单抗与细胞毒药物化学交联的概况

综述了近几年来单克隆抗体与细胞毒药物交联用于肿瘤治疗的一些化学方法，并对其优缺点进行了比较，同时对目前较流行的光敏交联。

Antitumor Activity of the Ganoderma Lucidum Spore Alcohol Extract in Vitro

Several cancer cell lines(epithelioma cells or leukemia cells)from human being or mouse were first used to study the antitumor activity of the Ganoderma lucidum spore alcohol extract(GLSAE)in vitro by the MTT test A comparision was made between the sporodermbroken(SB)and sporoderm nonbroken(SN)GLSAE It was showed that both GLSAE SB and GLSAE SN could inhibit the proliferation of these cancer cells,but the activity of GLSAE SB was much higher than that of GLSAE SN These results suggested that Ganoderma lucidum spore could probably be used for tumor treatment

Characterization of ST13 Protein Expression in Human Colorectal Cancer Tissues

Objective: To characterize the expression of ST13 protein in human tissuesfor investigation of the function of colorectal cancer related gene ST13. Methods: ST13 ORF wascloned and over-expressed in E.coli. The recombinant ST13 protein was purified by affinitychromatography. ST13 monoclonal antibodies were generated and affinity purified with the recombinantprotein. Immunoblot and immunohistochemical staining were employed to analyze ST13 proteinexpression in human tissues. Results: The expression and purification of the recombinant ST13protein were confirmed by SDS-PAGE. The protein yield reached about 2.5 mg/L of induced bacterialculture with a purity of 91.3%. Three strains of hybridoma were obtained with antibody titers from10~4 to 10~5 in ascites fluids and with high specificity for ST13 protein. Immunoblot showed thatthe apparent Mr of ST13 protein in SW480 cells and human tissues estimated by SDS-PAGE mobility wasapproximately 50 000, which was about 10 000 larger than the 41 324 calculated, but theglycosylation of the protein was excluded. Computer modeling revealed the protein to be ahydrophilic molecule. Immunohistochemical staining showed that ST13 protein was evenly distributedin cytoplasm and expressed in colon, stomach, liver, and other epithelial cells. Differences in thestaining intensity of the protein were observed between normal and cancer tissues as well as amongdifferent normal or carcinoma tissues. Conclusion: ST13 protein is a cytoplasmic molecule with anapparent Mr of 50 000. The protein is expressed in colorectal and other epithelial tissues. Theexpression level of the protein is down-regulated in colorectal cancer and varies among differentnormal and/or carcinoma tissues. Comparison of cDNA sequences and protein characteristics indicatesthat ST13 protein and hsp70-interacting protein (Hip) are same proteins, raising the possibilitythat ST13 protein is involved in the development of colorectal cancer through Hsp70 molecularchaperone machinery.

Influences of Melatonin on the Growth of HeLa Cells

Aim To investigate the influences of melatonin (MT) on the growth of HeLa cells in vitro. Methods Theantiprolfferation activities of MT were evaluated in HeLa cells by means of trypan blue dye exclusion and MTT vital staining.The morphological changes of HeLa cells induced by MT were observed under transmission electronic microscope. Cell divisioncycle influenced by MT was assessed by a flow cytometry. Results MT produced a certain inhibition of HeLa cells at the con-centration of 2 mmol@ L-1 and prolonged the TD. The fraction of cells inhibited was 61.0%. The IC. so of HeLa cells exposed toMT for 96 h was 2.039 mmol@ L- 1. The flow cytometric analyses showed that exposure to MT for 72 h reduced the number ofHeLa cells in phase S. Under electronic microscope, the HeLa cells exposed to MT for 72 h displayed morphological changesof necrosis, apoptosis, more hetero-chromosome and less somatic chromosome. Conclusion MT showed certain influences onthe growth of HeLa cells. Its mechanism may probably be attributable to reduction of the number of cells in phase S.

