Effects of Cadmium on Hepatocellular DNA Damage,Proto-Oncogene Expression and Apoptosis in Rats

Objective To study the effects of cadmium on hepatocellular DNA damage, expression of proto-oncogenes c-myc, c-fos, and c-jun as well as apoptosis in rats. Methods Cadmium chloride at the doses of 5, 10, and 20 μmol/kg was given to rats by i.p. and there were 5 male SD rats in each group. Hepatocellular DNA damage was measured by single cell gel electrophoresis （or comet assay）, while expression of proto-oncogenes c-myc, c-fos, and c-jun in rat hepatocytes were measured by Northern dot hybridization. C-Myc, c-Fos, and c-Jun were detected with immuno-histochemical method. Hepatocellular apoptosis was determined by TUNEL （TdT-mediated dUTP Nick End Labelling） and flow cytometry. Results At the doses of 5, 10, and 20 μmol/kg, cadmium chloride induced DNA damage in rat hepatocytes and the rates of comet cells were 50.20%, 88.40%, and 93.80%, respectively. Results also showed an obvious dose-response relationship between the rates of comet cells and the dose of cadmium chloride （r=0.9172, P〈0.01）. Cadmium chloride at the doses of 5, 10, and 20 μmol/kg induced expression of proto-oncogenes c-myc, c-fos, and c-jun. The positive brown-yellow signal for c-myc, c-fos, and c-jun was mainly located in the cytoplasm of hepatocytes with immunohistochemical method. TUNEL-positive cells were detected in cadmium-treated rat livers. Apoptotic rates （%） of cadmium-treated liver cells at the doses of 5, 10, and 20 μmol/kg were （17.24 ±2.98）, （20.58± 1.35）, and （24.06±1.77） respectively, being significantly higher than those in the control. The results also displayed an obvious dose-response relationship between apoptotic rates and the dose of cadmium chloride （r=0.8619, P〈0.05）. Conclusion Cadmium at 5-20 μmol/kg can induce hepatocellular DNA damage, expression of proto-oncogenes c-myc, c-fos, and c-jun as well as apoptosis in rats.

Current concepts in ameloblastoma-targeted therapies in B-raf proto-oncogene serine/threonine kinase V600E mutation: Systematic review

BACKGROUND Ameloblastomas are common benign epithelial odontogenic neoplasms that present an aggressive and unpredictable behavior that may modify treatment strategies.Different signaling pathways that participate in the progression of these tumors have been identified.B-raf proto-oncogene serine/threonine kinase(BRAF)is a protein involved in the behavior of ameloblastomas,and it is related to many cell mechanisms.BRAF gene mutations have been identified in ameloblastomas,of which the BRAF V600E(valine substituted by glutamic acid at amino acid 600)mutation has been the most common and can be present concomitantly with other mutations that may be involved in its behavior.Targeted therapies have been used as an alternative in the case of resistance or contraindications to conventional treatments.AIM To document the presence of BRAF V600E and additional mutations,their behavior,and targeted therapies in these tumors.METHODS An electronic literature search was conducted according to PRISMA guidelines in PubMed/MEDLINE,Cochrane,EMBASE,and SpringerLink using the terms“ameloblastomas”,“BRAF V600E”,“additional mutations”,and“targeted therapies”.Ameloblastomas were classified according to WHO guidelines.Inclusion criteria were articles in English,published not more than 10 years ago,and studies with laboratory works related to BRAF V600E.Articles were evaluated by two independent reviewers and retrieved for full-text evaluation.The EBLIP Critical Appraisal Checklist was used to evaluate the quality of the eligible studies.Descriptive statistical analysis was performed.RESULTS Two independent reviewers,with a substantial concordance indicated by a kappa coefficient of k=0.76,evaluated a total of 19 articles that were included in this study.The analysis registered 521 conventional ameloblastomas(AM),81 unicystic ameloblastomas(UA),13 ameloblastic carcinomas(AC),three metastatic ameloblastomas(MA),and six peripheral ameloblastomas(PA),of which the histopathological type,anatomic location,laboratory tests,expression of BRAF mutation,and additional mutations were registered.The BRAF V600E mutation was found in 297 AM(57%),63 UA(77.7%),3 AC(23%),1 MA(50%),and 5 PA(83.3%).Follicular type predominated with a total of 116 cases(40%),followed by plexiform type with 63 cases(22.1%).Furthermore,both types presented additional mutations,in which alterations in JAK3 P132T,SMARCB1,PIK3CA,CTNNB1,SMO,and BRAF G606E genes were found.Four case reports were found with targeted therapy to BRAF V600E.CONCLUSION The identification of BRAF V600E and additional mutations as an aid in targeted therapies has been a breakthrough in alternative treatments of ameloblastomas where surgical treatments are contraindicated.

