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Liver transplantation (LT) is an important treatment of unresectable hepatocellular carcinoma (HCC). However, the prognosis of tumor recurrence remains poor.If patients with a high risk of tumor recurrence after LT can be predicted preoperatively, suitable recipients are screened so that individualized monitoring and treatment protocols may be formulated for high-risk patients.Then better outcomes are obtained.Therefore it is imperative to accurately identify the relevant risk factors and select appropriate parameters for evaluate the risks of tumor recurrence before LT.This review summarized the latest researches of preoperative clinical predictors for recurrent HCC after LT.It was intended to provide references for selecting recipients and a proper management of high-risk patients.
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Objective:To investigate the value of aspartate aminotransferase/lymphocyte ratio (ALR), γ-glutamyltranspeptidase/lymphocyte ratio (GLR) and aspartate aminotransferase/alanine aminotransferase ratio (AAR) in predicting the recurrence of hepatocellular carcinoma after liver transplantation.Methods:The retrospective cohort study was conducted. The clinicopathological data of 178 patients with hepatocellular carcinoma who underwent liver transplantation in Tianjin First Central Hospital from July 2014 to June 2018 were collected. There were 156 males and 22 females, aged (54±9)years. All patients received the first time of orthotopic liver transplantation. Observation indicators: (1) follow-up; (2) the predictive value and cutoff value of each index for tumor recur-rence of patients with hepatocellular carcinoma after liver transplantation; (3) analysis of risk factors for tumor recurrence of patients with hepatocellular carcinoma after liver transplantation; (4) cons-truction and evaluation of the predictive model for tumor recurrence of patients with hepatocellular carcinoma after liver transplantation. Measurement data with normal distribution were represented as Mean± SD, and comparison between groups was conducted using the t test. Measurement data with skewed distribution were represented as M(range), and comparison between groups was conducted using the Mann-Whitney U test. Count data were expressed as absolute numbers, and comparison between groups was conducted using the chi-square test or Fisher exact probability. The Kaplan-Meier method was used to draw survival curve and the Log-rank test was used for survival analysis. Factors with P<0.05 in univariate analysis were included in multivariate analysis. Univariate analysis and multivariate analysis were performed by COX proportional risk regression model with forward method. The regression coefficient was used to build the prediction model. The receiver operating characteristic curve was drawn, and the area under curve (AUC) was used to evaluate the predictive ability of prediction model. Results:(1) Follow-up. All 178 patients with hepatocellular carcinoma were followed up for 36(range, 1?74)months after liver transplantation. During the follow-up, there were 41 patients died, 61 patients with tumor recurrence and 117 cases without tumor recurrence. The 3-, 5-year overall survival rates and 3-, 5-year tumor recurrence free survival rates of patients after liver transplantation were 72.8%, 69.9% and 57.3%, 52.8%, respectively. (2) The predictive value and cutoff value of each index for tumor recurrence of patients with hepatocellular carcinoma after liver transplantation. The AUC of preoperative serum alpha fetoprotein (AFP), tumor diameter, ALR, GLR, neutrophil to lymphocyte ratio, AAR in recipients were 0.76, 0.70, 0.69, 0.65, 0.64, 0.65 (95% confidence interval as 0.68?0.83, 0.61?0.79, 0.61?0.77, 0.57?0.74, 0.56?0.73, 0.56?0.74, P<0.05), and the corresponding best cutoff value of each index were 228.00 μg/L, 5.25 cm, 92.90, 122.40, 3.00, 2.42. (3) Analysis of risk factors for tumor recurrence of patients with hepato-cellular carcinoma after liver transplantation. Results of multivariate analysis showed the preoperative serum AFP >228.88 μg/L, number of tumor as multiple, tumor diameter >5.25 cm, ALR >92.90, AAR >2.42 were indepen-dent risk factors for tumor recurrence of hepatocellular carcinoma after liver transplantation ( hazard ratio=3.13, 1.90, 2.66, 2.40, 2.75, 95% confidence interval as 1.81?5.41, 1.08?3.35, 1.49?4.74, 1.40?4.11, 1.54?4.91, P<0.05). (4) Construction and evaluation of the predictive model for tumor recurrence of patients with hepatocellular carcinoma after liver transplantation. According to the results of multivariate analysis, the preoperative serum AFP, number of tumor, tumor diameter, ALR, AAR were used to construct the predictive model for tumor recurrence of hepatocellular carcinoma after liver transplantation. The AUC, best cutoff value, specificity and sensitivity of the predictive model were 0.83 (95% confidence interval as 0.76?0.89, P<0.05), 5.5, 80.3% and 73.8%. Of the 178 patients, there were 110 patients with low risk of tumor recurrence (scoring as 0?5) and 68 patients with high risk of tumor recurrence (scoring as 6?16) after liver transplantation. The 1-, 3-, 5-year tumor recurrence free survival rates and 1-, 3-, 5-year overall survival rates of patients with high risk of tumor recurrence were 27.7%, 18.2%, 18.2% and 63.7%, 48.9%, 48.9%, respectively. The above indicators of patients with low risk of tumor recurrence were 92.3%, 82.4%, 74.6% and 90.4%, 87.7%, 83.6%, respectively. There were significant differences of the above indicators between patients with high risk of tumor recurrence and low risk of tumor recurrence ( χ2=67.83, 21.95, P<0.05). Conclusions:The preoperative serum AFP, number of tumor, tumor diameter, ALR, AAR are independent influencing factors for tumor recurrence of hepato-cellular carcinoma after liver transplantation. The predictive model constructed based on the above indexes has a good prediction efficiency.