Antitumor Actinity of Puqietinone,a Novel Alkaloid fromthe Bulbs of Fritillaria puqiensis

从蒲圻贝母中分得的一种新生物碱蒲贝酮碱，按一定剂量灌胃给药，显示了强的抗小鼠艾氏腹水癌（ＥＡＳ，实体型），宫颈癌（Ｕ＿（１４），实体型）及肝癌（ＨｅＰＡ，实体型）的活性。

Antitumor activities of human autologous cytokineinduced killer(CIK)cells against hepatocellular carcinoma cells in vitro and in vivo

AIM: To characterize the anticancer function of cytokine-induced killer cells (CIK) and develop an adoptive immunotherapy for the patients with primary hepatocellular carcinoma (HCC), we evaluated the proliferation rate, phenotype and the antitumor activity of human CIK cells from healthy donors and HCC patients in vitro and in vivo. METHODS: Peripheral blood mononuclear cells (PBMC) from healthy donors and patients with primary HCC were incubated in vitro and induced into CIK cells in the presence of various cytokines such as interferon-gamma (IFN-gamma), interleukin-1 (IL-1), IL-2 and monoclonal antibody (mAb) against CD3. The phenotype and characterization of CIK cells were identified by flow cytometric analysis. The cytotoxicity of CIK cells was determined by (51)Cr release assay. RESULTS: The CIK cells were shown to be a heterogeneous population with different cellular phenotypes. The percentage of CD3+/CD56+ positive cells, the dominant effector cells, in total CIK cells from healthy donors and HCC patients, significantly increased from 0.1-0.13% at day 0 to 19.0-20.5% at day 21 incubation, which suggested that the CD3+ CD56+ positive cells proliferated faster than other cell populations of CIK cells in the protocol used in this study. After 28 day in vitro incubation, the CIK cells from patients with HCC and healthy donors increased by more than 300-fold and 500-fold in proliferation cell number, respectively. CIK cells originated from HCC patients possessed a higher in vitro antitumor cytotoxic activity on autologous HCC cells than the autologous lymphokine-activated killer (LAK) cells and PBMC cells. In in vivo animal experiment, CIK cells had stronger effects on the inhibition of tumor growth in Balb/c nude mice bearing BEL-7402-producing tumor than LAK cells (mean inhibitory rate, 84.7% vs 52.8%, P【0.05) or PBMC (mean inhibitory rate, 84.7% vs 37.1%, P【0.01). CONCLUSION: Autologous CIK cells are of highly efficient cytotoxic effector cells against primary hepatocellular carcinoma cells and might serve as an alternative adoptive therapeutic strategy for HCC patients.

Cancer metabolic reprogramming: importance, main features, and potentials for precise targeted anti-cancer therapies

Cancer cells are well documented to rewire their metabolism and energy production networks to support and enable rapid proliferation, continuous growth, survival in harsh conditions, invasion, metastasis, and resistance to cancer treatments. Since Dr. Otto Warhurg＇s discovery about altered cancer cell metabolism in 1930, thousands of studies have shed light on various aspects of cancer metabolism with a common goal to find new ways for effectively eliminating tumor cells by targeting their energy metabolism. This review highlights the importance of the main features of cancer metabolism, summarizes recent remarkable advances in this field, and points out the potentials to translate these scientific findings into life-saving diagnosis and therapies to help cancer patients.

Reversing multidrug resistance by RNA interference through the suppression of MDR1 gene in human hepatoma cells

AIM： To reverse the multidrug resistance （MDR） by RNA interference （RNAi）-mediated MDRI suppression in heparoma cells.METHODS： For reversing MDR by RNAi technology, two different short hairpin RNAs （shRNAs） were designed and constructed into pGenSil-1 plasmid, respectively. They were then transfected into a highly adriarnycin-resistant HepG2 hepatorna cell line （HepG2/ADM）. The RNAi effect on MDR was evaluated by real-time PCR, cell cytotoxicity assay and rhodarnine 123 （Rh123） efflux assy. RESULTS： The stably-transfected clones showed various degrees of reversal of MDR phenotype. Surprisingly, the MDR phenotype was completely reversed in two transfected clones. CONCLUSION： MDR can be reversed by the shRNAmediated MDRI suppression in HepG2/ADM cells, which provides a valuable clue to make multidrug-resistant hepatoma cells sensitive to anti-cancer drugs.

