Correlation between High Incidence of Colorectal Neoplastic Polyps and High-risk Adenomas in Patients with Diabetes Mellitus: A Retrospective Study.

BACKGROUND: Early detection and resection of colorectal polyps by routine colonoscopy screening can be effective in reducing the risk of colorectal cancer (CRC). OBJECTIVE: This study aimed to determine the association between diabetes mellitus (DM) and different types of colorectal polyps in the Chinese population. METHODS: A retrospective analysis was performed on inpatients admitted to the Gastroenterology Department of our hospital from January to December 2019. Clinical data, and colonoscopy and pathology findings of the subjects were collected. Bivariate analysis was used to assess factors associated with colorectal polyps. Significant variables from the bivariate evaluation were included in a stepwise multivariate logistic regression analysis to recognize independent predictors of neoplastic polyps and high-risk adenomas. RESULTS: The proportion of patients with DM was significantly higher in patients with neoplastic polyps and high-risk adenomas than in patients without polyps. Age ≥ 50 years, male gender, and a first-degree relative with a history of CRC were independent risk factors for neoplastic polyps and high-risk adenomas, even in non-smokers. An independent risk factor analysis that did not include a family history of CRC showed that age, gender, and alcohol consumption were independent risk factors for neoplastic polyps and high-risk adenomas. DM was an independent risk factor for high-risk adenomas (OR=2.902, 95% CI=1.221-6.899; p=0.016) after adjusting for age, gender, alcohol consumption, and body mass index. Thus, a history of DM significantly increases the risk of high-risk adenomas. CONCLUSION: This study demonstrated that patients with DM, age ≥ 50 years, male gender, alcohol consumption, and a first-degree relative with a history of CRC should undergo regular endoscopic screening and colonic polypectomy.

Epigenetic inactivation of HOXD10 is associated with human colon cancer via inhibiting the RHOC/AKT/MAPK signaling pathway.

BACKGROUND: To examine the influence of HOXD10 on the metabolism and growth of colon carcinoma cells by suppressing the RHOC/AKT/MAPK pathway. METHODS: Thirty-seven paired colon cancer and its adjacent samples from The Cancer Genome Atlas (TCGA) were analyzed. Chip Analysis Methylation Pipeline (ChAMP) analysis was employed for differential methylated points (DMPs) and the differential methylation regions (DMRs) screening. The HOXD10 mRNA expression and DNA methylation levels were detected by RT-PCR. The Cell proliferation, migration, invasion and apoptosis were respectively measured by MTT assay, transwell assay, wound healing assay and flow cytometry assay in carcinoma cell lines after treated with 5-aza-2'-deoxycytidine (5-Aza-dC) or transfected with HOXD10-expressing plasmid. The expression of HOXD10 and RHOC was revealed by immunohistochemistry in disparate differentiation colon carcinoma tissues, and the dephosphorylation of AKT and MAPK pathways were detected by RT-PCR and western blot. RESULTS: The bioinformatics analysis demonstrated that HOXD10 was hypermethylated and low-expressed in colorectal cancer tissues. The detection of RT-PCR indicated the similar results in colorectal cancer cell lines and tissues. The induction of demethylation was recovered by treatment with 5-Aza-dC and the HOXD10 in colorectal cancer cell lines was re-expressed by transfection with a HOXD10 expression vector. The demethylation or overexpression of HOXD10 suppressed proliferation, migration, invasion and promoted apoptosis in colorectal cancer cells. HXOD10 suppressed the tumor growth and detected an opposite trend of protein RHOC. AKT and MAPK pathways were notably inactivated after the dephosphorylation due to the overexpression of HOXD10. CONCLUSIONS: HOXD10 was suppressed in colon adenocarcinoma cells, which down-regulated RHOC/AKT/MAPK pathway to enhance colon cancer cells apoptosis and constrain the proliferation, migration and invasion.

Wnt and Nodal signaling simultaneously induces definitive endoderm differentiation of mouse embryonic stem cells.

