[Hemoglobin C Variant Affecting Glycated Hemoglobin Test Results: A Rare Case Report].

Hemoglobin (Hb) variants are common factors that affect the results of glycosylated hemoglobin (A1C) tests. Hemoglobin variants react differently to different testing methods. Herein, we presented the first ever report of the effect of hemoglobin C (Hb C) on the test results of A1C in the Chinese population. High performance liquid chromatography (HPLC) and capillary electrophoresis were performed to measure A1C. Hemoglobin electrophoresis was conducted to identify the hemoglobin variants. Hb sequencing was performed to determine the mutation sites on the ß chain. HPLC showed decreased A1C results, which could be corrected by electrophoresis, but the electrophoresis graph still showed abnormal peaks. The hemoglobin electrophoresis results suggested that there were hemoglobin variants, which hemoglobin sequencing results revealed to be Hb C. Uncommon variations in a specific population tend to be overlooked. To avoid clinical decision-making being affected by the results of a single test, we recommend that an explanatory reporting model be routinely adopted for A1C tests so that all reports always contain explanatory notes for the testing methodology and analysis of the graphs.

Anterior wall adenocarcinoma of bladder with similar clinicopathological and prognostic characteristics as common bladder carcinomas should not be treated as or classified into urachal adenocarcinomas.

PURPOSE: To discuss whether the dome or anterior wall of bladder adenocarcinoma (BAC) should be classified into urachal carcinoma (UrC) and the relationship of primary tumor location (PTL) as well as treatment with survival. METHODS: Surveillance, Epidemiology, and End Results 18 database was examined for eligible patients from 1975 to 2016. Patients were classified into adenocarcinoma originating from the urachus (UAC), the dome (D-BAC), the anterior wall (A-BAC), and the other sites adenocarcinoma of the bladder (O-BAC). The clinicopathological features, treatment, and survival were compared among the groups. RESULTS: Comparable clinicopathologic features were obtained between UAC and D-BAC, which were different from those of A-BAC and O-BAC; otherwise, the latter two had similar clinicopathologic features. Univariable and multivariable Cox regression analyses indicated that PTL was an independent predictor for survival. O-BAC conferred the worst prognosis then followed by A-BAC, D-BAC, and UAC. For non-metastatic UAC or D-BAC, partial cystectomy (with an en bloc resection of the urachus and umbilicus) is optimal for survival. However, the worse survival of non-metastatic D-BAC (compared with UAC) suggested different modalities, maybe more intensive surgery approaches, should be considered for D-BAC. CONCLUSION: This study illustrates that PTL of UAC and BAC was an independent predictor for survival. A-BAC had comparable characters and prognosis with O-BAC and should not be classified into and treated as UrC. For non-metastatic disease, non-metastatic D-BAC may need more intensive modality.

Prognostic Values of Radiosensitivity Genes and CD19 Status in Gastric Cancer: A Retrospective Study Using TCGA Database.

BACKGROUND: The correlation between the radiosensitivity genes combined with CD19 status and clinical outcome was investigated to identify gastric cancer (GC) patients who would benefit from radiotherapy combined with CAR-T cell therapy. METHODS: The gene expression and clinical features were downloaded from The Cancer Genome Atlas (TCGA) Stomach Cancer (STAD). To identify the hub radiosensitivity genes and CD19 status, 407 patients were categorized into two groups: radiosensitivity (RS) and radioresistance (RR) based on the prognosis. The chi-square test, Mann-Whitney test, and Kaplan-Meier survival analysis were applied to compare the differential expression in these groups and analyze the correlation between the gene expression and clinical outcome and features. Finally, the influencing factors for the prognosis of GC were investigated by multiple Cox regression, especially in RS patients. RESULTS: A total of 15 differential expression genes, containing two communities with 8 hub radiosensitivity genes, were identified. We also identified a 2-gene signature model with a negative coefficient and calculated the risk score for the prognosis of GC. Also, Helicobacter pylori infection was validated, and the high-risk score of radiosensitivity genes was the risk factor, and high CD19 expression was the protective factor for the prognosis. CONCLUSION: The radiosensitivity gene signature and CD19 expression predicted the clinical outcome of GC patients.

[Effect of Nifuroxazide on Proliferation, Migration, and Invasion of Thyroid Papillary Carcinoma Cells].