Anticancer effects of oligomeric proanthocyanidins on human colorectal cancer cell line, SNU-C4

AIM: Oligomeric proanthocyanidins (OPC), natural polyphenolic compounds found in plants, are known to have antioxidant and anti-cancer effects. We investigated whether the anti-cancer effects of the OPC are induced by apoptosis on human colorectal cancer cell line, SNU-C4.METHODS: Colorectal cancer cell line, SNU-C4 was cultured in RPMI 1640 medium supplemented with 10% fetal bovine serum. The cytotoxic effect of OPC was assessed by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenylt-etrazolium bromide (MTT) assay. To find out the apoptotic cell death, 4, 6-diamidino-2-phenylindole (DAPI) staining,terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) assay, reverse transcriptionpolymerase chain reaction (RT-PCR), and caspase-3 enzyme assay were performed.RESULTS: In this study, cytotoxic effect of OPC on SNUC4 cells appeared in a dose-dependent manner. OPC treatment (100 μg/mL) revealed typical morphological apoptotic features. Additionally OPC treatment (100 μg/mL)increased level of BAX and CASPASE-3, and decreased level of BCL-2 mRNA expression. Caspase-3 enzyme activity was also significantly increased by treatment of OPC (100 μg/mL) compared with control.CONCLUSION: These data indicate that OPC caused cell death by apoptosis through caspase pathways on human colorectal cancer cell line, SNU-C4.

Peripheral and mesenteric serum levels of CEA and cytokeratins,staging and histopathological variables in colorectal adenocarcinoma

AIM： To evaluate the differences that exist bet- ween peripheral and mesenteric serum levels of carcinoembryonic antigen （CEA） and cytokeratins in patients with colorectal adenocarcinoma. METHODS： One hundred and thirty-eight patients with colorectal adenocarcinoma who underwent surgery at Hospital Sao Paulo （Discipline of Surgical Gastroenterology of UNIFESP-EPM） between December 1993 and March 2000 were retrospectively analyzed. Differences between CEA and cytokeratin （TPA-M） levels in peripheral blood （P） and in mesenteric blood （M） were studied. Associations were investigated between peripheral and mesenteric levels and the staging and histopathological variables （degree of cell differentiation, macroscopic appearance, tumor dimensions and presence of lymphatic and venous invasion）. RESULTS： Differences were observed in the numerical values of the marker levels： CEA （M） （39.10 mg/1 ± 121.19 mg/L） vs CEA （P） （38.5 mg/L ± 122.55 mg/L）, P 〈 0.05; TPA-M （M） （325.06 U/L ±527.29 U/L） vs TPA-M （P） （279.48 U/L ±455.81 U/L）, P 〈 0.01. The mesenteric CEA levels were higher in more advanced tumors （P 〈 0.01）, in vegetating lesions （34.44 mg/L ± 93.07 mg/L） （P 〈 0.01） and with venous invasion （48.41 mg/L ± 129.86 mg/L） （P 〈 0.05）. Peripheral CEA was higher with more advanced staging （P 〈 0.01）and in lesions with venous invasion （53.23 mg/L ± 258.57 mg/L） （P 〈 0.05）. The patients demonstrated increased mesenteric and peripheral TPA-M levels with more advanced tumors （P 〈 0.01 and P 〈 0.01） and in non-ulcerated lesions [530.45 U/L =1= 997.46 U/L （P 〈 0.05） and 457.95 U/L ± 811.36 U/L （P 〈 0.01）]. CONCLUSION： The mesenteric levels of the tumor markers CEA and cytokeratins were higher than the peripheral levels in these colorectal adenocarcinoma patients, Higher levels of these biologic tumor markers are associated with an advanced state of cancerous dissemination

Review:Anticancer effects of Chinese herbal medicine,science or myth?

Currently there is considerable interest among oncologists to find anticancer drugs in Chinese herbal medicine (CHM). In the past, clinical data showed that some herbs possessed anticancer properties, but western scientists have doubted the scientific validity of CHM due to the lack of scientific evidence from their perspective. Recently there have been encouraging results, from a western perspective, in the cancer research field regarding the anticancer effects of CHM. Experiments showed that CHM played its anticancer role by inducing apoptosis and differentiation, enhancing the immune system, inhibiting angiogenesis, reversing multidrug resistance (MDR), etc. Clinical trials demonstrated that CHM could improve survival, increase tumor response, improve quality of life, or reduce chemotherapy toxicity, although much remained to be determined regarding the objective effects of CHM in human in the context of clinical trials. Interestingly, both laboratory experiments and clinical trials have demonstrated that when combined with chemotherapy, CHM could raise the efficacy level and lower toxic reactions. These facts raised the feasibility of the combination of herbal medicines and chemotherapy, although much remained to be investigated in this area.