Polymerase chain reaction-single strand conformational polymorphism analysis of rearranged during transfection proto-oncogene in Chinese familial hirschsprung's disease

AIM: To investigate the relationship between mutations of rearranged during transfection (RET) proto-oncogene and Chinese patients with Hirschsprung's disease (HD), and to elucidate the genetic mechanism of familial HD patient at the molecular level.METHODS: Genomic DNA was extracted from venous blood of probands and their relatives in two genealogies.Polymerase chain reaction (PCR) products, which were amplified using specific primers (RET, exons 11, 13, 15and 17), were electrophoresed to analyze the single-strand conformational polymorphism (SSCP) patterns. The positive amplified products were sequenced. Forty-eight sporadic HD patients and 30 normal children were screened for mutations of RET proto-oncogene simultaneously.RESULTS: Three cases with HD in one family were found to have a G heterozygous insertion at nucleotide 18 974 in exon 13 of RET cDNA (18 974insG), which resulted in a frameshift mutation. In another family, a heterozygosity for T to G transition at nucleotide 18 888 in the same exon which resulted in a synonymous mutation of Leu at codon 745 was detected in the proband and his father. Eight RET mutations were confirmed in 48 sporadic HD patients.CONCLUSION: Mutations of RET proto-oncogene may play an important role in the pathogenesis of Chinese patients with HD. Detection of mutated RET proto-oncogene carriers may be used for genetic counseling of potential risk for HD in the affected families.

Expressions of estrogen receptor subtypes and c-met proto-oncogene in endometrial carcinoma and their correlation

Objective To investigate the expressions of estrogen receptor(ER)subtypes and c-met proto-oncogene in human endometrial carcinomas and to assess the clinical significance of ER and c-met in this carcinoma.Methods Reverse transcription PCR(RT-PCR)was used to detect the expressions of ERα,ERβ and c-met proto-oncogene mRNA in 30 samples of endometrial carcinoma and 11 samples of normal endometrium.Results The expression of ERα in endometrial carcinoma(0.70±0.40)was significantly reduced in comparison to that in normal endometrium(1.14±0.56,P<0.05).A similar finding was made for the expression of ERβ in carcinoma(0.24±0.18)versus normal tissues(0.48±0.20,P<0.05).In contrast,c-met mRNA expression was increased in endometrial carcinoma(1.45±0.72)compared to that in normal endometrium(0.42±0.31,P<0.01).A decrease tendency of the expression of ERα was also found from Stage Ⅰ(0.82±0.41)to a more severe Stag Ⅱ-Ⅲ of endometrial carcinoma(0.42±0.17,P<0.05).The analysis of ERα and ERβ mRNA revealed a decrease tendency from shallow to deep invasion of the uterine muscles(P<0.05).We found that the expressions of ERα and ERβ were negatively correlated with c-met proto-oncogene with a coefficient correlation of-0.63(P<0.01)and-0.32(P<0.05),respectively.Conclusion ERα and ERβ are both involved in mutagenic action of carcinogen.C-met proto-oncogene plays an important role in the carcinogenesis and development of endometrial carcinoma.C-met and ER expressions show a negative correlation in the development of endometrial carcinoma.

Mutation of RET proto-oncogene in Hirschsprung's disease and intestinal neuronal dysplasia

AIM： To investigate the genetic relationship between Hirschsprung＇s disease （HD） and intestinal neuronal dysplasia （IND） in Chinese population.METHODS： Peripheral blood samples were obtained from 30 HD patients, 20 IND patients, 18 HD/IND combined patients and 20 normal individuals as control. Genomic DNA was extracted according to standard procedure. Exons 11,13,15,i7 of RET proto-oncogene were amplified by polymerase chain reaction （PCR）. The mutations of RET proto-oncogene were analyzed by single strand conformational polymorphism （SSCP） and sequencing of the positive amplified products was performed.RESULTS： Eight germline sequence variants were detected. In HD patients, 2 missense mutations in exon 11 at nucleotide 15165 G→A （G667S）, 2 frameshifc mutations in exon 13 at nucleotide 18974 （18974insG）, 1 missense mutation in exon 13 at nucleotide 18919 A→G （K756E） and 1 silent mutation in exon 15 at nucleotide 20692 G→A（Q916Q） were detected. In HD/IND combined patients, 1 missense mutation in exon 11 at nucleotide 15165 G→A and 1 silent mutation in exon 13 at nucleotide 18888 T→G （L745L） were detected. No mutation was found in IND patients and controls.CONCLUSION： Mutation of RET proto-oncogene is involved in the etiopathogenesis of HD. The frequency of REr proto-oncogene mutation is quite different between IND and HD in Chinese population, IND is a distinct clinical entity genetically different from HD.

