelial neoplasia or cancer. There were 204 (54.8%) lesions with long-axis diameter <10 mm and 168 (45.2%) lesions with length long-axis ≥ 10 mm. 238 (64.0%) lesions were found in the left side colon and rectum and 134 (36.0%) lesions in the right side colon. Gross classification under endoscopy: 16 flat type lesions (4.3%), 174 sessile lesions (46.8%), 117 semi-pedunculated lesions (31.5%), 59 pedunculated lesions (15.9%). Narrow-band imaging international colorectal endoscopic (NICE) classification: 85 (22.8%) type I lesions, 280 (75.3%) type II lesions, 4 (1.1%) type III lesions. Univariate analysis showed that lesion size, lesion location, lesion site and different WHO classifications were associated with malignant transformation of colorectal serrated adenoma (all P<0.05). For the serrated adenomas with different NICE classifications, there were statistically significant differences in the distribution of malignant lesions among groups (P=0.001). Multivariate analysis showed that the long-axis diameter of the lesion ≥10 mm (OR=6.699, 95% CI: 2.843-15.786) and the lesion locating in the left side colorectum (OR=2.657, 95% CI: 1.042-6.775) were independent risk factors for malignant transformation. Conclusions: Serrated adenomas mainly locate in the left side colon and rectum, and are prone to malignant transformation when the lesions are ≥10 mm in long-axis diameter or left-sided.
Adenoma/pathology* ; Adenomatous Polyps/pathology* ; Carcinogenesis ; Case-Control Studies ; Colonic Polyps/pathology* ; Colonoscopy ; Colorectal Neoplasms/pathology* ; Disease Progression ; Humans ; Precancerous Conditions/pathology* ; Retrospective Studies ; Risk Factors

Serrated polyposis syndrome (SPS) is closely associated with the initiation and development of colorectal cancer (CRC), however, there is few research on SPS in China. Serrated polyps can be divided into hyperplastic polyps, sessile serrated polyps and traditional serrated polyps. The diagnosis standard of SPS is as following: (1) There are at least 5 serrated lesions in proximal colon, and diameter of more than 2 lesions is >10 mm; (2) The patient has one serrated polyp with family history of SPS; (3) More than 20 serrated polyps can be found in the entire large bowel. The risk of SPS is relatively high in the development of colorectal cancer and 25%-70% of the SPS patients is diagnosed with synchronous or metachronous colorectal cancer during following-up. The clinical characteristics of SPS include that patients are relatively old; no significant racial difference exists in the morbidity; patients have family history of colorectal cancer. The mutation of BRAF or KRAS gene, which induces colorectal cancer through the RAS-RAF-MAPK signaling pathway, is often found in SPS as well as CpG island methylation phenotype (CIMP) and microsatellite instability (MSI). The difference between SPS and traditional familial adenomatous polyposis (FAP) should be noted because of the different pathology mechanism, clinical characteristics and the risk of malignancy. Nowadays, the common technologies of detecting serrated polyps are auto-fluorescence imaging (AFI) and narrow-band imaging (NBI), whose detective rate is around 55%. The SPS patients are advised to undergo the resection of all the serrated polyps with diameter larger than 3-5 mm and receive the colonoscopy examination every 1 or 2 year. Not only the research about SPS is on the initiation step and the molecular mechanism is still unknown, but also the scholars do not come to achieve agreement about the risk of SPS in the malignancy of colorectal cancer, which is essential for further research therefore.
Adenoma ; genetics ; pathology ; therapy ; Adenomatous Polyposis Coli ; genetics ; pathology ; therapy ; Colonic Polyps ; Colonoscopy ; Colorectal Neoplasms ; genetics ; pathology ; therapy ; DNA Methylation ; Genes, ras ; Humans ; Microsatellite Instability ; Mutation ; Phenotype ; Proto-Oncogene Proteins B-raf ; Syndrome