Systemic chemotherapy for hepatocellular carcinoma in non-cirrhotic liver:A retrospective study

AIM:To investigate the efficacy and toxicity of systemic chemotherapy in a retrospective study of patients with hepatocellular carcinoma(HCC)occurring in normal or fibrotic liver without cirrhosis. METHODS:Twenty-four patients with metastatic or locally advanced HCC in a normal or a fibrotic liver were given systemic chemotherapy(epirubicin,cis- platin and 5-fluorouracil or epirubicin,cisplatin and capecitabine regimens).Tumor response,time to pro- gression,survival,and toxicity were evaluated. RESULTS:There were 7 women and 17 men,mean age 54±10 years;18 patients had a normal liver and 6 had a fibrotic liver(F1/F2 on biopsy).Mean tumor size was 14 cm,5 patients had portal vein thrombosis and 7 had metastasis.Patients received a median of 4 chemotherapy sessions.Overall tolerance was good. There were 5 partial responses(objective response rate =22%),and tumor control rate was 52%.Second line surgical resection was possible in two patients.Median survival was 11 mo,and 1-and 2-year overall survival rates were 50%±10%and 32%±11%,respectively. CONCLUSION:In patients with HCC in a non-cirrhotic liver,chemotherapy was well tolerated and associated with an objective response rate of 22%,including two patients who underwent secondary surgical resection.

Anti-tumor effect of 5-aza-2'-deoxycytidine by inhibiting telomerase activity in hepatocellular carcinoma cells

AIM:To investigate the effect of the demethylating reagent 5-aza-2'-deoxycitidine(DAC) on telomerase activity in hepatocellular carcinoma(HCC) cell lines,SMMC-7721 and HepG2.METHODS:The related gene expression in cell lines was examined by real-time reverse transcription-polymerase chain reaction and Western blotting analysis.The telomerase activity was examined by telomeric repeat amplification protocol-enzyme-linked immunosorbent assay and DNA methylation was determined by methylation-specific polymerase chain reaction.RESULTS:The telomerase activity was significantly reduced in both cell lines treated with DAC,accompanied by downregulation of telomerase reverse transcriptase(hTERT).We also observed the effect of DAC on the methylation status of hTERT promoter and the expression of regulatory genes,such as c-myc,p15,p16,p21,E2F1,and WT1.The methylation status of hTERT promoter could be reversed in SMMC-7721 by DAC,but not in HepG2 cells.However,p16 expression could be reactivated by demethylation of its promoter,and c-Myc expression was repressed in both cell lines.Moreover,DAC could enhance the sensitivity to the chemotherapeutic agents,such as cisplatin,by induction of apoptosis of HCC cells.CONCLUSION:The DAC exerts its anti-tumor effects in HCC cells by inhibiting the telomerase activity.

Antithrombin reduces reperfusion-induced hepatic metastasis of colon cancer cells

AIM： To examine whether antithrombin （AT） could prevent hepatic ischemia/reperfusion （I/R）-induced hepatic metastasis by inhibiting tumor necrosis factor （TNF）-α-induced expression of E-selectin in rats. METHODS： Hepatic I/R was induced in rats and mice by clamping the left branches of the portal vein and the hepatic artery. Cancer cells were injected intrasplenically. The number of metastatic nodules was counted on day 7 after I/R. TNF-α and E-selectin mRNA in hepatic tissue, serum fibrinogen degradation products and hepatic tissue levels of 6-keto-PGF1α, a stable metabolite of PGI2, were measured. RESULTS： AT inhibited increases in hepatic metastasis of tumor cells and hepatic tissue mRNA levels of TNF-α and E-selectin in animals subjected to hepatic I/R. Argatroban, a thrombin inhibitor, did not suppress any of these changes. Both AT and argatroban inhibited I/R-induced coagulation abnormalities. I/R-induced increases of hepatic tissue levels of 6-keto-PGF1α were significantly enhanced by AT. Pretreatment with indomethacin completely reversed the effects of AT. Administration of OP-2507, a stable PGI2 analog, showed effects similar to those of AT in this model. Hepatic metastasis in congenital AT-deficient mice subjected to hepatic I/R was significantly increased compared to that observed in wild-type mice. Administration of AT significantly reduced the number of hepatic metastases in congenital AT-deficient mice. CONCLUSION： AT might reduce I/R-induced hepatic metastasis of colon cancer cells by inhibiting TNF-α-induced expression of E-selectin through an increase in the endothelial production of PGI2. These findings also raise the possibility that AT might prevent hepatic metastasis of tumor cells if administered during the resection of liver tumors.

