转车原理

介绍了一种搭车方法 ,以及讨论了搭车的一般规律 .运用矩阵知识和简单运算 ,以表格形式建立数学模型 ,给出制定搭车策略的一般方法 .最后得出查找中间站的定理。

Predictive value of Ki67 and p53 in locally advanced rectal cancer:Correlation with thymidylate synthase and histopathological tumor regression after neoadjuvant 5-FU-based chemoradiotherapy

AIM: To investigate the predictive value of Ki67 and p53 and their correlation with thymidylate synthase (TS) gene expression in a rectal cancer patient cohort treated according to a standardized recommended neoadjuvant treatment regimen.METHODS: Formalin fixed, paraffin embedded pre-therapeutical tumor biopsies (n = 22) and post-therapeutical resection specimens (n = 40) from patients with rectal adenocarcinoma (clinical UICC stage Ⅱ/Ⅲ) receiving standardized neoadjuvant 5-fluorouracil (5-FU) based chemoradiotherapy were studied for Ki67 and p53 expression by immunohistochemistry and correlated with TS mRNA expression by quantitative TaqMan real-time PCR after laser microdissection. The results were compared with histopathological tumor regression according to a standardized semiquantitative score grading system.RESULTS: Responders (patients with high tumor regression) showed a significantly lower Ki67 expression than non-responders in the pre-therapeutical tumor biopsies (81.2% vs 16.7%; P < 0.05) as well as in the post-therapeutical resection specimens (75.8% vs 14.3%; P < 0.01). High TS mRNA expression was significantly correlated with a high Ki67 index and low TS mRNA expression was significantly correlated with a low Ki67 index in the pre-therapeutical tumor biopsies (corr. coef. = 0.46; P < 0.01) as well as in the post-therapeutical resection specimens (corr. coef. = 0.40; P < 0.05). No significant association was found between p53 and TS mRNA expression or tumor regression.CONCLUSION: Ki67 has, like TS, predictive value in rectal cancer patients after neoadjuvant 5-FU based chemoradiotherapy. The close correlation between Ki67 and TS indicates that TS is involved in active cell cycle processes.

Overlapping expression of microRNAs in human embryonic colon and colorectal cancer

MicroRNAs （miRNAs） are essential for regulating cell differentiation and maintaining the pluripotent state of stem cells. Although dysregulation of specific miRNAs has been associated with certain types of cancer, to date no evidence has linked miRNA expression in embryonic and tumor tissues. We assessed the expression of mature miRNAs in human embryonic colon tissue, and in colorectal cancer and paired normal colon tissue. Overlapping miRNA expression was detected between embryonic colonic mucosa and colorectal cancer. We have found that the miR-17-92 cluster and its target, E2F1, exhibit a similar pattern of expression in human colon development and colonic carcinogenesis, regulating cell proliferation in both cases. In situ hybridization confirmed the high level of expression of miR-17-5p in the crypt progenitor compartment. We conclude that miRNA pathways play a major role in both embryonic development and neoplastic transformation of the colonic epithelium.

Overexpression of S100A4 is closely associated with progression of colorectal cancer

AIM： To investigate whether S100A4 played an important role in the development or progression of colorectal cancer. METHODS： A total of 124 colorectal adenocarcinoma tissue specimens were analyzed by immunohistochemistry for the expression of S100A4 protein and subsequently investigated for the gene mutations in the coding region of S100A4 gene. The specimens were collected over a 3-year period in the laboratories at our large teaching hospital in Seoul, Republic of Korea. RESULTS： Normal colonic epithelium either failed to express or showed focal weak expression of S100A4. Moderate to strong cytoplasmic expression of S100A4 was seen in 69 （55.6%） of the 124 colorectal carcinoma tissue specimens. S100A4 expression was detected in 43 （69.4%） of 62 specimens with lymph node metastasis. Statistically, overexpression of S100A4 was significantly associated with Dukes＇ stage and lymph node metastasis. Nuclear staining was also observed in 24 （19.4%） of 124 samples and closely associated with Dukes＇ stage. However, there was no significant correlation between overexpression of S100A4 and other investigated clinico-pathologic parameters, including tumor localization, tumor size, and survival period. In mutational analysis, no gene mutation was found in the analyzed genomic area of colorectal cancer. CONCLUSION： Overexpression of S100A4 may be closely related with the aggressiveness of colorectal carcinoma.

