OBJECTIVE: To study the expression of tumor associated vascular insulin receptor (TVIR) in colorectal cancer with or without metabolic syndrome (MS) and its relationship with the pathological features of colorectal cancer. METHODS: The expression of TVIR in 220 colorectal cancer specimens was detected by tissue microarray and immunohistochemistry. The relationships between the expression of TVIR and the pathological features (pathological subtypes, histological grade, invasion depth, lymph node metastasis and TNM stage) of colorectal cancer with/without MS were analyzed. RESULTS: The insulin receptor expression was observed in colorectal cancer tissue or border area between cancer and normal tissue, but not in normal intestinal tissue. The high-expression rates of TVIR in MS group was remarkably lower than that of non-MS group (21.6%vs. 41.0%, CONCLUSIONS s: High-expression of TVIR is associated with aggressive pathological features such as invasion, lymph node metastasis and high TNM stage of colorectal cancer, especially for those patients without MS. TVIR could be a useful biological marker for prognosis of colorectal cancer.
Biomarkers, Tumor/genetics* ; Colorectal Neoplasms/physiopathology* ; Gene Expression Regulation, Neoplastic ; Humans ; Neoplasm Staging ; Prognosis ; Receptor, Insulin/genetics*

OBJECTIVETo predict and identify the target gene of miR-145, and to explore the underlying mechanism of the inhibition of miR-145 on drug resistance to Oxaliplatin (L-OHP) in human colorectal cancer cells.

METHODSL-OHP-resistant human colorectal cancer cell line (HCT116/L-OHP) was established in vitro by exposing to increased concentrations of L-OHP in cell culture medium. MiR-145-mimics and its negative control (NC-miRNA) were transfected into HCT116/L-OHP cells using liposome to establish HCT116/L-OHPover-expressing miR-145 and HCT116/L-OHP. The target genes of miR-145 were predicted by bioinformatic analysis, and validated by dual luciferase activity assay. After determination of G protein coupled receptor 98(GPR98) as target gene, corresponding plasmids were constructed and transfected to establish HCT116/L-OHPover-expressing GPR98 and HCT116/L-OHP. HCT116/L-OHP cells over-expressing both GPR98 and miR-145 (HCT116/L-OHP) were acquired through modification of the binding sites of GPR98 cDNA with miR-145. CCK-8 assay was used to assess the proliferation (A value) and sensitivity to L-OHP (the lower the IC50, the stronger the sensitivity) in HCT116/L-OHP cells. Real-time quantitative PCR was used to measure the mRNA expression of miR-145 and GPR98. Western blot was used to examine the protein expression of GPR98 and drug-resistant associated protein, such as P-glycoprotein (gp), multiple drug-resistance protein 1(MRP1), cancer-inhibition gene PTEN.

RESULTSHCT116/L-OHP cell line was successfully established with ICof (42.34±1.05) mg/L and miR-145 mRNA expression of 0.27±0.04, which was higher than (9.81±0.95) mg/L (t=39.784, P=0.000) and lower than 1.00±0.09 (t=13.021, P=0.000) in HCT116 cells. Based on HCT116/L-OHP cells, HCT116/L-OHPcells were established successfully, with relative miR-145 expression of 10.01±1.05, which was higher than 1.06±0.14 in HCT116/L-OHPand 1.00±0.16 in HCT116/L-OHP (F=161.797, P=0.000). GPR98 was identified to be the target gene of miR-145. The relative mRNA and protein expressions of GPR98 in HCT116/L-OHPcells were 8.48±0.46 and 1.71±0.09, respectively, which were higher than those in HCT116/L-OHP(mRNA: 3.65±0.40, protein: 1.21±0.10) and HCT116/L-OHP (mRNA: 3.49±0.35, protein: 1.22±0.08; all P<0.05). The A value was 1.31±0.10, and the relative protein expressions of P-gp and MRP1 were 1.53±0.18 and 1.49±0.20 in HCT116/L-OHPcells, which were higher than those in HCT116/L-OHP (A value: 0.82±0.08, relative protein expression: 1.00±0.06 and 1.21±0.13, all P<0.05). The A value was 0.89±0.08, and the relative protein expressions of P-gp and MRP were 1.02±0.24 and 1.38±0.25 in HCT116/L-OHPcells, which were higher than those in HCT116/L-OHP(A value: 0.20±0.05, relative protein expression: 0.20±0.07, 0.55±0.10, all P<0.05). The relative protein expression of PTEN in HCT116/L-OHPcells was 0.12±0.03, which was lower than 1.25±0.14 in HCT116/L-OHP cells(P<0.05). In addition, relative protein expressions of P-gp and MRP1 were 1.02±0.24 and 1.38±0.25 in HCT116/L-OHPcells, which were higher than those in HCT116/L-OHPcells (0.20±0.07 and 0.55±0.10), while PTEN expression in HCT116/L-OHPcells was lower as compared to HCT116/L-OHPcells (1.41±0.16 vs. 1.98±0.13, P<0.05).