Malignant pheochromocytoma in neurofibromatosis; mutation screening of RET proto-oncogene, VHL and SDH gene

AIM: To investigate pathogenic mutations related to malignant pheochromocytoma in neurofibromatosis(NF).METHODS: We present a patient with NF and metastatic pheochromocytoma in whom genetic screening for presence of pathogenic mutations in RET protooncogene, von Hippel-Lindau(VHL) and succinate dehydrogenase complex subunits B(SDHB) genes were investigated. RET proto-oncogene mutation screening for exons 10, 11, 13, 14, 15, 16 were examined by polymerase chain reaction(PCR) and direct DNA sequencing in patient. Mutation screening for exons 1, 2, 3 of VHL gene was carried out. Both forward and reverse strandswere subjected to direct sequencing after PCR amplification. The entire coding sequence of SDHB gene was screened for the presence of pathogenic mutations by PCR-sequencing.RESULTS: A 45-year-old man presented with abdominal pain and hypertension over the previous year. The patient was a known case of neurofibromatosis type 1(NF1) who presented at the age of 15 years with hyperpigmented and hypopigmented lesions. After complete evaluation for hypertension, biochemical tests and imagings indicated a malignant pheochromocytoma of 120 mm × 70 mm in size. The patient underwent left adrenalectomy, nephrectomy and splenectomy. After surgery the symptoms improved and blood pressure was controlled. After 5 years he was admitted again for evaluation of hypertensive crisis. Biochemical tests were again consistent with pheochromocytoma and disease relapse. Imaging studies and liver biopsy confirmed metastatic pheochromocytoma to the liver and para-aortic area. 131 Iodine-metaiodobenzylguanidine therapy was carried out. Genetic screening of VHL(exons 1, 2, 3), RET proto-oncogene(exons 10, 11, 13, 14, 15, 16) and SDH complex subunits revealed no pathogenic mutation. CONCLUSION: We conclude that mutations in the NF1 gene are responsible for the patient's clinical findings. However, would be helpful to further examine somatic mutations for a more precise study of genotypephenotype correlation.

THE PRELIMINARY APPLICATION OF IN SITU HYBRIDI-ZATION IN DETECTING PROTO-ONCOGENES EXPRESSION IN HUMAN LEUKEMIC CELLS

An in situ hybridization technique with 35S labelled proto-oncogene probes (c-myc & c-fes) was used to detect their expression in bone marrow cells of 22 cases of leukemia of various types and immature granulocytes and erythroblasts of 16 nomal myelograms as controls. Both c-myc and c-fes were detectable in leukemic cells as well as in immature granulocytes and erythroblasts of normal bone marrow, but the expression extent varied in different cases. The levels of c-myc expression in leukemic cells were higher than those in controls (P<0.001). There was no difference of c-fes expression in two groups of bone marrow cells (P>0.05). This technique provides us a new method in studying variations of proto-oncogene expression in leukemic cells.

A NOVEL Ser73Gly VARIATION OF SUCCINATE DEHYDROGENASE,SUBUNIT D AND A Cys634Gly MUTATION IN Ret PROTO-ONCOGENE OBSERVED IN A CHINESE MULTIPLE ENDOCRINE NEOPLASIA TYPE 2A PATIENT

Multiple endocrine neoplasia type 2A （ MEN2A ） is an autosomal dominant cancer syndrome that is characterized by medullary thyroid carcinoma （MTC）, pheochromaocytoma （50% - 60% of cases ）, and hyperplasia of the parathyroid glands （ 20% - 30% of cases ）. MEN-2A comprises a heterogeneous group of neoplastic disorders that most commonly have a single missense substitution of the Ret proto-oncogene （RET） involving exons 10 and 11. Here, we reported a novel case of MEN2A associated with two variations in two distinct genes, Cys634Gly in RET and a rare Ser73Gly substitution in succinate dehydrogenase, subunit D （SDHD）. Because the patient presented with medullary thyroid carcinoma and pheochromocytoma but without parathyroid gland involvement, we speculated that this clinical feature could be correlated with the two substitutions. This is the first report of a MEN2A case involving two different changes one in the RET gene and the other in the SDHD gene.