Narrow-band imaging (NBI) is a new imaging technology that was developed in 2006 and has since spread worldwide. Because of its convenience, NBI has been replacing the role of chromoendoscopy. Here we review the efficacy of NBI with/without magnification for detection, characterization, and management of colorectal polyps, and future perspectives for the technology, including education. Recent studies have shown that the next-generation NBI system can detect significantly more colonic polyps than white light imaging, suggesting that NBI may become the modality of choice from the beginning of screening. The capillary pattern revealed by NBI, and the NBI International Colorectal Endoscopic classification are helpful for prediction of histology and for estimating the depth of invasion of colorectal cancer. However, NBI with magnifying colonoscopy is not superior to magnifying chromoendoscopy for estimation of invasion depth. Currently, therefore, chromoendoscopy should also be performed additionally if deep submucosal invasive cancer is suspected. If endoscopists become able to accurately estimate colorectal polyp pathology using NBI, this will allow adenomatous polyps to be resected and discarded; thus, reducing both the risk of polypectomy and costs. In order to achieve this goal, a suitable system for education and training in in vivo diagnostics will be necessary.
Adenomatous Polyps ; Capillaries ; Classification ; Colonic Polyps ; Colonoscopy ; Colorectal Neoplasms ; Diagnosis ; Education ; Mass Screening ; Narrow Band Imaging ; Pathology ; Polyps*

PURPOSE: Colonoscopic polypectomy and surveillance are important to prevent colorectal cancer and identify additional relative risk factors for adequate surveillance. In this study, we evaluated risk factors related to recurrent high-risk polyps during the surveillance of patients with high-risk polyps. MATERIALS AND METHODS: We included 434 patients who had high-risk polyps (adenoma > or =10 mm, > or =3 adenomas, villous histology, or high-grade dysplasia) on the baseline colonoscopy and underwent at least one surveillance colonoscopy from 2005 to 2011 at Severance Hospital. Data regarding patient characteristics, bowel preparation and polyp size, location, number, and pathological diagnosis were retrospectively collected from medical records. Patients with recurrent high-risk polyps were compared with patients with low-risk or no polyps during surveillance. RESULTS: Patients were predominantly male (77.4%), with a mean age of 61.0+/-8.6 years and mean follow-up of 1.5+/-0.8 years. High-risk polyps recurred during surveillance colonoscopy in 51 (11.8%) patients. Results of multivariate analysis showed that male gender, poor bowel preparation, and a larger number of adenomas were independent risk factors for recurrent high-risk polyps (p=0.047, 0.01, and <0.001, respectively). Compared with high-risk polyps found during initial colonoscopy, high-risk polyps on surveillance colonoscopy had higher proportions of small adenomas, low-risk pathology, and fewer adenomas overall, but there was no difference in location. CONCLUSION: Male patients and those with poor bowel preparation for colonoscopy or higher numbers of adenomas were more likely to experience recurrent high-risk polyps.
Adenomatous Polyps/pathology/*surgery ; Aged ; *Colectomy ; Colonic Neoplasms/*pathology ; Colonic Polyps/pathology/*surgery ; *Colonoscopy ; Female ; Follow-Up Studies ; Humans ; Male ; Middle Aged ; Multivariate Analysis ; Neoplasm Recurrence, Local/*diagnosis ; Retrospective Studies ; Risk Factors

BACKGROUNDSporadic fundic gland polyps (FGPs) are common gastric polyps. Some studies reported that FGPs dramatically increased due to proton pump inhibitors (PPIs) use and a decreased prevalence of Helicobacter pylori (H. pylori) infection in Western countries. However, data are still controversial. This study aimed to identify the relationships between these two factors and FGPs in China.

METHODSConsecutive patients with FGPs detected were retrospectively analyzed. Data including patients' age, sex, symptoms, H. pylori infection, history of PPIs use, and the polyps were documented. Each patient was compared with two randomly selected age- and sex-matched controls with similar symptoms in the same period.

RESULTSDuring the period from March 2011 to March 2012, a total of 328 patients were diagnosed as FGPs in 23 047 patients who underwent routine esophagogastroduodenoscopy and 656 patients without FGPs as controls. The mean age was (55.12±12.61) years, and 75.91% were women. The prevalence of H. pylori in patients with FGPs was significantly lower than in those without FGPs (22.30% (64/287) vs. 42.26% (224/530), P < 0.001, OR 0.392, 95% CI 0.283-0.544). Overall, a total of 54 patients with FGPs (54/328, 16.46%) and 136 patients without FGPs (136/656, 20.73%) received PPIs therapy (P = 0.110). According to the different duration of PPIs use, no significant differences of PPIs use were found between the cases and controls among all subgroups. Moreover, the PPIs use was also similar, regardless of age, sex, H. pylori infection, and the number of polyps.