CONCLUSIONMiR-145 inhibits drug resistance to L-OHP of HCT116 cells through suppressing the expression of target gene GPR98.

ATP Binding Cassette Transporter, Sub-Family B ; drug effects ; ATP-Binding Cassette, Sub-Family B, Member 1 ; drug effects ; Cell Line, Tumor ; drug effects ; physiology ; Colorectal Neoplasms ; physiopathology ; Down-Regulation ; drug effects ; genetics ; Drug Resistance, Neoplasm ; drug effects ; genetics ; physiology ; HCT116 Cells ; drug effects ; physiology ; Humans ; In Vitro Techniques ; MicroRNAs ; genetics ; pharmacology ; Multidrug Resistance-Associated Proteins ; drug effects ; Organoplatinum Compounds ; pharmacology ; PTEN Phosphohydrolase ; drug effects ; RNA, Messenger ; Receptors, G-Protein-Coupled ; drug effects ; genetics

OBJECTIVETo investigate the effect of ASCT2 gene (glutamine transporter) knock-down by shRNA on biological behaviors of colorectal cancer cells.

METHODSshRNA was transfected into colorectal cancer cells Lovo and SW480 to knockdown ASCT2 mediated by Lipofectamine 2000. Reverse transcription-PCR and Western blot were used to examine the mRNA and protein expression of ASCT2. MTT and transwell assay were used to determine the proliferation and invasiveness of Lovo and SW480 cells. Radioactive-tracer was used to detect the uptake of glutamine.

RESULTSASCT2 mRNA and protein levels were significantly down-regulated by shRNA in Lovo and SW480 cells(P<0.01). MTT and transwell assays showed that ASCT2 knock-down could significantly inhibit the proliferation of Lovo and SW480 cells (A490) and decrease the number of invasive Lovo and SW480 cells from the membrane (both P<0.01). The number of membrane Lovo cells in shASCT group and control group was 46.3±5.9 and 197.7±9.1, respectively while the number of membrane SW480 cells in shASCT group and control group was 29.7±3.8 and 139.0±9.5, respectively. Radioactive-tracer showed that shASCT2 transfection could significantly reduce the uptake of glutamine, with an inhibition rate of 79.15% in Lovo and 67.22% in SW480 cells (both P<0.01).

CONCLUSIONSASCT2 plays an oncogenic role in colonic cancer, and its promotion mechanism may be associated with glutamine metabolism. ASCT2 may be a novel therapeutic target of colonic cancer.

Amino Acid Transport System ASC ; drug effects ; genetics ; physiology ; Cell Line, Tumor ; physiology ; Cell Proliferation ; genetics ; Colorectal Neoplasms ; genetics ; physiopathology ; Down-Regulation ; drug effects ; Gene Knockdown Techniques ; methods ; Glutamine ; drug effects ; genetics ; physiology ; Humans ; Minor Histocompatibility Antigens ; drug effects ; genetics ; physiology ; Neoplasm Invasiveness ; genetics ; physiopathology ; Oncogenes ; drug effects ; genetics ; RNA, Messenger ; physiology ; RNA, Small Interfering ; pharmacology ; Transfection

OBJECTIVETo explore the predictive value of combination detection of Pgp1 expression in cancer tissue and serum CEA level for the prognosis of colorectal cancer (CRC) patients.

METHODSClinicopathological data, complete 5-year follow-up data and CRC tissue samples of 153 CRC patients with stage I( to II( tumor undergoing radical operation in our department from January 2004 to August 2006 were retrospectively collected. Immunohistochemical staining was used to detect the expression level of Pgp1. The combined evaluation of staining intensity and positive cell percentage was performed to determine the expression level of Pgp1. Pgp1 staining (-) and (+) was defined as low expression; and staining (++) and (+++) as high expression. Electrochemiluminescence immunoassay was used to detect the level of serum CEA. CEA > 5 μg/L was defined as positive. χand Fisher's exact test were performed to analyze the association of Pgp1 expression with CEA level and clinicopathological variables. Moreover, Kaplan-Meier method was used to analyze the survival. Univariate and multivariate Cox proportional hazard regression models were used to evaluate the roles of Pgp1 expression combined with serum CEA level in prognosis prediction.