Effect of cisplatin-based concurrent radiochemotherapy on malignant degree of advanced cervical cancer and expression of proto-oncogene and tumor suppressor genes

Objective:To study the effect of cisplatin-based concurrent radiochemotherapy on the malignant degree of advanced cervical cancer and the expression of proto-oncogene and tumor suppressor genes.Methods: A total of 82 patients with advanced cervical cancer who were treated in our hospital between July 2013 and December 2016 were collected and divided into control group and observation group according to random number table, with 41 cases in each group. The control group of patients received radiotherapy alone, while the observation group of patients received cisplatin-based concurrent radiochemotherapy. Tumor marker levels in serum as well as proto-oncogene and tumor suppressor gene expression in tumor tissue were compared between two groups of patients before and after treatment.Results:Before treatment, differences in tumor marker levels in serum as well as proto-oncogene and tumor suppressor gene expression in tumor tissue were not statistically significant between two groups of patients. After treatment, serum tumor markers SCC, CA50, CA724 and CEA levels of observation group were significantly lower than those of control group;proto-oncogene DEK, c-myc and PIK3CA mRNA expression in tumor tissue were significantly lower than those of control group;tumor suppressor genes p53, SOCS-1, FHIT and PTEN mRNA expression in tumor tissue were significantly higher than those of control group.Conclusions:Cisplatin-based concurrent radiochemotherapy can effectively reduce the tumor malignancy and balance the proto-oncogene / tumor suppressor gene expression in patients with advanced cervical cancer.

RET proto-oncogene mutation analysis in a pedigree with multiple endocrine neoplasia 2A

Objective To discuss clinical diagnosis and treatment of multiple endocrine neoplasia ( MEN) 2A,and report the mutation of RET proto-oncogene in a pedigree of three patients with MEN 2A. Methods Bilateral adrenalectomy was performed on two of the three

Effect of Jinguo Weikang Capsule(金果胃康胶囊) on Proto-oncogene Expression of Gastric Mucosa in Rats with Gastric Precancerous Lesions

Objective： To study the effect of Jinguo Weikang Capsule （金果暖康胶囊, JWC） on the gene expression of H-ras, epidermal growth factor receptor （EGFR）, P53 and C-myc of the gastric mucosa in rats with gastric precancerous lesions, and to investigate the action mechanism of JWC on gastric precancerous lesions. Methods： A rat model with paratypical proliferation of the gastric epithelium mucosa was established by using ^60Co irradiation. Rats were divided into the normal group, model group, high-, medium-, low-dose JWC treatment groups, and the vitacoenzyme control group, and were treated for 30 days. The expression of H-ras, EGFR, P53 and C-myc genes of the gastric mucosa was detected by using immunohistochemical methods. Results： The expression and over-expression rates of H-ras, EGFR, P53 and C-myc gene in the high- and medium-dose JWC treatment groups were significantly lower （P〈0.05） as compared with those of the model group. Conclusion： JWC can inhibit the expression of the H-ras, EGFR, P53 and C-myc genes expression of the gastric mucosa in rats, which may be one of mechanisms involved in suppressing or reversing gastric carcinogenesis.

Effects of recombinant human transforming growth factor-β_1 or/and interleukin-6 on growth inhibition and proto-oncogene c-myc expression in human leukemia cells