CONCLUSIONSporadic FGPs may not be induced by PPIs therapy but negatively correlate with H. pylori infection in China, which is not the same with the data in Western countries.

Adenomatous Polyps ; epidemiology ; Adult ; Aged ; China ; epidemiology ; Endoscopy, Digestive System ; Female ; Gastric Fundus ; drug effects ; pathology ; Helicobacter Infections ; epidemiology ; Humans ; Male ; Middle Aged ; Proton Pump Inhibitors ; adverse effects ; Retrospective Studies ; Stomach Neoplasms ; epidemiology

OBJECTIVE: To explore the relationship between the Helicobacter pylori (H.pylori) infection and gastric mucosa change and blood-lipid in people undergoing the physical examination in Changsha. METHODS: A total of 2 264 people undergoing physical examination were divided into an H. pyloripositive group (n=1 068) and an H. pylori-negative group (n=1 196). Gastric mucosa change was diagnosed by gastroscopy, blood-lipid and blood sugar were detected, and the statistical analysis was performed. RESULTS: The incidence rate of H.pylori infection was 47.2%. The incidence rate of gastric mucosal erosion, gastric ulcer, duodenal ulcer, gastric mucosal atrophy, gastric polyp, dyslipidemia, increase of triglyceride were (TG) and decrease of the high density lipoprotein cholesterol (HDL-C) in the H.pylori-positive group were all higher than those in the H.pylori-negative group (P<0.01 or P<0.05). In the H. pylori-positive group, the level of TG in people with gastric mucosal erosion, gastric ulcer and duodenal ulcer was higher than that in people with normal gastric mucosa or mild gastritis, and HDL-C was lower than that in people with normal gastric mucosa or mild gastritis. CONCLUSION H. pylori infection can induce the gastric mucosa injury and dyslipidemia, which may result in the occurrence and development of coronary heart disease by increasing TG and decreasing HDL-C, thus increasing the risk of atherosclerosis.
Adenomatous Polyps ; Cholesterol, HDL ; blood ; Duodenal Ulcer ; microbiology ; physiopathology ; Dyslipidemias ; microbiology ; Gastric Mucosa ; microbiology ; pathology ; Gastritis ; microbiology ; physiopathology ; Helicobacter Infections ; physiopathology ; Helicobacter pylori ; Humans ; Lipids ; blood ; Physical Examination ; Stomach Neoplasms ; Stomach Ulcer ; microbiology ; physiopathology ; Triglycerides ; blood

Adenomatous Polyps ; pathology ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; Endoscopy, Digestive System ; Female ; Gastric Fundus ; pathology ; Humans ; Male ; Middle Aged ; Retrospective Studies ; Stomach Neoplasms ; pathology

OBJECTIVE: To investigate the relationship between the expression of leptin, p-mTOR protein and the pathogenesis, development and clinicopathological features in colon carcinoma. METHODS: The expression of leptin and p-mTOR protein was evaluated by immunohistochemical methods in 40 normal colon mucosas, 40 colon adenomatous polyps and 108 cases of colon carcinomas. The relationship between the staining pattern and clinicopathogical features was examined. RESULTS: The positive rates of detection of leptin in normal colon mucosa, adenomatous polyps and colon carcinomas were 10% (4/40), 27.5% (11/40), and 71.3% (77/108), respectively; with significant differences among the three groups (P<0.05). The positive rates of p-mTOR protein in the normal colon mucosa, the adenomatous polyps, and the colon carcinomas were 2.5% (1/40), 20% (8/40), and 61.1% (66/108), respectively; with significant differences among the three groups (P<0.05). The expression of leptin and p-mTOR proteins were related to invasive depth, TNM stages, lymph node metastasis, distant metastasis and tumor differentiation (P<0.05), but not to age, sex, or site (P>0.05). In colon carcinoma tissues, leptin expression was positively correlated with p-mTOR expression (P<0.01). CONCLUSION Leptin and p-mTOR proteins may play important roles in the occurrence and development of colon carcinoma. The detection of leptin and p-mTOR may be helpful for evaluation of the prognosis of the patient with colon carcinoma.
Adenocarcinoma ; metabolism ; pathology ; Adenomatous Polyps ; metabolism ; pathology ; Aged ; Colon ; metabolism ; Colonic Neoplasms ; metabolism ; pathology ; Female ; Humans ; Intestinal Mucosa ; metabolism ; Leptin ; metabolism ; Male ; Middle Aged ; Neoplasm Metastasis ; Phosphorylation ; Prognosis ; TOR Serine-Threonine Kinases ; metabolism