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OBJECTIVE To promote the standardization and integrity of the informed consent form for clinical trials of registered anti-tumor drugs， and to protect the legitimate rights and interests of the subjects. METHODS The ethical review resolutions of clinical trial projects of registered anti-tumor drugs that were initially reviewed by the Ethics Committee of our hospital from July 1st， 2020 to July 1st， 2022 were summarized to statistically analyze the problematic items according to the “Quality Analysis Form of Informed Consent” prepared by our hospital. RESULTS Of the 316 clinical trials of registered anti- tumor drugs that were initially reviewed， 257 （81.3%） had problems with the contents of informed consent form， mainly domestic multi-center trials and phase Ⅲ trials. The main problems included the vague notification of the test fee bearer （68.5%）， the incomplete notification of the test content （59.1%）， the insufficient notification of rights and interests and risks （58.4%）， the insufficient notification of personal information protection （56.0%）， and the nonstandard expression of the informed consent form （52.5%）. CONCLUSIONS There is still a gap between the informed consent form of the clinical trials of registered anti-tumor drugs in our hospital and the requirements of the new version of Good Clinical Practice for Drugs （GCP）. The parties involved in the test can take a number of measures to improve the standardization and integrity of the informed consent form， and the research team should design the informed consent form in strict accordance with the requirements of the new GCP and pay attention to the comprehensive notification about the test. The Ethics Committee can provide the sponsor and researcher with the template of informed consent form and the key points of writing， continue to strengthen the examination ability， improve the examination quality， and effectively protect the safety and interests of the subjects.
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Objective: To analyze the situation and influencing factors of school meals leftover among primary and secondary school students in the area of the Nutrition Improvement Program for Rural Compulsory Education Students, improve the quality of school meals, develop healthy dietary behavior, and reduce food waste. Methods: In 2019, among the 50 monitoring counties that implemented the Compulsory Education Student Nutrition Improvement Program, two primary schools and two junior schools were randomly selected according to different food supply patterns.This study randomly selected one or two classes from grade 3 to grade 9. Basic information and school meals of 26 778 students were collected by using a student questionnaire. Multivariate logistic regression was used to analyze the influencing factors of leftovers rate. Results: 54.93% (14 709) of students wasted school meals, in which the highest rate was the staple food, with the main reason as "not in favor". 11.87% (1 743) of the students wasted school meals 6-7 days a week, with 54.20% (7 957) of students wasted but in less amount. The leftover rate of staple food was the highest (29.78%), followed by vegetables and meat. The main reason of leftovers was that they didn't like this kind of food (33.52%). The rate of school meal waste was higher for girls (OR=1.19,95%CI:1.13-1.25), junior high school students (OR=1.17, 95%CI: 1.11-1.25), resident students (OR=1.06, 95%CI: 1.00-1.12), lower economic level (OR=1.06, 95%CI: 1.00-1.12), parents working outside their houses (OR=1.22, 95%CI: 1.13-1.30), health education classes (OR=1.70, 95%CI: 1.40-2.06), company-based meals (OR=1.89, 95%CI: 1.71-2.07) and school meals were not as good as home food(OR=1.89, 95%CI: 1.78-2.00)(P<0.05). Conclusions: It is common for poor rural primary and middle school students in central and western China to waste school meals, and the reasons were affected by many factors. Reducing food waste requires the joint efforts of individuals, families, schools and society.