RESULTSOf 153 patients, 105 were males and 48 females with mean age of 59 (27 to 90) years; 41 cases were rectal cancer, and 112 cases colon cancer; 23 patients were TNM stage I( tumor, and 130 patients stage II( tumor; median follow-up time was 64 months; 30 cases were dead. Positive rate of Pgp1 expression in colorectal cancer tissues was 66.0%(101/153). The expression of Pgp1 was associated with gender, tumor location, and survival during the follow-up (all P<0.05). The preoperative positive rate of serum CEA was 28.1% (43/153). The preoperative serum CEA level was associated with tumor recurrence and survival (all P<0.05). Kaplan-Meier analysis showed the overall 5-year survival rate was 81.7%. The 5-year survival rate of patients with high expression of Pgp1 was 88.1%, which was significantly higher than 69.2% of those with low expression of Pgp1(P=0.003). The 5-year survival rate of patients with preoperative positive serum CEA was 72.1%, which was significantly lower than 86.1% of those with preoperative negative serum CEA(P=0.023). Furthermore, the 5-year survival rate of patients with negative Pgp1 plus positive CEA was 66.7%, which was significantly lower than 91.0% of those with positive Pgp1 plus negative CEA(P=0.002). Univariate analysis showed that gender, Pgp1 expression level, preoperative serum CEA level, and Pgp1 combined with CEA were significantly associated with the prognosis of patients(all P<0.05). Multivariate analysis showed that Pgp1 expression was an independent prognostic factor of CRC [HR(95%CI:1.261 to 64.224), P=0.028].

CONCLUSIONSLow expression of Pgp1 in cancer tissue indicates poor prognosis in patients with stage I( and II( tumor. Combination detection of Pgp1 expression and serum CEA can be applied to predict the prognosis of patients with stage I( and II( colorectal cancer.

Adult ; Aged ; Aged, 80 and over ; Biomarkers, Tumor ; blood ; physiology ; Carcinoembryonic Antigen ; blood ; physiology ; Colonic Neoplasms ; physiopathology ; secretion ; Colorectal Neoplasms ; physiopathology ; secretion ; Female ; Fluorescent Antibody Technique ; Humans ; Hyaluronan Receptors ; metabolism ; Kaplan-Meier Estimate ; Male ; Middle Aged ; Multivariate Analysis ; Neoplasm Proteins ; blood ; physiology ; Neoplasm Recurrence, Local ; physiopathology ; Neoplasm Staging ; Predictive Value of Tests ; Prognosis ; Proportional Hazards Models ; Rectal Neoplasms ; physiopathology ; secretion ; Retrospective Studies ; Sex Factors ; Survival Rate

OBJECTIVETo investigate the association of peripheral nerve invasion (PNI) with clinicopathological factors and prognosis of colorectal cancer.

METHODSClinicopathological data and Surgical specimens of 372 colorectal cancer patients who underwent radical resection from January 2011 to June 2012 in The Second Affiliated Hospital of Harbin Medical University were collected. Histopathological evaluation of tissue samples was conducted with hematoxylin and eosin-stained sections. PNI was considered positive when cancer cells were observed inside the nerve sheath, or when at least 33% of the nerve periphery was surrounded by cancer cells. The relationship between PNI and clinicopathological factors of colorectal cancer was analyzed by χtest or Fisher's exact test. Three-year overall survivals of PNI positive and negative patients were determined using the Kaplan-Meier method. Detection results were compared using log-rank test.