Adenomatous Polyposis Coli ; genetics ; pathology ; Colonic Neoplasms ; classification ; genetics ; pathology ; Colorectal Neoplasms, Hereditary Nonpolyposis ; diagnosis ; genetics ; DNA Glycosylases ; metabolism ; Humans ; Intestinal Polyps ; pathology ; Lymphatic Metastasis ; Neoplasm Staging ; Neuroendocrine Tumors ; classification ; pathology ; Precancerous Conditions ; pathology ; Rectal Neoplasms ; classification ; genetics ; pathology ; World Health Organization

OBJECTIVETo study the expression levels of ANXA1 and ANXA2 and elucidate their clinicopathological significance in adenocarcinoma, peritumoral tissues, adenomatous polyp and chronic cholecystitis of gallbladder.

METHODSEnVision(TM) immunohistochemical staining was used to detect the expression of ANXA1 and ANXA2 in paraffin-embedded tissue sections from resected specimens of adenocarcinoma (n = 108), peritumoral tissue (n = 46), adenomatous polyp (n = 15) and chronic cholecystitis (n = 35).

RESULTSThe positive rates and scores of ANXA1 and ANXA2 were significantly higher in adenocarcinoma (59.3%, 56.5%; 3.2 ± 0.9, 3.4 ± 0.8) than those in peritumoral tissues (34.8%, 1.1 ± 0.8, P < 0.01; 30.4%, 1.0 ± 0.8, P < 0.01), adenomatous polyp (26.7%, 0.9 ± 0.7, P < 0.05 or P < 0.01; 26.7%, 0.9 ± 0.8, P < 0.05 or P < 0.01) and chronic cholecystitis (17.1%, 0.7 ± 0.9, P < 0.01; 20.0%, 0.8 ± 0.8, P < 0.01). The benign lesions with positive ANXA1 and/or ANXA2 expression showed mild to severe atypical hyperplasia of the gallbladder epithelium. The positive rates of ANXA1 and/or ANXA2 were significantly lower in the well-differentiated adenocarcinoma, in a maximal diameter of < 2 cm, with no metastasis to lymph nodes and no invasion to surrounding tissues than those in the moderately or poorly-differentiated adenocarcinoma, in a maximal diameter of ≥ 2 cm, with metastasis to lymph nodes and invasion in surrounding tissues (P < 0.05 or P < 0.01). A high consistence was found between the expression levels of ANXA1 and ANXA2 (χ(2) = 67.84, P < 0.01), and a close positive correlation between the scores of ANXA1 and ANXA2 (r = 0.78, P < 0.01) in gallbladder adenocarcinoma. Kaplan-Meier analysis and multivariate Cox regression analysis showed that ANXA1 or ANXA2 was not an independent prognostic predictor in gallbladder adenocarcinoma.

CONCLUSIONThe expression levels of ANXA1 and/or ANXA2 may be important biological markers in the carcinogenesis, progression and biological behaviors of gallbladder adenocarcinoma.

Adenocarcinoma ; metabolism ; pathology ; surgery ; Adenocarcinoma, Mucinous ; metabolism ; pathology ; surgery ; Adenomatous Polyps ; metabolism ; pathology ; Adult ; Aged ; Annexin A1 ; metabolism ; Annexin A2 ; metabolism ; Cholecystectomy ; methods ; Cholecystitis ; metabolism ; pathology ; Female ; Gallbladder ; metabolism ; pathology ; Gallbladder Neoplasms ; metabolism ; pathology ; surgery ; Humans ; Lymphatic Metastasis ; Male ; Middle Aged ; Neoplasm Invasiveness ; Proportional Hazards Models ; Survival Rate