Induced differentiation of definitive endoderm (DE) from embryonic stem cells (ESCs) has been the recent focus of studies investigating regeneration and transplantation of organs of the digestive system. Poor cell survival is the most important challenge to DE differentiation from ESCs. This study aimed to optimize culture conditions to promote the differentiation of mouse ESCs into DE, and to investigate the roles of the Wnt and Nodal signaling pathways in the DE differentiation. The mouse ESCs were treated with or without leukemia inhibitory factor, Wnt3a and Activin A alone or together, and examined the DE differentiation by the DE marker CXCR4 and the ESC marker Oct4. The result showed the optimal induction of differentiation was achieved in cells simultaneously treated with Wnt3a and Activin A. Induction of CXCR4 was also earlier when there was simultaneous activation of Wnt and Nodal signaling compared to the groups treated with only Wnt3a or Activin A alone. These findings provide the basis for the induced differentiation of ESCs for the generation of functional, mature cells of gastrointestinal lineage, which can be potentially used for cell replacement therapy, disease modeling, as well as drug discovery studies.

Lgr5 positive stem cells sorted from small intestines of diabetic mice differentiate into higher proportion of absorptive cells and Paneth cells in vitro.

Intestinal epithelial stem cells (IESCs) can differentiate into all types of intestinal epithelial cells (IECs) and Leucine-rich repeat-containing G protein-coupled receptor 5 (Lgr5) is a marker for IESC. Previous studies reported enhanced proliferation of IECs in diabetic mice. In this study, the in vitro differentiation of Lgr5 positive IESCs sorted from diabetic mice was further investigated. The diabetic mouse model was induced by streptozotocin (STZ), and crypt IECs were isolated from small intestines. Subsequently, Lgr5 positive IESCs were detected by flow cytometry (FCM) and sorted by magnetic activated cell sorting (MACS). Differentiation of the sorted IESCs was investigated by detecting the IEC markers in the diabetic mice using immunostaining, quantitative real-time reverse-transcription polymerase chain reaction (qRT-PCR), and Western blot analysis, which was compared with normal mice. We found that the proportion of Lgr5 positive cells in the crypt IECs of diabetic mice was higher than that of control mice (P < 0.05). Lgr5 positive IESCs could be significantly enriched in Lgr5 positive cell fraction sorted by MACS. Furthermore, the absorptive cell marker sucrase-isomaltase (SI) and the Paneth cell marker lysozyme 1 (Lyz1) were more highly expressed in the differentiated cells derived from Lgr5 positive IESCs of diabetic mice in vitro (P < 0.05). We demonstrate that the number of Lgr5 positive IESCs is significantly increased in the small intestines of STZ-induced diabetic mice. Lgr5 positive IESCs sorted from the diabetic mice can differentiate into a higher proportion of absorptive cells and Paneth cells in vitro. We characterized the expression of Lgr5 in the small intestine of diabetic mice, and sorted Lgr5 positive intestinal epithelial stem cells (IESCs) for investigating their differentiation in vitro. We proved that the quantity of Lgr5 positive IESCs was significantly increased in the small intestines of diabetic mice. IESCs sorted from the diabetic mice can differentiate into a higher proportion of absorptive cells and Paneth cells in vitro.

Gemcitabine Adjuvant Therapy for Resected Pancreatic Cancer: A Meta-analysis.

Gemcitabine (GEM) is an approved treatment for unresectable pancreatic cancer; however, its role in treating resected pancreatic cancer is less clear. The aim of this study was to investigate the evidence of the role of adjuvant GEM therapy on survival in resected pancreatic cancer. Four phase III randomized trials of adjuvant GEM in patients with resected pancreatic cancer were identified and the hazard ratio (HR) for overall survival were used in this meta-analysis; 2 studies compared GEM treatment with best supportive care and 2 studies with 5-fluorouracil/folinic acid therapy. The pooled data (n=2017 patients) indicated that the overall survival data were homogenous among the studies (Q=4.371; I=31.37%; P=0. 224). The combined HR significantly favors GEM over the other treatments. The overall HR was 0.88 (range, 0. 720 to 0.940; P=0.014). The results indicate that GEM prolongs overall survival compared with other treatments after the resection of pancreatic cancer.