Aberrant expression of krUppel-like factor 6 protein in colorectal cancers

AIM： TO investigate whether krüppel-like factor 6 （KLF6） plays an important role in the development and/or progression of colorectal cancer. METHODS： A total of 123 formalin-fixed and paraffinembedded colorectal cancer specimens were analyzed by immunohistochemistry using tissue microarray for the expression of KLF6 protein. The specimens were collected over a 3-year period in the laboratories at our large teaching hospital in Seoul, Republic of Korea. The correlation of KLF6 expression with clinicopathologic parameters was analyzed by χ^2 test and Bartholomew test. RESULTS： Normal colonic epithelium showed weak to moderate expression of KLF6, whereas reduced KLF 6 expression or loss of KLF6 expression was seen in 45 （36.6%） of the 123 colorectal carcinoma specimens. Interestingly, aberrant expression of KLF6 was detected in 25 （43.1%） of 58 cases with metastasis to regional lymph node and in 31 （47.0%） of 66 tumors more than 5 cm in size. Statistically, loss of KLF6 expression was significantly associated with tumor size （P〈0.05）. However, there was no significant correlation between KLF6 expression and Dukes＇ stage （Bartholomew test, P〉 0.05）, tumor location and lymph node metastasis （χ^2 test, P〉0.05）.CONCLUSION： Loss of KLF6 expression may be a common and early event in colorectal carcinogenesis.

Correlation of N-myc downstream-regulated gene 1 expression with clinical outcomes of colorectal cancer patients of different race/ethnicity

AIM： To evaluate the role of N-myc downstream- regulated gene 1 （NDRG1） expression in prognosis and survival of colorectal cancer patients with different ethnic backgrounds. METHODS： Because NDRG1 is a downstream target of p53 and hypoxia inducible factor-1α （HIF-1α）, we examined NDRG1 expression together with p53 and HIF-1α by irnmunohistochernistry. A total of 157 colorectal cancer specimens including 80 from Japanese patients and 77 from US patients were examined. The correlation between protein expression with clinicopathological features and survival after surgery was analyzed. RESULTS： NDRG1 protein was significantly increased in colorectal tumor compared with normal epithelium in both Japanese and US patient groups. Expression of NDRG1 protein was significantly correlated with lymphatic invasion, venous invasion, depth of invasion, histopathological type, and Dukes＇ stage in Japanese colorectal cancer patients. NDRG1 expression was correlated to histopathological type, Dukes＇ stage and HIF-1α expression in US-Caucasian patients but not in US-African American patients. Interestingly, Kaplan-Meier survival analysis demonstrated that NDRG1 expression correlated significantly with poorer survival in US-African American patients but not in other patient groups. However, in p53-positive US cases, NDRG1 positivity correlated significantly with better survival. In addition, NDRG1 expression also correlated significantly with improved survival in US patients with stages Ⅲ and IV tumors without chemotherapy. In Japanese patients with stages Ⅱ and Ⅲ tumors, strong NDRG1 staining in p53- positive tumors correlated significantly with improved survival but negatively in patients without chemotherapy. CONCLUSION： NDRG1 expression was correlated with various clinicopathological features and clinical outcomes in colorectal cancer depending on the race/ethnicity of the patients. NDRG1 may serve as a biological basis for the disparity of clinical outcomes of colorectal cancer patients with different ethnic backgrounds.

Gene expression profiling:Canonical molecular changes and clinicopathological features in sporadic colorectal cancers

AIM： To investigate alternative or subordinate pathways involved in colorectal tumorigenesis and tumor growth, possibly determining at-risk populations and predicting responses to treatment. METHODS： Using microarray gene-expression analysis, we analyzed patterns of gene expression relative to canonical molecular changes and clinicopathological features in 84 sporadic colorectal cancer patients, standardized by tumor location. Subsets of differentially expressed genes were confirmed by real-time reverse-transcript polymerase chain reaction （RT-PCR）. RESULTS： The largest number of genes identified as being differentially expressed was by tumor location, and the next largest number by lymphovascular or neural invasion of tumor cells and by mismatch repair （NMR） defects. Amongst biological processes, the immune response was significantly implicated in entire molecular changes observed during colorectal tumorigenesis （P 〈 0.001）. Amongst 47 differentially expressed genes, seven （PISD, NIBP, BAI2, STOML1, MRPL21, MRPL16, and MKKS） were newly found to correlate with tumorigenesis and tumor growth. Most location-associated molecular changes had distinct effects on gene expression, but the effects of the latter were sometimes contradictory. CONCLUSION： We show that several differentially expressed genes were associated with canonical molecular changes in sporadic colorectal cancers, possibly constituting alternative or subordinate pathways of tumorigenesis. As tumor location was the dominant factor influencing differential gene expression, location-specific analysis may identify location-associated pathways and enhance the accuracy of class prediction.