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Female , Humans , Food Services , Meals , Refuse Disposal , Schools , StudentsABSTRACT
α-Hederagenin (H), derived from Hedera nepalensis var.sinensis, is a pentacyclic oleane-type triterpenoid that exhibits clear cytotoxicity to different tumor cell lines.In this study,a series of novel C-28 derivatives of hederagenin (H) were designed and synthesized in attempt to develop potent tumor resistance reverse activities agents. Previous research showed that H6 displayed robust reverse activity for paclitaxel resistance in KBV cells. Importantly, Co-treatment of paclitaxel with H6 significantly reduced the tumor weight to 42%. Pleasingly, H6 enhanced the efficacy of paclitaxel against KBV cancer cell-derived xenograft tumors in nude mice.Mechanism studies had found that H6 activated permeability glycoprotein(P-gp)ATPase,reduced intracellular ATP levels and inhibited efflux of P-gp substrates,thus enhancing the antitumor activity of paclitaxel on KBV cells.Molecular docking analysis of homology P-gp and H6 then conducted using the Surflex-Dock module.H6 showed a high binding affinity docking score with a total score of 5.4148,much higher than that of H(0.1414).The nov-el C-28 derivatives of H was synthesized from H6 via three-step reaction. The reversal activity of all synthesized H derivatives were tested using the MTT assay.The results showed that the derivatives of nitrogen groups at C-28 displayed same even potent activity than parent compound H6.In addition,its underlying mechanism of action and in vivo activity are in explore.
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OBJECTIVE:To provide theoretic basis for the design and synthesis of novel high-activity biaryl aminothiazineβ-amyloid precursor protein cleaving enzyme 1 (BACE1) inhibitor,the research and development of new AD therapy drugs. METHODS:Totally 41 molecules of biaryl aminothiazine BACE1 inhibitors were selected. By SYBYL-X 2.0 software package, CoMFA and CoMSIA method were used to construct 3D-QSAR model of derivatized compounds. Surflex-dock molecular docking was applied to analyze binding mode of the compounds with BACE1. RESULTS:The q2 value of 3D-QSAR model established by CoMFA and CoMSIA method were all higher than 0.5,indicating good predictability. The established three dimensional contour plots could manifest the effect of substituents at different sites on activity of compounds. Surflex-dock analysis showed that biaryl aminothiazine and amino acid residues as ASP80, ASP276 and TYR246 in BACE1 had a key effect on hydrogen bonds. CONCLUSIONS:3D-QSAR model established on the basis of biaryl aminothiazine derivatized compounds show good predictability,which provides guidance for the structure optimization of the compound. TYR246 may be another potential active functional residue of biaryl aminothiazine inhibitor compound molecule combined with BACE1. Through 3D-QSAR analysis and molecular docking,new biaryl aminothiazine BACE1 inhibitor can be designed and synthesized so as to research and develop new drugs for AD.
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In this study, we searched multiple databases for all relevant original articles (1996-2013). To investigate blood lead levels (BLL) and possible risk factors for lead exposure among children in China A total of 388 articles met our inclusion criteria. The overall geometric mean (GM) BLL was 71 µg/L, and the prevalence of elevated BLL (EBLL, defined as BLL ⋝ 100 µg/L) was 18.48% among children. The prevalence of EBLL remained significantly higher among boys. In children less than 6 years of age, there were significantly increasing trends in both BLL and prevalence of EBLL in an age-dependent manner. The ban on leaded gasoline significantly reduced the BLL as well as EBLL prevalence; however, children whose parents had lower educational levels or were exposed to lead in the workplace had a higher EBLL prevalence. Despite its decline over time, the average BLL among children in China remains higher than the average level most recently reported in the United States. Childhood lead poisoning remains a public health problem in China.