Association of serum levels of CEA, CA199, CA125, CYFRA21-1 and CA72-4 and disease characteristics in colorectal cancer.

Identifying predictive biomarkers for colorectal cancer would facilitate diagnosis and treatment of the disease. This study aimed to investigate the association of the serological biomarkers CEA, CA19-9, CA125, CYFRA21-1 and CA72-4 with patient characteristics and disease outcomes in colorectal cancer. Patients (N = 373) with colorectal cancer were evaluated for the association of CEA, CA19-9, CA125, CYFRA21-1, and CA72-4 pre and post-surgery and at disease recurrence with demographics, disease characteristics including pathological types, degree of differentiation, invasion depth, abdominal lymph node metastasis, TMN stage, Dukes stage, location of cancer and metastasis, and disease outcomes. It was more common for a patient to express these markers prior to surgery and at disease recurrence than following surgery. Overall, the serum levels of CEA, CA19-9, CA125, CYFRA21-1, and CA72-4 were not associated with age, gender, pathological type and location of cancer (all P-values >0.05), but were associated with the poor tumor differentiation, higher tumor invasion, greater degree of abdominal lymph node metastasis, and higher TNM and Duke stage tumors (all P-values < 0.01). CEA expression was associated with older ages (median age 65 years). Multivariate analysis indicated that CEA was correlated with overall survival and none of the markers correlated with disease recurrence. The expression of CEA, CA19-9, CA125, CYFRA21-1, and CA72-4 was associated with specific disease characteristics which tended to indicated more advanced disease and disease recurrence consistent with these biomarkers being useful for detecting colorectal cancer.

Enhanced proliferation in colorectal epithelium of patients with type 2 diabetes correlates with ß-catenin accumulation.

AIMS: ß-Catenin accumulation promotes proliferation. However, the correlation between proliferation of colorectal epithelium and ß-catenin in type 2 diabetes mellitus (DM) patients remains unclear. METHODS: Colorectal epithelium samples from distal ends of colorectal adenocarcinomas without histological aberrances were divided into two groups: DM patients with type 2 DM for more than 1year (n=27) and non-DM patients without hyperglycemia (n=20). Samples from patients without colorectal epithelial disease or hyperglycemia served as a control group (n=6). Proliferative index was calculated as the percentage of proliferating cell nuclear antigen positive cells. Wnt/ß-catenin signaling was assessed immunohistochemically and phosphorylation of ß-catenin was assessed by immunofluorescence. RESULTS: Compared with the non-DM or control group, the proliferative index and expression of lactate dehydrogenase A and Wnt/ß-catenin signaling were significantly higher in the DM group (all p<0.01). The proliferative index correlated positively with ß-catenin expression (Spearman correlation coefficient=0.55; p<0.01). Reduced phosphorylation at serine 33/37 and increased phosphorylation at serine 675 of ß-catenin were detected in the DM group (all p<0.01). CONCLUSIONS: Enhanced proliferation, accompanied by increased aerobic glycolysis, was detected in colorectal epithelium of patients with diabetes. ß-Catenin accumulation with altered phosphorylation correlated with the proliferative changes.

Abnormal differentiation of intestinal epithelium and intestinal barrier dysfunction in diabetic mice associated with depressed Notch/NICD transduction in Notch/Hes1 signal pathway.