Identification of differently expressed genes in human colorectal adenocarcinoma

AIM： To investigate the differently expressed genes in human colorectal adenocarcinorna.METHODS： The integrated approach for gene expression profiling that couples suppression subtractive hybridization, high-throughput cDNA array, sequencing, bioinformatics analysis, and reverse transcriptase real- time quantitative polymerase chain reaction （PCR） was carried out. A set of cDNA clones including 1260 SSH inserts amplified by PCR was arrayed using robotic printing. The cDNA arrays were hybridized with florescent-labeled probes prepared from RNA of human colorectal adenocarcinoma （HCRAC） and normal colorectal tissues.RESULTS： A total of 86 genes were identified, 16 unknown genes and 70 known genes. The transcription factor Sox9 influencing cell differentiation was downregulated. At the same time, Heat shock protein 10 KDis downregulated and Calmoulin is up-regulated.CONCLUSION： Downregulation of heat shock protein 10 KD lost its inhibition of Ras, and men attenuated the Ras GTPase signaling pathway, increased cell proliferation and inhibited cell apoptosis. Down-regulated transcription factor Sox9 influences cell differentiation and cell-specific gene expression. Down-regulated Sox9 also decreases its binding to calmodulin, accumulates calmodulin as receptor-activated kinase and phosphorylase kinase due to the activation of PhK.

Tiaml gene expression and its significance in colorectal carcinoma

AIM: To explore the expression of Tiam1 gene in colorectal carcinoma and its correlation with tumor metastasis. METHODS: Expressions of Tiaml gene in 8 colorectal carcinoma cell lines were detected by reverse transcriptase-polymerase chain reaction. In vitro invasiveness was determined by means of Matrigel invasion assay. The correlation of Tiaml expression with the invasive ability was also analyzed. RESULTS: Tiaml gene was highly expressed in LoVo and SW620, which were established from metastatic colorectal carcinomas in comparison with LS174T, SW480, HCT116, LST, HRT-18 and Hee8693, which were established from primary colorectal carcinomas. In vitro cell invasivion demonstrated that LoVo and SW620 had a higher invasive ability than LS174T, SW480, HCT116, LST, HRT-18 and Hee8693. The expression of Tiaml gene was highly related to the metastatic potential of colorectal carcinoma cells. CONCLUSION: Tiaml gene may play an important role in invasion and metastasis of colorectal carcinoma and is a metastasis-related gene.

Expression of ST13 in colorectal cancer and adjacent normal tissues

AIM: To investigate the in situ expression of suppressionof tumorigenecity 13 (ST13) mRNA in both colorectal cancer and adjacent normal tissues.METHODS: Colorectal cancer cell lines SW1116, SW620and CoLo205 were enrolled to confirm the feasibility of the in situ hybridization procedure. Seven colorectal cancer and adjacent normal tissues were included for RNA-RNA in situ hybridization.RESULTS: The expression of ST13 in the seven normal colon tissues was positive and the positive signals appeared in mucosal cells. Only three of the seven colorectal cancer tissues had positive hybridization signals that appeared in adenocarcinoma cells.CONCLUSION: The expression of ST13 decreases in colorectal cancer tissue compared with that in adjacent normal tissue. ST13 is mostly expressed in colorectal epithelia and adenocarcinoma cells.

Telomerase activity and human telomerase reverse transcriptase expression in colorectal carcinoma