RESULTSOf 372 colorectal cancer patients, 133 (35.8%) were PNI positive. Among the PNI positive patients, 63 cases were male and 70 cases female; 76 cases were more than 60 years old and 57 cases less than 60 years old; tumors of 6 cases located in the ileocecal colon, of 33 cases in the ascending colon, of 7 cases in the transverse colon, of 8 cases in the descending colon, of 22 cases in the sigmoid colon, and of 57 cases in the rectum; tumor diameter was greater than 4 cm in 83 cases, and less than 4 cm in 50 cases; tumors of 48 cases were moderately or highly differentiated, and of 85 cases poorly-differentiation; tumor invasion depth in 2 cases, T2 in 7 cases, T3 in 93 cases, T4 in 31 cases; lymphatic metastasis was N0 phase in 56 cases, N1 in 41 cases, and N2 in 36 cases; tumors were stage I( in 2 cases, stage II( in 40 cases, of stage III( in 75 cases and stage IIII( in 16 cases. The positive rate of PNI was significantly associated with tumor location (χ=11.20, P=0.048), tumor size (χ=21.80, P=0.000), differentiation (χ=60.90, P=0.000), depth of invasion (χ=19.00, P=0.000), lymph node metastasis (χ=19.70, P=0.000) and TNM staging (χ=70.80, P=0.000), but not with sex, age or vascular invasion(P>0.05). The median follow-up time was 48 (8 to 62) months. Kaplan-Meier survival curve showed that the 3-year survival rate of PNI positive patients was 52.6%, significantly lower than that of PNI negative patients(78.3%, P=0.000). Further analysis of patients with stage II( and III( colorectal cancer showed that the 3-year survival rates of PNI positive patients were 62.3% and 43.5%, respectively, which were significantly lower than those of PNI negative patients with stage II( and III((91.7% and 79.4%), and the differences were statistically significant(P=0.000).

CONCLUSIONSPNI is a poor prognostic factor of colorectal cancer. It may be a complement of the classic TNM staging classification in stratifying colorectal cancer patients, especially in stages II( and III(.

Aged ; Colorectal Neoplasms ; diagnosis ; epidemiology ; mortality ; pathology ; Female ; Follow-Up Studies ; Humans ; Kaplan-Meier Estimate ; Lymphatic Metastasis ; pathology ; Male ; Middle Aged ; Neoplasm Grading ; statistics & numerical data ; Neoplasm Invasiveness ; pathology ; physiopathology ; Neoplasm Staging ; statistics & numerical data ; Peripheral Nervous System Neoplasms ; mortality ; pathology ; Prognosis ; Retrospective Studies ; Risk Factors ; Survival Rate

OBJECTIVETo investigate the risk factors of metachronous bone metastasis after radical resection of colorectal cancer within 5 years.

METHODSClinical data of 1 749 patients with colorectal cancer, of whom 50(2.8%) patients developed metastasis to bone after operation, in the Department of Colorectal Surgery, Changhai Hospital of The Second Military Medical University from January 2001 to December 2010 were analyzed retrospectively. Univariate and multivariate analysis were performed to find the risk factors of metachronous bone metastasis from colorectal cancer using Chi square test and Logistic regression, respectively.

RESULTSOf 50 colorectal cancer cases with bone metastasis, 29 were male and 21 were female. The age was ≥ 60 years old in 28 cases. Tumors of 36 cases were located in the rectum and of 14 cases located in the colon. Pathology examination showed 43 cases were adenocarcinomas, 7 cases were mucinous adenocarcinoma. Forty-two cases had T3-4 stage lesions, 30 cases had lymph node metastasis, 14 cases had pulmonary metastasis, and 5 cases had liver metastasis. Univariate Chi square test indicated that factors associated with the metachronous bone metastasis of colorectal cancer within 5 years were tumor site (χ=4.932, P=0.026), preoperative carbohydrate antigen 199 (CA199) level (χ=4.266, P=0.039), lymph node metastasis (χ=13.054, P=0.000) and pulmonary metastasis(χ=35.524, P=0.000). The incidence of bone metastasis in patients with rectal cancer (3.6%, 36/991) was higher compared to those with colon cancer (1.8%, 14/758). The incidence of bone metastasis in patients with higher(> 37 kU/L) preoperative serum CA199 level (4.9%, 12/245) was higher compared to those with lower serum CA199 level (2.5%, 38/1504). The incidence of bone metastasis in patients with lymph node metastasis(4.8%,30/627) and pulmonary metastasis (11.6%, 14/121) was significantly higher compared to those without lymph node metastasis (1.8%, 20/1122) and pulmonary metastasis(2.2%, 36/1628), respectively. Logistic multivariate analysis showed that rectal cancer(OR:0.508, 95%CI:0.268 to 0.963, P=0.038), lymph node metastasis (OR:2.291, 95%CI:1.273 to 4.122, P=0.006) and metachronous pulmonary metastasis(OR:4.796, 95%CI:2.473 to 9.301, P=0.000) were the independent risk factors of metachronous bone metastasis of colorectal cancer within 5 years.