Proliferative change and intestinal barrier dysfunction in intestinal mucosa of diabetes have been described, but the differentiation characteristics of intestinal epithelial cells (IECs) and the mechanisms in the IECs development remain unclear. To explore the intestinal epithelial constitution patterns and barrier function, the diabetic mouse model was induced by streptozotocin. Tight junctions between IECs were significantly damaged and the serum level of D-lactate was raised in diabetic mice (P < 0.05). The expression of Zo1 and Ocln in the small intestine of diabetic mice were lower, while the markers for absorptive cell (SI) and Paneth cell (Lyz1) were significantly higher than in control mice (P < 0.05). The expression of Msi1, Notch1, and Dll1 in small intestine gradually increased throughout the course of hyperglycemia in diabetic mice (P < 0.05). However, the expression of NICD, RBP-jκ, Math1, and Hes1 had a reverse trend compared with Msi1 and Notch1. Intestinal absorptive cells and Paneth cells had a high proliferation rate in diabetic mice. However, the intestinal barrier dysfunction associated with the decreased expressions of Zo1 and Ocln was detected throughout hyperglycemia. In conclusion, downregulation of Notch/Hes1 signal pathway caused by depressed Notch/NICD transduction is associated with the abnormal differentiation of IECs and intestinal barrier dysfunction in diabetic mice.

5-Aminosalicylates reduce the risk of colorectal neoplasia in patients with ulcerative colitis: an updated meta-analysis.

BACKGROUND: Although the chemopreventive effect of 5-aminosalicylates on patients with ulcerative colitis has been extensively studied, the results remain controversial. This updated review included more recent studies and evaluated the effectiveness of 5-aminosalicylates use on colorectal neoplasia prevention in patients with ulcerative colitis. METHODS: Up to July 2013, we searched Medline, Embase, Web of Science, Cochrane CENTRAL, and SinoMed of China for all relevant observational studies (case-control and cohort) about the effect of 5-aminosalicylates on the risk of colorectal neoplasia among patients with ulcerative colitis. The Newcastle-Ottawa Scale was used to assess the quality of studies. Adjusted odds ratios (ORs) were extracted from each study. A random-effects model was used to generate pooled ORs and 95% confidence intervals (95%CI). Publication bias and heterogeneity were assessed. RESULTS: Seventeen studies containing 1,508 cases of colorectal neoplasia and a total of 20,193 subjects published from 1994 to 2012 were analyzed. 5-aminosalicylates use was associated with a reduced risk of colorectal neoplasia in patients with ulcerative colitis (OR 0.63; 95%CI 0.48-0.84). Pooled OR of a higher average daily dose of 5-aminosalicylates (sulfasalazine ≥ 2.0 g/d, mesalamine ≥ 1.2 g/d) was 0.51 [0.35-0.75]. Pooled OR of 5-aminosalicylates use in patients with extensive ulcerative colitis was 1.00 [0.53-1.89]. CONCLUSION: Our pooled results indicated that 5-aminosalicylates use was associated with a reduced risk of colorectal neoplasia in patients with ulcerative colitis, especially in the cases with a higher average daily dose of 5-aminosalicylates use. However, the chemopreventive benefit of 5-aminosalicylates use in patients with extensive ulcerative colitis was limited.

Celiac plexus block for treatment of pain associated with pancreatic cancer: a meta-analysis.

Pancreatic ductal adenocarcinoma has a high rate of neural invasion (80 to 100%) and can be associated with moderate to severe pain in pancreatic cancer. Treatment of pain with celiac plexus blockage (CPB) combined with the three-step ladder utilization of pharmaceutical analgesics following WHO guidelines is used, but the evidence in randomized controlled trials is inconsistent. This meta-analysis identified and compared seven randomized control trials of pain relief from pancreatic cancer, by treatment with medical management alone to celiac plexus blockade with medical management. While no evidence of potential publication bias was detected, group size and statistical power may account for some of the inconsistent conclusions. The combined CPB groups had a significantly lower pain score at 4 weeks, but significance was not maintained at 8 weeks. The combined CPB groups required significantly less drug use compared to the combined control groups treated with pharmaceutical analgesics.

Clinical features and expressions of Foxp3 and IL-17 in type 1 autoimmune pancreatitis in China.