AIM： To study the activity of telomerase and the expression of human telomerase reverse transcriptase （hTERT） in colorectal carcinoma and its adjacent tissues, normal mucosa and adenomatoid polyp, and to evaluate their relation with carcinogenesis and progression of colorectal carcinoma. METHODS： Telomerase activity and hTERT expression were determined in 30 samples of colorectal carcinoma and its adjacent tissues, normal mucosa and 20 samples of adenomatoid polyp by modified telomeric repeat amplification protocol （TRAP）, enzyme-linked immunosorbent assay （ELISA） and immunohistochemical method. RESULTS： Telomerase activity and hTERT expression were 83.33% （25/30） and 76.67% （23/30） respectively in colorectal carcinoma, which were obviously higher than those in paracancerous tissues （13.33%, 16.67%）, normal mucosa （3.33%, 3.33%） and adenomatoid polyp （10%, 10%）. There was a significant difference between colorectal carcinoma and other tissues （P=0.027）. The telomerase activity and hTERT expression were higher in colorectal carcinoma with lymphatic metastasis than in that without lymphatic metastasis （P=0.034）. When the histological classification and clinical stage were greater, the telomerase activity and hTERT expression increased, but there was no significant difference between them. In colorectal carcinoma, the telomerase activity was correlated with hTERT expression （positive vs negative expression of telomerase activity and hTERT, P=0.021）. CONCLUSION： Telomerase activity is closely correlated with the occurrence, development and metastasis of colorectal carcinoma. Overexpression of hTERT may play a critical role in the regulation of telomerase activity.

Frequent mutations of the CA simple sequence repeat in intron 1 of EGFR in mismatch repair-deficient colorectal cancers

AIM:To investigate the polymorphic simple sequencerepeat in intron 1 of the epidermal growth factor receptorgene(EGFR)(CA-SSRⅠ),which is known to affect theefficiency of gene transcription as a putative target of themismatch repair(MMR)machinery in colorectal tumors.METHODS:The CA-SSRⅠgenotype was analyzed ina total of 86 primary colorectal tumors,selected upontheir microsatellite instability(MSI)status[42 with highfrequency MSI(MSI-H)and 44 microsatellite stable(MSS)]and their respective normal tissue.The effect of the CA-SSRⅠgenotype on the expression of the EGFR gene wasevaluated in 18 specimens using quantitative real-timereverse transcription PCR and immunohistochemistry.RESULTS:Mutations in CA-SSRⅠwere detected in 86%(36 of 42)of MSI-H colorectal tumors and 0%(0 of 44)ofMSS tumors,indicating the EGFR gene as a novel putativespecific target of the defective MMR system(P<0.001).Impaired expression of EGFR was detected in most ofthe colorectal tumors analyzed[6/12(50%)at the mRNAlevel and 15/18(83%)at the peptide level].However,noassociation was apparent between EGFR expression andCA-SSRⅠstatus in tumors or normal tissues.CONCLUSION:Our results suggest that CA-SSRⅠsequence does not contribute to the regulation of EGFRtranscription in colon,and should thus not be consideredas a promising predictive marker for response to EGFRinhibitors in patients with colorectal cancer.

Pin1 overexpression in colorectal cancer and its correlation with aberrant β-catenin expression

AIM： To investigate clinical significance of Pin1 and β-catenin expression in colorectal cancers and to demonstrate the relationship of their expression. METHODS： The role of Pin1 and β-catenin protein in colorectal tumorigenesis and their clinicopathologic significance were analyzed by immunohistochemistry, and correlation between Pin1 and β-catenin protein expressions was also studied in 124 patients with colorectal cancer who were surgically treated. RESULTS： Normal colonic epithelium either failed to express or showed focal and weak expression of Pin1 and β-catenin. Overexpression of Pin1 and β-catenin protein was found in 23 （18.54%） and 50 （40.3%） of 124 colorectal cancers, respectively. Overexpression of both proteins was not related to the lymph node metastasis, tumor stage and survival period after excision. Survival analysis results indicated that tumor stage was a valuable predictor of survival. Interestingly, a significant correlation was found between Pin1 and β-catenin protein expression. CONCLUSION： Overexpression of Pin1 and β-catenin may be closely related with the development and/or progression of colorectal carcinoma and further supports that Pin1 overexpression might contribute to the upregulation of β-catenin.

Effect of preoperative FOLFOX chemotherapy on CCL20/CCR6 expression in colorectal liver metastases

AIM： To evaluate the influence of preoperative FOLFOX chemotherapy on CCL20/CCR6 expression in liver metastases of stage IV colorectal cancer （CRC） patients.（/7 = 53） and in patients who did not receive FOLFOX chemotherapy prior to liver surgery （n = 29）. RESULTS： Of the 53 patients who received FOLFOX, time to liver surgery was n〈 1 mo in 14 patients, 〈 1 year in 22 patients and 〉 1 year in 17 patients, respectively. In addition, we investigated the proliferation rate of CRC cells in liver metastases in the different patient groups. Both CCL20 and CCR6 mRNA and protein ex- pression levels were significantly increased in patients who received preoperative FOLFOX chemotherapy ~〈 12 mo before liver surgery （P 〈 0.001） in comparison to patients who did not undergo FOLFOX treatment. Further, proliferation of CRLM cells as measured by Ki-67 was increased in patients who underwent FOLFOX treat- ment. CCL20 and CCR6 expression levels were significantly increased in CRLM patients who had undergone preoperative FOLFOX chemotherapy. CONCLUSION： This chemokine/receptor up-regulation could lead to increased proliferation/migration through an autocrine mechanism which might be used by surviving metastatic cells to escape cell death caused by FOLFOX.