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Child , Child, Preschool , Female , Humans , Male , China , Environmental Exposure , Lead , Blood , Risk FactorsABSTRACT
Benzene is an established leukotoxin and leukemogen in humans. We have previously reported that exposure of workers to benzene and to benzene metabolite hydroquinone in cultured cells induced DNA-dependent protein kinase catalytic subunit (DNA-PKcs) to mediate the cellular response to DNA double strand break (DSB) caused by DNA-damaging metabolites. In this study, we used a new, small molecule, a selective inhibitor of DNA-PKcs, 2-(morpholin-4-yl)-benzo[h]chomen-4-one (NU7026), as a probe to analyze the molecular events and pathways in hydroquinone-induced DNA DSB repair and apoptosis. Inhibition of DNA-PKcs by NU7026 markedly potentiated the apoptotic and growth inhibitory effects of hydroquinone in proerythroid leukemic K562 cells in a dose-dependent manner. Treatment with NU7026 did not alter the production of reactive oxygen species and oxidative stress by hydroquinone but repressed the protein level of DNA-PKcs and blocked the induction of the kinase mRNA and protein expression by hydroquinone. Moreover, hydroquinone increased the phosphorylation of Akt to activate Akt, whereas co-treatment with NU7026 prevented the activation of Akt by hydroquinone. Lastly, hydroquinone and NU7026 exhibited synergistic effects on promoting apoptosis by increasing the protein levels of pro-apoptotic proteins Bax and caspase-3 but decreasing the protein expression of anti-apoptotic protein Bcl-2. Taken together, the findings reveal a central role of DNA-PKcs in hydroquinone-induced hematotoxicity in which it coordinates DNA DSB repair, cell cycle progression, and apoptosis to regulate the response to hydroquinone-induced DNA damage.
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Humans , Apoptosis , Physiology , Benzene , Toxicity , Catalysis , Chromones , Pharmacology , DNA Damage , Genetics , DNA Repair , Physiology , DNA-Activated Protein Kinase , Metabolism , K562 Cells , Morpholines , Pharmacology , Protein SubunitsABSTRACT
Benzene is an established leukotoxin and leukemogen in humans. We have previously reported that exposure of workers to benzene and to benzene metabolite hydroquinone in cultured cells induced DNA-dependent protein kinase catalytic subunit (DNA-PKcs) to mediate the cellular response to DNA double strand break (DSB) caused by DNA-damaging metabolites. In this study, we used a new, small molecule, a selective inhibitor of DNA-PKcs, 2-(morpholin-4-yl)-benzo[h]chomen-4-one (NU7026), as a probe to analyze the molecular events and pathways in hydroquinone-induced DNA DSB repair and apoptosis. Inhibition of DNA-PKcs by NU7026 markedly potentiated the apoptotic and growth inhibitory effects of hydroquinone in proerythroid leukemic K562 cells in a dose-dependent manner. Treatment with NU7026 did not alter the production of reactive oxygen species and oxidative stress by hydroquinone but repressed the protein level of DNA-PKcs and blocked the induction of the kinase mRNA and protein expression by hydroquinone. Moreover, hydroquinone increased the phosphorylation of Akt to activate Akt, whereas co-treatment with NU7026 prevented the activation of Akt by hydroquinone. Lastly, hydroquinone and NU7026 exhibited synergistic effects on promoting apoptosis by increasing the protein levels of pro-apoptotic proteins Bax and caspase-3 but decreasing the protein expression of anti-apoptotic protein Bcl-2. Taken together, the findings reveal a central role of DNA-PKcs in hydroquinone-induced hematotoxicity in which it coordinates DNA DSB repair, cell cycle progression, and apoptosis to regulate the response to hydroquinone-induced DNA damage.
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<p><b>OBJECTIVE</b>To investigate the application of BPDE-albumin adducts as monitoring biomarkers for coke oven workers exposed to polycyclic aromatic hydrocarbons (PAHs) and to explore possible relationship between BPDE-albumin adducts and urinary 1-hydroxypyrene (1-OHP) levels in them.</p><p><b>METHODS</b>Thirty-seven coke oven workers from a coke plant and 47 controls without the occupational exposure to PAHs were recruited in this study. The levels of plasma BPDE-albumin adducts and urinary 1-OHP were analyzed using high performance liquid chromatography.</p><p><b>RESULTS</b>The median levels of BPDE-albumin adducts (42.10 fmol/mg albumin) and urinary 1-OHP (5.46 micromol/mol creatinine) were significantly higher in coke oven workers than in controls (14.16 fmol/mg albumin, 2.96 micromol/mol creatinine, respectively; P<0.01). Multiple logistic regression analysis showed that coke oven workers were at higher risk of having BPDE-albumin adduct levels above 25.30 micromol/mg albumin (OR=1.79, P<0.01) and urinary 1-OHP levels above 4.13 micromol/mol creatinine (OR=2.45, P<0.05). There was a positive correlation between the levels of BPDE-albumin adducts and urinary 1-OHP in all subjects (rs=0.349, P<0.01).</p><p><b>CONCLUSION</b>BPDE-albumin adduct is a useful biomarker for monitoring long-term exposure to PAHs, and plasma BPDE-albumin adducts level is significantly correlated to urinary 1-OHP levels in coke oven workers.</p>