BACKGROUND: Autoimmune pancreatitis (AIP) is a distinct type of pancreatitis associated with a presumed autoimmune mechanism. The aim of this study was to analyze the clinical features and expressions of forkhead box P3 (Foxp3) and interleukin-17 (IL-17) in type 1 AIP in China and to identify factors for differentiation of AIP from non-AIP chronic pancreatitis (CP). MATERIAL AND METHODS: We retrospectively reviewed pancreatic specimens with diagnosis of type 1 AIP and non-AIP CP at Sun Yat-Sen Memorial Hospital in China from January 2000 to December 2013. The clinical symptoms, serological data, imaging findings, histopathology, and immunohistochemical findings of Foxp3 and IL-17 in the 2 groups were analyzed. RESULTS: Twenty-nine patients with type 1 AIP and 20 patients with non-AIP CP were enrolled. Obstructive jaundice was more common in type 1 AIP than in non-AIP CP (62.1% vs. 30.0%, P=0.042). The diffuse or segmental enlargement of the pancreas was more frequent in type 1 AIP than in non-AIP CP (72.4% vs. 40.0%, P=0.038). Histopathology of type 1 AIP presented dense lymphoplasmacytic infiltration, "snowstorm-like" fibrosis and abundant immunoglobulin (Ig) G4+ cells. Foxp3+ cells were more frequently observed in type 1 AIP than in non-AIP CP. IL-17+ cell infiltration was similar between the 2 groups. Furthermore, a positive correlation was found between Foxp3+ and IgG4+ cell counts in the pancreas of patients with type 1 AIP. CONCLUSIONS: Type 1 AIP has distinctive symptoms, image, and pathological characteristics, which could be used for differentiation from non-AIP CP. Foxp3+ cells might be helpful to distinguish type 1 AIP from non-AIP CP.

Enteral nutrition within 48 hours of admission improves clinical outcomes of acute pancreatitis by reducing complications: a meta-analysis.

BACKGROUND: Enteral nutrition is increasingly advocated in the treatment of acute pancreatitis, but its timing is still controversial. The aim of this meta-analysis was to find out the feasibility of early enteral nutrition within 48 hours of admission and its possible advantages. METHODS AND FINDINGS: We searched PubMed, EMBASE Databases, Web of Science, the Cochrane library, and scholar.google.com for all the relevant articles about the effect of enteral nutrition initiated within 48 hours of admission on the clinical outcomes of acute pancreatitis from inception to December 2012. Eleven studies containing 775 patients with acute pancreatitis were analyzed. Results from a pooled analysis of all the studies demonstrated that early enteral nutrition was associated with significant reductions in all the infections as a whole (OR 0.38; 95%CI 0.21-0.68, P<0.05), in catheter-related septic complications (OR 0.26; 95%CI 0.11-0.58, P<0.05), in pancreatic infection (OR 0.49; 95%CI 0.31-0.78, P<0.05), in hyperglycemia (OR 0.24; 95%CI 0.11-0.52, P<0.05), in the length of hospitalization (mean difference -2.18; 95%CI -3.48-(-0.87); P<0.05), and in mortality (OR 0.31; 95%CI 0.14-0.71, P<0.05), but no difference was found in pulmonary complications (P>0.05). The stratified analysis based on the severity of disease revealed that, even in predicted severe or severe acute pancreatitis patients, early enteral nutrition still showed a protective power against all the infection complications as a whole, catheter-related septic complications, pancreatic infection complications, and organ failure that was only reported in the severe attack of the disease (all P<0.05). CONCLUSION: Enteral nutrition within 48 hours of admission is feasible and improves the clinical outcomes in acute pancreatitis as well as in predicted severe or severe acute pancreatitis by reducing complications.

Prognosis of 153 patients with decompensated hepatitis B virus-related cirrhosis is improved after 3-year continuous lamivudine treatment.