CONCLUSIONPatients with rectal cancer, lymph node metastasis and metachronous pulmonary metastasis are high risk groups of metachronous bone metastasis after radical resection of colorectal cancer within 5 years.

Adenocarcinoma ; surgery ; Aged ; Biomarkers, Tumor ; blood ; Bone Neoplasms ; epidemiology ; secondary ; Chi-Square Distribution ; Colonic Neoplasms ; surgery ; Colorectal Neoplasms ; surgery ; Colorectal Surgery ; statistics & numerical data ; Disease-Free Survival ; Female ; Humans ; Incidence ; Liver Neoplasms ; secondary ; Logistic Models ; Lung Neoplasms ; secondary ; Lymphatic Metastasis ; physiopathology ; Male ; Middle Aged ; Multivariate Analysis ; Prognosis ; Rectal Neoplasms ; surgery ; Retrospective Studies ; Risk Factors

Tripolinolate A (TLA) is recently identified as a new compound from a halophyte plant Tripolium vulgare and has been shown to have significant in vitro activity against the proliferation of colorectal cancer and glioma cells. This study was designed to further investigate the effects of TLA on the proliferation of human normal cells, and the apoptosis and cell cycle in colorectal cancer cells, and the growth of tumors in the colorectal cancer-bearing animals. The data obtained from this study demonstrated that: 1) TLA had much less cytotoxicity in the human normal cells than the colorectal cancer cells; 2) TLA remarkably induced apoptosis in the human colorectal cancer cells and blocked cell cycle at G/M phase, and 3) TLA had significant anti-colorectal cancer activity in the tumor-bearing animals.
Animals ; Antineoplastic Agents, Phytogenic ; administration & dosage ; chemistry ; Apoptosis ; drug effects ; Asteraceae ; chemistry ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Colorectal Neoplasms ; drug therapy ; physiopathology ; Drugs, Chinese Herbal ; administration & dosage ; chemistry ; Esters ; administration & dosage ; chemistry ; G2 Phase ; drug effects ; Humans ; Male ; Mice ; Mice, Inbred BALB C ; Phenols ; administration & dosage ; chemistry

Considering the great potential of natural products as anticancer agents, the present study was designed to explore the molecular mechanisms responsible for anticancer activities of Mesua ferrea stem bark extract against human colorectal carcinoma. Based on MTT assay results, bioactive sub-fraction (SF-3) was selected for further studies using HCT 116 cells. Repeated column chromatography resulted in isolation of less active α-amyrin from SF-3, which was identified and characterized by GC-MS and HPLC methods. α-amyrin and betulinic acid contents of SF-3 were measured by HPLC methods. Fluorescent assays revealed characteristic apoptotic features, including cell shrinkage, nuclear condensation, and marked decrease in mitochondrial membrane potential in SF-3 treated cells. In addition, increased levels of caspases-9 and -3/7 levels were also observed in SF-3 treated cells. SF-3 showed promising antimetastatic properties in multiple in vitro assays. Multi-pathway analysis revealed significant down-regulation of WNT, HIF-1α, and EGFR with simultaneous up-regulation of p53, Myc/Max, and TGF-β signalling pathways in SF-3 treated cells. In addition, promising growth inhibitory effects were observed in SF-3 treated HCT 116 tumour spheroids, which give a hint about in vivo antitumor efficacy of SF-3 phytoconstituents. In conclusion, these results demonstrated that anticancer effects of SF-3 towards colon cancer are through modulation of multiple molecular pathways.
Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Cell Line, Tumor ; Colorectal Neoplasms ; drug therapy ; metabolism ; pathology ; physiopathology ; ErbB Receptors ; genetics ; metabolism ; HCT116 Cells ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit ; genetics ; metabolism ; Magnoliopsida ; chemistry ; Neoplasm Metastasis ; prevention & control ; Plant Bark ; chemistry ; Plant Extracts ; pharmacology ; Signal Transduction ; drug effects ; Wnt Proteins ; genetics ; metabolism

OBJECTIVETo explore the inhibitory effect of combined administration of bear bile powder (BBP) and cyclophosphamide (Cytoxan, CTX) on colorectal cancer liver metastasis by regulating tumor promotion inflammation microenvironment.