Correlation of IL-8 with induction, progression and metastatic potential of colorectal cancer

AIM： To investigate the expression profile of IL-8 in inflammatory and malignant colorectal diseases to evaluate its potential role in the regulation of colorectal cancer （CRC） and the development of colorectal liver metastases （CRLM）.METHODS： IL-8 expression was assessed by quantitative real-time PCR （Q-RT-PCR） and the enzyme-linked immunosorbent assay （ELISA） in resected specimens from patients with ulcerative colitis （UC, n = 6） colorectal adenomas （CRA, n = 8）, different stages of colorectal cancer （n = 48） as well as synchronous and metachronous CRLM along with their corresponding primary colorectal tumors （n = 16）.RESULTS： IL-8 mRNA and protein expression was significantly up-regulated in all pathological colorectal entities investigated compared with the corresponding neighboring tissues. However, in the CRC specimens IL-8 revealed a significantly more pronounced overexpression in relation to the CRA and UC tissues with an average 30-fold IL-8 protein up-regulation in the CRC specimens in comparison to the CRA tissues. Moreover, [L-8 expression revealed a close correlation with tumor grading. Most interestingly, IL-8 up-regulation was most enhanced in synchronous and metachronous CRLM, if compared with the corresponding primary CRC tissues. Herein, an up to 80-fold IL-8 overexpression in individual metachronous metastases compared to normal tumor neighbor tissues was found.CONCLUSION： Our results strongly suggest an association between IL-8 expression, induction and progression of colorectal carcinoma and the development of colorectal liver metastases.

Absence of FHIT expression is associated with apoptosis inhibition in colorectal cancer

Objective： To investigate the expression of fragile histidine triad （FHIT） protein in normal colorectal tissue, colorectal adenoma and colorectal cancer （CRC）, and to study the relationships between the expression of FHIT protein and the clinical pathology, the apoptosis-associated protein （Bcl-2, Bax, Survivin）, apoptosis in colorectal cancer. Methods： Tissue microarray （TMA） and immunohistochemistry SP were used to detect the expression of FHIT gene, Bcl-2, Bax and Survivin in 16 cases of the normal colorectal tissue, 16 cases of colorectal adenoma and 80 cases of the colorectal cancer. TUNEL was used to detect the apoptosis index （Al） in 80 cases of the colorectal cancer. Results： （1） The positive rates of FHIT gene expression in normal colorectal tissue, colorectal adenoma and adenocancer were 93.75%, 68.75% and 46.25% respectively. There were no significant differences in the relationships between the FHIT gene expression and histological types, the gender as well as the age （P〉0.05）. There were significant relationships between FHIT gene expression and lymph node metastasis, histological grades, Duke＇s system as well as the 5-year survival rate after operation. （2） The positive rates of Bax, Bcl-2 and Survivin in colorectal adenocancer were 72.50%, 51.25%, 77.50% respectively. The expression of FHIT gene was positively correlated with that of Bcl-2, Bax and Survivin. （3） The mean AI in FHIT negative tumors was significantly lower than that in FHIT positive tumors （P〈0.01）. Conclusion： FHIT gene may play a role in the oncogenesis and progression of colorectal cancer. The abnormal regulation of apoptosis may play an important role in the pathogenesis of colorectal cancer.