BACKGROUND: The long-term effectiveness and safety of lamivudine in patients with decompensated hepatitis B virus-related cirrhosis are still not clear. The present study attempted to describe the clinical outcomes of lamivudine therapy in these special patients over three years. METHODS: This study was a retrospective, controlled cohort study which involved 153 patients with decompensated hepatitis B virus-related cirrhosis. Of these, 86 patients received lamivudine 100 mg daily accompanied with general internal treatment, and the other 67 were given general internal treatment only. Significant clinical responses were recorded after years of antiviral treatment. RESULTS: The patients in both groups were matched in terms of age, sex and laboratory results at baseline. After years of therapy, the Child-Pugh-Turcotte scores and laboratory values of the patients receiving lamivudine were remarkably improved compared to the patients in the control group. The mortality rate and the incidence of cirrhosis-related complications were much lower in the lamivudine group than in the control group. Genotypic resistance tyrosine, methionine, aspartate, aspartate mutations developed in 26.7 percent of the patients during 3-year lamivudine treatment, and cirrhosis-related death and the hepatocellular carcinoma were more likely to occur in patients with these mutations than in the other patients who were treated with lamivudine. CONCLUSIONS: Continuous long-term lamivudine treatment in patients with decompensated hepatitis B virus-related cirrhosis delays clinical progression, and significantly improves hepatic function and prognosis. However, the use of a retrospective control cohort precludes drawing definitive conclusions.

[Study on moxa sticks burning temperature-time-space curves].

OBJECTIVE: To study the burning characteristics of moxa stick. METHODS: A self-designed moxa stick burning temperature measuring device, which was assembled with ALTEC intelligence digital setter and SJ-600 thermocouple, was used to conduct next four experiences: 1) embedding a thermocouple inside a moxa stick to measure peak burning temperature; 2) pulling a thermocouple embedded in the moxa stick at the proper rate to detect combustion stability; 3) elucidating temperature distribution of transverse section by measuring the temperature in the center, radius midpoint and lateral; 4) drawing temperature-time-space curves by pulling the thermocouples in the former three observation points. RESULTS: The experiment indicated that the burning temperature peak of three-year moxa stick (Hubei Herbal Medicine St. Qichun Technology Co., Ltd.) was 848 degrees C which had good combustion stability. Furthermore, the temperature in the center, radius midpoint and lateral of transverse section were 843 degrees C, 731 degrees C and 410 degrees C, respectively, and its burning temperature-time-space curves was drawn, which showed the real-time burning temperature and the peak burning temperature and were regarded as ultimate indice to integrate the formers. CONCLUSION: The measuring system elaborately reflecting the burning features of moxa stick may provide reference for manufacture industry of moxa stick quality criteria for its convenience and accuracy.

Musashi1 expression cells derived from mouse embryonic stem cells can be enriched in side population isolated by fluorescence activated cell sorter.

BACKGROUND: Purifying stem cells is an inevitable process for further investigation and cell-therapy. Sorting side population (SP) cells is generally regarded as an effective method to enrich for progenitor cells. This study was to explore whether sorting SP could enrich for the Musashi1 (Msi1) positive cells from Msi1 high expression cells (Msi1(high) cells) derived from mouse embryonic stem cells (ESCs) in vitro. RESULTS: In this study, Msi1(high) cell population derived from ESCs were stained by Hoechst 33342, and then the SP and non-SP (NSP) fractions were analyzed and sorted by fluorescence activated cell sorter. Subsequently, the expressions of Msi1 and other markers for neural and intestinal stem cells in SP and NSP were respectively detected. SP and NSP cells were hypodermically engrafted into the backs of NOD/SCID mice to form grafts. The developments of neural and intestinal epithelial cells in these grafts were investigated. SP fraction was identified and isolated from Msi1(high) cell population. The expression of Msi1 in SP fraction was significantly higher than that in NSP fraction and unsorted Msi1(high) cells (P< 0.05). Furthermore, the markers for neural cells and intestinal epithelial cells were more highly expressed in the grafts from SP fraction than those from NSP fraction (P< 0.05). CONCLUSIONS: SP fraction, isolated from Msi1(high) cells, contains almost all the Msi1-positive cells and has the potential to differentiate into neural and intestinal epithelial cells in vivo. Sorting SP fraction could be a convenient and practical method to enrich for Msi1-positive cells from the differentiated cell population derived from ESCs.