Objective To examine the effect of recombinant human transforming growth factor β1 (rhTGF β1) alone or recombinant human interleukin 6 (rhIL 6) alone or in combination on proliferation inhibition of the human leukaemia cell line. Methods In the present study, using the human monoblastic cell line (U 937 ) and human promyelocytic cell line (HL 60 ) as an in vitro model, we analyzed the effect of two cytokins on proliferation inhibition with rate of 3H TdR incorporation, the cellular content of DNA, DNA indices, the cell cycle and the expression of c myc mRNA. Results With administration of rhTGF β 1 and rhIL 6, U 937 cell growth was inhibited and the rate of 3H TdR incorporation inhibition was increased. There was a decrease in the cellular content of DNA and DNA indices. And no change in the cell cycle was observed after administration of rhTGF β 1 or rhIL 6. However, there was an increase in G 0/G 1 phase cells and a decrease in G 2M+S phase cells after administration of combination of rhTGF β 1 and rhIL 6. It was also found that rhIL 6 could inhibit proliferative responses of HL 60 cells, meanwhile the inhibition could be enhanced by rhTGF β 1. The rate of 3H TdR incorporation inhibition rose up to 39.89%, and DNA index fell to 1.00 following induction by rhIL 6 plus rhTGF β 1. Furthermore, G 0/G 1 phase cells increased while G 2M+S cells decreased. Conclusions These results suggest that combination of rhTGF β 1 and rhIL 6 acted in synergy to inhibit proliferation of both U 937 and HL 60 cell lines. Molecular hybridization test show that rhTGF β 1 alone, rhIL 6 alone or rhTGF β 1 and rhIL 6 in combination can inhibit U 937 and HL 60 cells expression of c myc mRNA in a time and dose dependent manner. rhTGF β 1 and rhIL 6 in combination synergistically inhibited c myc expression, which may be one of the machanisms for the actions of the two cytokines.

In vitro triplex formation and functional analysis of TFOs designed against human c-sis/PDGF-B proto-oncogene

PDGF (platelet derived growth factor) has been shown to play animportant role in tumorigenesis, tumor growth, atherosclerosis and inflammation and other various pathologic settings. PDGF-B chain gene is 92% homologous to v-sis oncogene of the simian sarcoma virus. Thus PDGF-B gene is also called c-sis proto-oncogene. This report provides 3 TFOs (triplex-forming oligonucleotides) to inhibit the expression of c-sis/PDGF-B gene. The results from gel mobility shift analysis, in vitro transcription, DNase I footprinting and protein binding assays demonstrate that the TFOs we designed can form sequence-specific stable triplex with the target, and can effectively suppress the downstream gene transcription and inhibit transcription factors binding. They can be used for preparation of drugs to inhibit tumor growth and for the therapy of atherosclerosis, inflammation, etc.

AMPLIFICATIONS OF PROTO-ONCOGENES IN OVARIAN CARCINOMA

Thirty-two cases of ovarian carcinoma, two of normal ovaries, four of benign epithelial ovarian tumor, and three of borderline epithelial ovarian tumor were studied using Southern blot hybridization of DNA. In 15 of the 32 cases of ovarian carcinoma, peripheral lymphocytes were also studied. The amplification rate of C-myc, C-N-ras, C-Ki-ras and C-erbB-2 in ovarian carcinoma were 50%, 44%, 31% and 25% respectively. The amplification of C-Ki-ras and C-N-ras took place chiefly in cases of early stage and those of good differentiation. The amplification of C-N-ras was also found in cases of advanced stage. The amplifications of C-myc and C-erbB-2 were chiefly found in cases above stage Ⅲ and those of poor differentiation. A total of 83% of the patients who died were found to have amplifications of more than 2 proto-oncogenes, with which the amplification of C-erbB-2 was involved.

QUANTITATIVE DETECTION OF AMPLIFICATION OF PROTO-ONCOGENES IN BREAST CANCER

In the present study, dot-blot hybridization, serial dilution analysis and densitomctric scanning were used to detect amplification of proto- oncogenes including c-erbB2, c-myc, int-2 and c-Ha-ras in 104 paraffin-embedded breast cancers. Expression of c-erbB2 was also examined by immunohistochemistry. Amplification of c-erbB2. c-myc and int-2 genes was found in 34.7%, 17.8% and 11.9% of breast cancers respectively. However amplification of c-Ha-ras was not detected in all cases. In 11.9% of cases co-amplification of two or more oncogenes was observed. Positive immunostain-ing of c-erbB2 was seen in 23.8% of the cases and it was significantly associated, but not always corresponding to the amplification of the gene. There was no difference between primary and metastatic breast cancer in the alterations of proto-oncogenes examined in this study, which suggested that the amplification and overexpression of these proto-oncogenes occured prior to and maintained in the process of metastasis of breast cancer. Statistical analysis showed that high-scale of immunopositive staining of c-erbB2 and high-fold co-amplification of proto-oncogenes were significantly correlated with large size of the tumour and the number of involved lymph nodes. Our results indicate that the alterations of multiple oncogenes are involved in the development of breats cancer and some of them may have prognostic importance for breast cancer patients.