Survivin expression in early hepatocellular carcinoma and post-treatment with anti-cancer drug under hypoxic culture condition

AIM： To investigate the expression of survivin during the early stages of hepatocellular cardnoma （HCC）.METHODS： Immunohistochemical expression of survivin in liver tumor and non-tumor tissue specimens taken from 17 patients was compared. In addition, to determine the survivin expression in response to anticancer drugs in early stage HCC, the survivin expression was determined after the treatment of the HCC cells with anti-cancer drugs under hypoxic culture conditions.RESULTS： Survivin proteins were expressed in 64.7% of cells in early HCC specimens. A correlation between the survivin expression rate in the peritumoral hepatocytes and the rate of expression in the HCC specimens （low-rate group vs high-rate group） was observed. The survivin protein concentration in HCC cells was increased by the combination of hypoxia and anti-cancer drugs.CONCLUSION： This study suggests that survivin could be used as a therapeutic target in early HCC.

Purification and characterization ofα-L-fucosidase from human primary hepatocarcinoma tissue

AIM: To purify and characterizeα-L-fucosidase from human liver cancer tissue and to detect the localization ofα-L-fucosidase in tumor tissue. METHODS: Cation exchange chromatography on CM-52 and ultrafiltration were used to separateα-Lfucosidase (AFU) from crude extract of liver cancer tissue. 4-methylumbelliferyl-α-L-fucopyranoside was used as a fluorescent substrate to quantify the purified AFU activity in each step. A polyclonal antibody (pAb) against the purified AFU was obtained by anion exchange chromatography on DEAE-52 after ammonium sulfate fractionation and ultrafiltration. Immuohistochemical staining was used to observe the expression of AFU in malignant and adjacent liver tissues. RESULTS: Humanα-L-fucosidase was purified 74-fold to apparent homogeneity with 15% yield. SDSPAGE indicated the presence of one subunit of molecular weight of 55 Ku. The specific activity of AFU in pooled fraction by chromatography was 10085 IU/mg. Western blot analysis indicated that the pAb could recognize one protein band of molecular weight of 55 Ku. The expression of AFU was observed in cytoplasm membrane of liver cancer tissue but not in that of adjacent tissue. CONCLUSION: The purifiedα-L-fucosidase from primary hepatocarcinoma (PHC) is different in its properties fromα-L-fucosidase in human other organs. The polyclonal antibody prepared in this experiment can be applied to the diagnosis of PHC.

Treatment of hepatoma with liposome-encapsulated adriamycin administered into hepatic artery of rats

AIM： To observe the therapeutic effects of liposomeencapsulated adriamycin （LADM） on hepatoma in comparison with adriamycin solution （FADM） and adriarnycin plus blank liposome （ADM ＋ BL） administered into the hepatic artery of rats. METHODS： LADM was prepared by pH gradient-driven method. Normal saline, FADM （2 mg/kg）, ADM＋BL （2 mg/kg）, and LADM （2 mg/kg） were injected via the hepatic artery in rats bearing liver W256 carcinosarcoma, which were divided into four groups randomly. The therapeutic effects were evaluated in terms of survival time, tumor enlargement ratio, and tumor necrosis degree. The difference was determined with ANOVA and Dunnett test and log rank test. RESULTS： Compared to FADM or ADM ＋ BL, LADM produced a more significant tumor inhibition （tumor volume ratio： 1.243±0.523 vs 1.883±0.708, 1.847±0.661, P 〈 0.01）, and more extensive tumor necrosis. The increased life span was prolonged significantly in rats receiving LADM compared with FADM or ADM＋BL （231.48 vs 74.66, 94.70） （P 〈 0.05）. CONCLUSION： The anticancer efficacies of adriamycin on hepatoma can be strongly improved by liposomal encapsulation through hepatic arterial administration.

A preliminary analysis of antineoplastic activity ofparvovirus MVMp NS-1 proteins

Human gastric cancer MKN-45 cells were transfectedwith pULB 3238, a plasmid carrying MVMp NS-1 genewith its original P4 promoter replaced by the glucocorticoid inducible promoter MMTV-LTR. After the integration and expression of NS-1 gene, some of the transfectantsdied, while others remained alive, but the growth featuresof survived cells were changed. For further study on theantineoplastic function of parvoviral NS-1 protein in vivo,transgenic mice carrying NS-1 genes were established byconventional method. Among 4 founders, one of them wasfound to be able to transmit the transgene to around 50%of their offsprings. RT-PCR was performed to indicate theexpression of NS-1 gene in transgenic mice and its mRNAappeared in a variety of tissues. The expression of integrated NS-1 gene may correlate with the decreased incidence of tumor induced in vivo by chemical carcinogens.