Musashi 1-positive cells derived from mouse embryonic stem cells can differentiate into neural and intestinal epithelial-like cells in vivo.

Msi1 (Musashi 1) is regarded as a marker for neural and intestinal epithelial stem cells. However, it is still unclear whether Msi1-positive cells derived from mouse embryonic stem cells have the ability to differentiate into neural or intestinal epithelial cells. A pMsi1-GFP (green fluorescent protein) reporter plasmid was constructed in order to sort Msi1-positive cells out of the differentiated cell population. The GFP-positive cells (i.e. Msi1-positive cells) were sorted by FACS and were hypodermically engrafted into the backs of NOD/SCID (non-obese diabetic/severe combined immunodeficient) mice. The presence of neural and intestinal epithelial cells in the grafts was detected. Msi1 was highly expressed in the GFP-positive cells, but not in the GFP-negative cells. The markers for neural cells (Nestin and Tubulin ß III) and intestinal epithelial cells [FABP2 (fatty acid binding protein 2), Lyz (lysozyme) and ChA (chromogranin A)] were more highly expressed in the grafts from Msi1-positive cells than those from Msi1-negative cells (P<0.05). The grafts from the Msi1-negative cells contained more mesodermal-like tissues than those from the Msi1-positive cells. The pMsi1-GFP vector can be used to sort Msi1-positive cells from a cell population derived from mouse embryonic stem cells. The Msi1-positive cells can differentiate into neural and intestinal epithelial-like cells in vivo.

[Value of fecal and blood adenomatous polyposis coli gene and K-ras gene mutation detection in colorectal neoplasm screening].

OBJECTIVE: To explore the value of detection of adenomatous polyposis coli (APC) gene and K-ras gene mutations in fecal and blood samples in colorectal neoplasm screening. METHODS: From 84 subjects undergoing colonoscopic examination (including 31 with colorectal carcinoma, 26 with colorectal adenoma, and 27 healthy subjects) between October, 2003 and March, 2004, 5 ml of heparinized peripheral blood and 3-5 g fecal specimens were collected. The DNA was extracted from the specimens for detecting the mutation of APC and K-ras gene using polymerase chain reaction-single strand conformation polymorphism and the results were analyzed statistically. RESULTS AND CONCLUSION: (1) The incidence of APC gene mutation was 41.9% and 57.7% in the plasma, and 34.8% and 26.8% in the fecal specimens of colorectal carcinoma patients and adenoma patients, respectively, both higher than that in normal subjects (P<0.05), suggesting high consistency between fecal and plasma APC gene mutation detection (K=0.811, P<0.05). (2) The incidence of plasma K-ras mutation was 48.4% in colorectal carcinoma patients, 3.8% in adenoma patients and 0% in normal control subjects, and in the feces, the incidences were 54.8%, 7.7% and 11.1%, respectively. The mutation rate was higher in carcinoma patients than in adenoma patients and normal subjects (P<0.05). Fecal K-ras gene mutation detection was consistent with plasma detection (K=0.662, P=0.000). (3) APC gene mutation detection showed a low sensitivity and specificity in the diagnosis of colorectal carcinoma, but K-ras mutation detection showed a high specificity. The diagnostic sensitivity increased when combining APC and K-ras gene detection in the plasma or fecal specimens, but there was no evidence to suggest that APC and K-ras mutation detection in the plasma could be better than detection in the feces. (4) For colorectal carcinoma, APC gene mutation is associated with lymphoid node metastasis, but not with the patient's gender, age, tumor location, differentiation, distant organ metastasis or CEA level (P>0.05), and the mutation of K-ras gene is related to the degree of tumor differentiation.