C634Y mutation in RET-induced multiple endocrine neoplasia type 2A:A case report

BACKGROUND Multiple endocrine neoplasia type 2(MEN2)is a rare,autosomal dominant endocrine disease.Currently,the RET proto-oncogene is the only gene implicated in MEN2A pathogenesis.Once an RET carrier is detected,family members should be screened to enable early detection of medullary thyroid carcinoma,pheochromocytoma,and hyperparatitity.Among these,medullary thyroid carcinoma is the main factor responsible for patient mortality.Accordingly,delineating strategies to inform clinical follow-up and treatment plans based on genes is paramount for clinical practitioners.CASE SUMMARY Herein,we present RET proto-oncogene mutations,clinical characteristics,and treatment strategies in a family with MEN2A.A family study was conducted on patients diagnosed with MEN2A.DNA was extracted from the peripheral blood of family members,and first-generation exon sequencing of the RET protooncogene was conducted.The C634Y mutation was identified in three family members spanning three generations.Two patients were sequentially diagnosed with pheochromocytomas and bilateral medullary thyroid carcinomas.A 9-yearold child harboring the gene mutation was diagnosed with medullary thyroid carcinoma.Surgical resection of the tumors was performed.All family members were advised to undergo complete genetic testing related to the C634Y mutation,and the corresponding treatments administered based on test results and associated clinical guidelines.CONCLUSION Advancements in MEN2A research are important for familial management,assessment of medullary thyroid cancer invasive risk,and deciding surgical timing.

Effect of heparin on apoptosis in human nasopharyngeal carcinoma CNE2 cells

In order to study the mechanism of the effect of heparin on apoptosis in carcinoma cells, the nasopharyngeal carcinoma cell line CNE2 was used to identify the effect of heparin on apoptosis associated with the expression of c-myc, bax, bcl-2 proteins by use of Hoechst 33258 staining, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL), agarose gel electrophoresis, and flow cytometry, as well as Western blot analysis. The results showed that heparin induced apoptosis of CNE2 cells including the morphologic changes such as reduction in the volume, and the nuclear chromatin condensation, as well as the 'ladder pattern' revealed by agarose gel electrophoresis of DNA in a concentration-dependent manner. The number of TUNEL-positive cells was dramatically increased to 33.6+/-1.2% from 2.8+/-0.3% by treatment with heparin in different concentrations (10 to approximately 40 kU/L). The apoptotic index was increased to 32.5% from 3.5% by detecting SubG1 peaks on flow cytometry. Western blot analysis showed that levels of bcl-2, bax and c-myc were significantly overexpressed by treatment with the increase of heparin concentrations. These results suggest that heparin induces apoptosis of CNE2 cells, which may be regulated by differential expression of apoptosis-related genes.

Function of apoptosis and expression of the proteins Bcl-2,p53 and C-myc in the development of gastric cancer

INTRODUCTIONIn China ,the incidence and mortality of gastric cancer rank the second among all cancers. Recent development of cancer [1-20].The aim of this study was investigat the insight of apoptosis and bcl-2, p53 and C-myc protein expression in the development of gastric cancer .

Paclitaxel induces apoptosis in human gastric carcinoma cells

AIM;To investigate the apoptosis in gastric cancer cells induced by paclitaxel,and the relation between this apoptosis and expression of Bcl-2 and Bax. METHODS:In in vitro experiments,MTT assay was used to determine the cell growth inhibitory rate.Transmission electron microscope and TUNEL staining method were used to quantitatively and qualitively detect the apoptosis status of gastric cancer cell line SGC-7901 before and after the paclitaxel treatment.Immunohistochemical staining was used to detect the expression of apoptosis-regulated gene Bcl-2 and Bax. RESULTS:Paclitaxel inhibited the growth of gastric cancer cell line SGC-7901 in a dose-and time-dependent manner. Paclitaxel induced SGC-7901 cells to undergo apoptosis with typically apoptotic characteristics,including morphological changes of chromatin condensation,chromatin crescent formation,nucleus fragmentation and apoptotic body formation.Paclitaxel could reduce the expression of apoptosis-regulated gene Bcl-2,and improve the expression of apoptosis-regulated gene Bax. CONCLUSION:Paclitaxel is able to induce the apoptosis in gastric cancer.This apoptosis may be mediated by down- expression of apoptosis-regulated gene Bcl-2 and up- expression of apoptosis-regulated gene Bax.