Reversal of Adriamycin Resistance of Hepatocellular Carcinoma by Targeting with Recombined Adenovirus Caning Antisense mdr1 RNA

OBJECTIVE Chemotherapy is an important therapy for hepatocellular carcinoma （HCC）. However, it is not effective in many cases due to recurrence and metastasis even if the initial treatment produces a response. Multidrug resistance （MDR） is considered to be one of the considerable causes. The aim of this study was to reverse MDR of HepG2/ADM cells by blocking mdr1 with an adenovirus vector carrying antisense mdr1 in a tumor transplantated in athymic mice. METHODS PCMV IE was removed from the pshuttle vector. A 0.3 kb AFP promoter was inserted into the pshuttle vector and pCMV changed into pAFP. The pAFP and asmdr1 PCR products were doubly digested with Kpnl and Apal, the digested products were ligated by T4 ligase, the asmdr1 gene was inserted into pAFP and a newly plasmid pAFP-asmdr1 was constructed. Following digestion with PI-SceI/I-Ceu I, pAFP-asmdr1 was ligated with Adeno-X genome DNA and amplified in E.coli XL1-Blue. The HEK293 cells were transfected and virus collected. The HepG2 MDR cells （HepG2/ADM） were induced by graded resistance to ADM and were inoculated into athymic mice. After adeno-asmdr1 was injected, the expression of mdr1-mRNA and the volume of the transplantated tumor and its cells were observed. RESULTS Following injection with Adeno-asmdr1, the tumor volume in the ADM＋Adeno-asmdr1 group did not increase. However the tumor volume in the PBS plus ADM group did significantly increase （P〈0.05）. In the tumor xenograft cells, mdr1 mRNA in the xenografts was assessed by RT-PCR and was found to be reduced at 1 week and 4 weeks in the ADM＋asmdr1 group, but it was stable in the ADM group. It was only 20% in the ADM＋asmdr1 group compared to the ADM group at the 4th week （P〈0.05）. Evidence of apoptosis was observed in the tumor xenograft cells treated with Adeno-asmdr1, but there was rare or no apoptosis in the group treated with ADM and PBS. CONCLUSION Adenovirus carrying antisense mdr1 RNA can partially reverse the MDR of HepG2/ADM cells and inhibit tumor growth by down-regulating mdr1 mRNA resulting in tumor cell apoptosis.

Significance of serum tumor markers CA50 and CEA in gastric cancer

AIMS The CAS0 and CEA are well-described human tumor-as- sociated antigens most useful clinically in gastrointestinal cancer. In this study we compared these markers in sera from patients with malignant and benign digestive tract diseases. METHODS Using a side-phase radioimmunoassay,CA50 and CEA serum levels were measured in 33 control subjects and 86 patients with gastric cancer(n=34),gastric ulcer(n=27)and chronic atrophic gastritis(n=25).Carcinoma of the stomach was found in the antrum(n=22),in the body(n=3),and the fundus(n=9),and histopathologically,was divided into adeno- carcinoma(n=21),squamous cancer(n=4)and not divided (n=9).Gastric ulcer,when present,appeared in the antrun(18 patients),the body(3)and the fundus(9)and chronic atrophic gastritis was all associated with intestinal metaplasia(IM). RESULTS The normal ranges established for CA50 and CEA in the control group were 16.26+6.14 kU/L and 3.12±1.03/μg/L respectively.In the patients with gastric cancer,serum levels of CA50(112.67±38.36 kU/L)and CEA(10.28±3.76μg/L) were elevated significantly(P<0.01,respectively),the former being>22 kU/L in 18 of 34 patients(53%;range,5-1 550 kU/ L),and the latter>5 μg/L in 19 of 34 patients(55.8%,range, 0.5-17.4 μg/L).A statistically significant correlation was found between the levels of CA50 and GEA(r=0.648,P<0.01). The serum levels of CA50(46.4±25.9 kU/L,P<0.01 )and CEA(6.85±2.43 μg/L,P<0.01)were much lower in patients with gastric ulcer or chronic atrophic gastritis(P>0.05). CONCLUSIONS Based on these results,it is concluded that CA50 and CEA are indicators for advanced gastric cancer,and af- ter surgery,their serum levels may decrease considerably. Overall,there is such a close correlation between them that in clinical practice they might be of great value to the diagnosis of gastric cancer.