METHODThe CRC liver metastasis mode in mice was established through in situ spleenic injection of SL4 tumor cells into spleens. The mice were randomly divided into 5 groups: the model group, the CTX (80 mg x kg(-1)) treatment group, the CTX + BBP high dose (300 mg x kg(-1)) group, the CTX + BBP middle dose (150 mg x kg(-1)) group and the CTX + BBP low dose (75 mg x kg(-1)) group. Mice were orally administered with drugs for 12 days, and sacrificed on the 13'h day for weighing their spleens and lives, HE staining, and immunofluorescence analysis. Their peripheral blood, and metastatic tumor in spleens and lives were analyzed with flow cytometry.

RESULTSpleen and liver weights of the: CTX treatment group and other doses groups were significantly lower than that of the model group. HE staining and immunofluorescence analysis showed that lymphocyte infiltration was detected in normal tissues, and macrophages infiltration was observed around the tumor tissues. Flow cytometry analysis showed that the number of T-lymphocytes in peripheral blood of different doses groups were much higher than that of the CTX treatment group (P < 0.05), with the rise in the ratio of CD4/CD8; the total number of lymphocytes in spleen cell suspension increased in different doses groups, compared to the CTX treatment group, with notable increase in B cells (P < 0.05) and significant decrease in CD11b, F4/80 cells (P < 0.05). The combined treatment showed less monocyte macrophages in liver metastasis than that of the CTX treatment group.

CONCLUSIONThe combined treatment of bear bile powder and cyclophosphamide has the effect in not only protecting liver and increase immunity, but also in anti-inflammation and antitumor by regulating tumor microenvironment and reducing the collection of mononuclear macrophages. Particularly, the combined administration of low dose of bear bile powder and CTX shows the most significant effect in reducing inflammatory cell infiltration.

Animals ; Bile ; chemistry ; Colorectal Neoplasms ; drug therapy ; mortality ; pathology ; Combined Modality Therapy ; Cyclophosphamide ; administration & dosage ; Humans ; Liver Neoplasms ; drug therapy ; mortality ; physiopathology ; secondary ; Male ; Mice ; Mice, Inbred C57BL ; Tumor Microenvironment ; drug effects ; Ursidae

BACKGROUND/AIMS: Serrated adenomas of the colon show mixed characteristics of both hyperplastic and adenomatous polyps. Serrated adenomas are known to progress via the serrated pathway than the adenoma-carcinoma pathway. The aim of this study was to evaluate the characteristics of traditional serrated adenomas compared to hyperplastic polyps and tubular adenomas by using immunohistochemical staining for p53, Bcl-2, and Ki-67. METHODS: Age, sex, location, size and the immunoexpression of p53, Bcl-2, and Ki-67 were retrospectively analyzed in 20 traditional serrated adenomas, 20 hyperplastic polyps, and 20 tubular adenomas from January 2007 to December 2012 at The Catholic University of Korea, Yeouido St. Mary's Hospital. RESULTS: There was no difference in Bcl-2 and p53 expression between traditional serrated adenomas and hyperplastic polyps. Ki-67 Expression of traditional serrated adenomas was higher than that of hyperplastic polyps (p=0.001). Ki-67 and p53 expression was similar between traditional serrated and tubular adenomas. Bcl-2 expression of traditional serrated adenomas was lower than that of tubular adenomas (p=0.001). Regarding the expression of p53, Bcl-2, and Ki-67 in traditional serrated adenomas, there were no statistical differences among age, sex, location, and size. CONCLUSIONS: Our study suggested that Ki-67 may be helpful in distinguishing traditional serrated adenomas from hyperplastic polyps, and p53 expression may be ineffective in distinguishing between traditional serrated and tubular adenomas. From Bcl-2 expression, it is suggested that the tumorigenesis of traditional serrated adenomas is lower than that of tubular adenomas.
Adenoma/genetics/metabolism/*physiopathology ; Aged ; Colonic Polyps/physiopathology ; Colorectal Neoplasms/genetics/metabolism/*physiopathology ; Female ; *Gene Expression Regulation, Neoplastic ; Humans ; Immunohistochemistry ; Ki-67 Antigen/*genetics/metabolism ; Male ; Middle Aged ; Proto-Oncogene Proteins c-bcl-2/*genetics/metabolism ; Retrospective Studies ; Tumor Suppressor Protein p53/*genetics/metabolism