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Adult , Humans , Male , 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide , Coal Mining , Workforce , Coke , Environmental Monitoring , Mutagens , Occupational Exposure , Plasma , Chemistry , Polycyclic Aromatic Hydrocarbons , Pyrenes , Serum Albumin , Urinalysis , Urine , ChemistryABSTRACT
<p><b>OBJECTIVE</b>To study the effect of TTRAP expression on apoptosis induced by hydroquinone in HL-60 cells in vitro, and explore the relationship between TTRAP expression and the apoptosis.</p><p><b>METHODS</b>Apoptotic and necrotic rate was examined by flow cytometer with Anti-AnnexinV/FITC Plus PI staining. The mRNA expression of TTRAP was detected by RT-PCR. The differences in different treated groups were compared.</p><p><b>RESULTS</b>After different concentrations of hydroquinone to the cells for 0, 4, 8, 12 h culture, were added, the cell apoptotic rate in different concentrations of hydroquinone groups was significantly higher than that in blank control groups. The optimal concentration of hydroquinone was 200 micromol/L, lasting for 8 h. When it was 250 micromol/L, the necrotic rate increased significantly. The apoptosis induced by hydroquinone was associated with the culture time at the concentration of 200 micromol/L, and the peak apoptotic time was 8 h. Then the apoptotic rate decreased and necrotic rate increased. Furthermore, with the concentrations of hydroquinone increased and time lasted for 8 h, the apoptotic rate of cells increased, the amount of TTRAP expression in the mRNA level also increased accordingly. When the concentrations of hydroquinone was above 250 micromol/L, necrotic rate increased sharply, and the amount of TTRAP expression decreased.</p><p><b>CONCLUSION</b>Hydroquinone could induce apoptosis of HL-60 cells. The up-regulation of TTRAP expression may promote hydroquinone to induce HL-60 cells to go into apoptosis in vitro with dose-effect and time-effect relationship.</p>
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Humans , Apoptosis , Flow Cytometry , HL-60 Cells , Hydroquinones , Pharmacology , Up-RegulationABSTRACT
<p><b>OBJECTIVE</b>To investigate the protective effect of tert-butylhydroquinone on bone marrow cells in rats from cytotoxicity induced by benzene in vitro.</p><p><b>METHODS</b>The bone marrow cells in rats were divided into two groups randomizedly. Cells of the control group were stimulated by 0, 5, 10, 15, 20 mmol/L benzene for 2, 4, 6 hours respectively. Cells of the tBHQ-pretreated group were treated by 100 micromol/L tBHQ for 12 hours followed by the same conditions as the control group. The DNA damage was detected by single cell gel electrophoresis assay (SCGE) and cell apoptosis was examined by flow cytometry. The activities of NAD (P) H: quinone oxidoreductase (NQO1) in bone marrow cells of rats were also measured before benzene treatment in two groups.</p><p><b>RESULTS</b>In control group, the DNA damage and the apoptosis of bone marrow cells was increased with the growing concentration and time of benzene treatment. The DNA migration and the lengths of DNA migration of the bone marrow cells in the rats under 5, 10, 15, 20 mmol/L benzene treatment in the tBHQ-pretreated group were significantly lower than those in control group at the same time point (P < 0.05). The apoptosis of the bone marrow cells in the rats stimulated by 15, 20 mmol/L benzene for 2 hours and 10, 15, 20 mmol/L benzene for 4 hours as well as 5, 10, 15, 20 mmol/L benzene for 6 hours were also significantly lower than those in control group (P < 0.05). The activities of NQO1 in the bone marrow cells in the rats were increased after tBHQ treatment (P < 0.01) (1.62 +/- 0.16 min(-1).mg(-1) vs. the control group: 0.95 +/- 0.08 min(-1).mg(-1)).</p><p><b>CONCLUSION</b>The benzene can induce the DNA damage and the apoptosis of bone marrow cells in rats in a time dependent and dose dependent manner to some extent. The tBHQ can protect the bone marrow cells in rats from the cytotoxicity induced by benzene, which can be partly explained by the increase of the NQO1 activity induced by tBHQ.</p>