B_7 molecule mRNA expression in colorectal carcinoma

AIM： To observe the status of tumor-associated B7 molecule mRNA expression in human colorectal cancer tissue by/n situ hybridization. METHODS： The mRNA expression patterns of cancer- associated B7-1,B7H1t,B7H2, ICOS in 22 specimens of human colorectal cancer tissue were monitored by in situ hybridization （ISH） with digoxin-labeled oligonucleotide probes. RESULTS： B7-1, B7H1,B7H2,ICOS mRNA were detected in both cancer cells and tumor infiltrating lymphocytes （TIL）. The mRNA expression level of these molecules in tumor cells was higher than that in TIL （0.76±0.54-1.62±0.82 vs 0.38±0.19-0.65±0.33, P〈0.001）. There was no relationship between expression level of tested B7 family molecules and patients＇ sex, age, differentiation status of cancer and regional lymph node metastasis. CONCLUSION： Th2 cytokine predominant in tumor microenvironment might be related to the expression of B7H1t B7H2 co-signal molecules in tumor cells and TIL. 2005 The WJG Press and Elsevier Inc. All rights reserved

DNA end binding activity and Ku70/80 heterodimer expression in human colorectal tumor

AIM： TO determine the DNA binding activity and protein levels of the Ku70/80 heterodimer, the functional mediator of the NHEJ activity, in human colorectal carcinogenesis. METHODS： The Ku70/80 DNA-binding activity was determined by electrophoretic mobility shift assays in 20 colon adenoma and 15 colorectal cancer samples as well as matched normal colonic tissues. Nuclear and cytoplasmic protein expression was determined by immunohistochemistry and Western blot analysis. RESULTS： A statistical found in both adenomas y significant difference was and carcinomas as compared to matched normal colonic mucosa （P〈0.00）. However, changes in binding activity were not homogenous with approximately 50% of the tumors showing a clear increase in the binding activity, 30% displaying a modest increase and 15% showing a decrease of the activity.Tumors, with increased DNA-binding activity, also showed a statistically significant increase in Ku70 and Ku86 nuclear expression, as determined by Western blot and immunohistochemical analyses （P〈0.001）. Cytoplasmic protein expression was found in pathological samples, but not in normal tissues either from tumor patients or from healthy subjects. CONCLUSION： Overall, our DNA-binding activity and protein level are consistent with a substantial activation of the NHEJ pathway in colorectal tumors. Since the NHEJ is an error prone mechanism, its abnormal activation can result in chromosomal instability and ultimately lead to tumorigenesis.

Correlation between expression and differentiation of endocan in colorectal cancer

AIM: To investigate the expression frequency of endocan in colorectal cancer and analyze the relationship between endocan expression and clinical parameters and to study the role of endocan in colorectal carcinogenesis. METHODS: Expression of endocan in 72 tumor tissue samples of colorectal cancer as well as in 27 normal mucous membrane tissue samples was analyzed using in situ hybridization, immunohistochemistry on tissue microarray, Western blot and reverse-transcript polymerase chain reaction (RT-PCR). RESULTS: The expression of endocan was higher in normal colon and rectum tissue samples than in cancerous tissue samples (mRNA = 92.6%, protein = 36%), and was lower in colorectal cancer tissue samples (mRNA = 70.4%, protein = 36.1%). No correlation was found between staining intensity and clinical parameters such as sex, age, tumor size andTNM stage. However, the expression of endocan was positively correlated with the tissue differentiation in colorectal cancer. CONCLUSION: The expression of endocan is down- regulated in colorectal cancer and is positively correlated with the tissue differentiation in colorectal cancer, suggesting that the expression of endocan is associated with development and differentiation of colorectal cancer.

The expression of chemokine MCP-1 in colorectal carcinoma and its relationship to the infiltration of macrophage

Objective: To study the expression of MCP-1 in colorectal carcinoma and its relationship to the infiltration of the macrophage and to the biological behaviour of infiltration and metastasis of colorectal carcinoma. Methods: The expression of the MCP-1 mRNA was assessed in colorectal carcinoma collected freshly from surgical specimen by RT-PCR and the expres- sion of the MCP-1 protein was assessed in colorectal carcinoma collected from surgical specimen by immunohistochemistry. The tumor infiltrating cell and macrophage were also investigated by immunohistochemistry. Results: All the 12 specimens of colorectal carcinoma detected by RT-PCR expressed the MCP-1 mRNA; MCP-1 protein was detected in 90℅ (36/40) cases of the tumor; The expression of the MCP-1 protein in colorectal carcinoma correlated negatively with its state of metastasis and the Dukes’ stage. But a postive correlation was found between the expression of MCP-1 and the infiltrated macrophage. The stron- ger expression of MCP-1, the more number of the infiltrated macrophage. Conclusion: The expression of chemokine MCP-1 in colorectal carcinoma may influence its biological behaviour of infiltration and metastasis, and can attract the immuno-cell to the local of the tumor, such as Macrophage.