Subject(s)
Animals , Male , Rats , Apoptosis , Benzene , Toxicity , Bone Marrow Cells , Cell Biology , Cells, Cultured , DNA Damage , Dose-Response Relationship, Drug , Enzyme Inhibitors , Pharmacology , Hydroquinones , Pharmacology , NAD(P)H Dehydrogenase (Quinone) , Metabolism , Rats, WistarABSTRACT
<p><b>OBJECTIVE</b>To investigate the differential expression of apoptosis genes in patients with different degrees of benzene poisoning by cDNA microarray.</p><p><b>METHODS</b>Peripheral mononuclear cells were isolated from seven patients with benzene poisoning of different degrees (suspected 1 case, moderate 2, severe 2), and seven age and sex matched normal control subjects. Total RNA was extracted and purified, followed by reverse transcription to cDNAs with concomitant incorporation of fluorescent dCTP (Cy3 or Cy5). Then 177 genes associated with cell apoptosis were hybridized against the cDNAs probes in microarray. Fluorescent signals were scanned to detect apoptosis genes differentially expressed in patients and normal subjects.</p><p><b>RESULTS</b>Forty one genes were found to be differentially expressed between benzene-poisoned patients and normal controls; among the 41 genes, three were up-regulated among patients with mild to moderate degrees of benzene poisoning and one up-regulated among all patients. The total amount of differentially expressed genes of apoptosis decreased with the aggravation of benzene poisoning.</p><p><b>CONCLUSIONS</b>Differential expression of apoptosis genes was found in patients with benzene poisoning, suggesting a role of altered apoptosis in benzene-induced hematotoxicity.</p>
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Female , Humans , Apoptosis , Genetics , Benzene , Poisoning , Case-Control Studies , Gene Expression Profiling , Oligonucleotide Array Sequence Analysis , Methods , RNAABSTRACT
<p><b>OBJECTIVE</b>To screen DNA replication, and damage repair genes associated with benzene poisoning by using gene expression profile analysis.</p><p><b>METHODS</b>Leucocytes in peripheral blood of seven patients and seven normal controls were collected and total RNA was extracted. The cDNA probes were prepared by labeling cell RNA with Cy3-dUTP and Cy5-dUTP with reverse transcription. The arrays with 141 genes were hybridized against the cDNA probe mixture, and the fluorescent signals were scanned.</p><p><b>RESULTS</b>Twenty five differentially expressed genes were screened out. Among these genes, 16 genes were up-regulated and 9 down-regulated. They were DNA replication genes such as PRIM2A, ORC1L etc; DNA synthesis, recombination and repair genes such as POLK etc; DNA damage signaling/repair proteins and DNA ligases such as RECQL, PRKDC, G22P1, ERCC3, ERCC1, CRY1, CHES1, BRCA2, APEX etc; proteins involved in recombination such as RECQL; and other DNA synthesis, recombination, and repair proteins such as SKIV2L, RBMS1, SON, SET.</p><p><b>CONCLUSIONS</b>Some DNA replication, and damage repair genes associated with benzene poisoning show differential expression, which provides the basis for screening biomarkers of benzene poisoning.</p>
Subject(s)
Female , Humans , Benzene , Poisoning , Case-Control Studies , DNA Damage , Genetics , DNA Repair , Genetics , Gene Expression Profiling , Oligonucleotide Array Sequence AnalysisABSTRACT
<p><b>OBJECTIVE</b>To detect target genes for further study by way of analyzing the gene expression profiles of benzene poisoning by using cDNA microarray.</p><p><b>METHODS</b>Peripheral mononuclear cells were isolated from seven patients with benzene poisoning of different degrees, and sevene age-and sex-matched normal subjects. Total RNA was extracted and purified, followed by revese transcription to cDNAs with concomitant incorporation of fluorescent dCTP (Cy3 or Cy5). The cDNAs were used as probes in microarray of 2780 cloned cDNA. Fluorescent signals were scanned to detect genes differentially expressed in patients and normal subjects.</p><p><b>RESULTS</b>Among 7 pieces of cDNA microarray of 2780 tumour related genes, the expression of 16 genes, such as GRO1, TGFBR3, LYN ctc was upregulated, whereas the expression of 28 genes, such as FOSB, DJ-1, MCT-1 etc was down-regulated.</p><p><b>CONCLUSION</b>Abnormal expression of tumour related genes of patients exposed to benzene suggests that they may be the key genes, which play important role in benzene-induced leucocythemia. cDNA microarray technique is useful to indicate the expression mode of benzene poisoning tumour related genes, and to find rapidly and effectively new research object and the way of gene therapy.</p>