OBJECTIVE: To explore the effect of nifuroxazide on proliferation, migration, and invasion of thyroid papillary carcinoma cells. METHODS: BCPAP and TPC-1 cell lines treated with different concentration (0, 1.25, 2.5, 5, 10, 20 µmol/L) of nifuroxazide, respectively. Cell viability and proliferation of BCPAP and TPC-1 was evaluated by MTT and colony formation assay. Apoptosis analysis and cell nuclear changes were determined by staining with Hoechst 33258 and visualized by a fluorescence microscope after treatment with nifuroxazide. Western blot analysis was used to evaluate protein expressions of apoptosis and invasion of BCPAP cells treated (48 h) with nifuroxazide. Transwell assay was conducted to evaluate ability of cell migration and invasion. RESULTS: After being treated with nifuroxazide (0, 1.25, 2.5 µmol/L and 0, 1.25 µmol/L) for 24, 48, 72 h respectively, decreased proliferations of BCPAP and TPC-1 cell lines were not obvious ( P>0.05). However, treated BCPAP and TPC-1 cells with higher concentration respectively (5, 10, 20 µmol/L and 5, 10 µmol/L) of nifuroxazide for 24, 48, 72 h, the inhibitory effects were significantly obvious ( P<0.05), and the inhibitory effects were increased in a CM(155mm]concentration- and time-dependent manner. The inhibition in proliferation of TPC-1 cell with nifuroxazide (2.5, CM)]5 µmol/L) took effect from 72 h and 48 h ( P<0.05), respectively. Clone formations of BCPAP and TPC-1 cells were significantly inhibited after being exposed to nifuroxazide (2.5, 5 µmol/L) for 10 d ( P<0.05). Hoechst 33258 staining assay showed that nifuroxazide (10 µmol/L) treatment resulted in cell shrinking, nuclear fragmentation and formation of condensed nuclei with bright-blue fluorescence. After 48 h, the percentage of apoptotic cells of BCPAP and TPC-1 significantly increased respectively as the concentration of nifuroxazide with 10 µmol/L ( P<0.005). Pro-apoptotic protein CC-3 and Bax expression levels increased significantly ( P<0.05), and the expression of anti-apoptotic protein Bcl-2 decreased significantly ( P<0.05) in BCPAP cells after nifuroxazide-treatment (10 µmol/L) for 48 h. The percentage of migrations and invasions of BCPAP and TPC-1 significantly decreased ( P<0.05) in the presence of nifuroxazide (10 µmol/L, 48 h). Nifuroxazide (10 µmol/L) treatment significantly decreased the expressions of matrix metalloproteinase (MMP)-2 and MMP-9 in BCPAP cells ( P<0.05) . Expression of MMPs family inhibitor-tissue inhibitors of metalloproteinase (TIMP)-2 increased ( P<0.05). CONCLUSION: Nifuroxazide inhibits the proliferation of thyroid cancer cells BCPAP and TPC-1, induceds the cell apoptosis by up-regulating the expressions of CC-3 and Bax proteins in vitro, and blocks migration and invasion of cells in vitro by reducing protein expressions of MMP-2 and MMP-9.

[Serum Wnt5a and Its Associations with Liver Steatosis and Fibrosis in Overweight and Obese People].

OBJECTIVES: To determine serum Wnt5a and its associations with liver steatosis and fibrosis in overweight and obese people. METHODS: The study participants were recruited from those who visited our hospital for health examinations. They were divided into three groups according to body mass index (BMI), controlled attenuation parameter (CAP)values and elasticity (E) values of liver fibroscan: Control ( n=27), Mild NAFLD (non-alcoholic fatty liver disease, n=51) and Moderate/severe NAFLD ( n=56). The waist circumference (WC), hip circumference (HC), oral glucose tolerance test (OGTT), insulin releasing test (IRT), liver function, blood lipid, serum Wnt5a and ß-catenin of those participants were measured. RESULTS: The three groups of participants had no significant differences in age, gender, BMI, WC or HC ( P>0.05). Significant differences appeared in fasting glucose, 2 h postprandial glucose and fasting insulin level between the three groups ( P<0.05), but not in 2 h postprandial insulin level ( P>0.05).The participants with NAFLD had higher levels of serum Wnt5a and ß-catenin than controls ( P<0.05). Wnt5a level was correlated with CAP value ( r=-0.19, P<0.000 1), but barely with E value ( r=0.02, P=0.241). CONCLUSIONS: Wnt5a may play a role at different stages of NAFLD in overweight/obese people.

[The Preliminary Investigation of GLP-1 Receptor Agonist on Liver Steatosis in Obese Mice].

OBJECTIVES: To investigate the effects of glucagon-like peptide-1 (GLP-1) receptor agonist, exenatide, on liver function and steatosis in obese mice. METHODS: Male c57BL/6J mice (8 weeks old) were divided into high-fat-diet group (for obesity model construction) and chow diet group. 12 weeks later, mice of high-fat diet group were randomly divided into high-dose exenatide group [H group, intraperitoneal injection 0.02 µg/ (g·d) , high-fat-diet], low-dose exenatide group [L group, intraperitoneal injection 0.01 µg/ (g·d) , high-fat-diet], saline group (NS group, intraperitoneal injection of saline, high-fat-diet) , diet control group (D group, shifted to chow diet) and high-fat control group (M group, high-fat-diet) for 4-week treatments , respectively. The body mass and serum biochemical indicators of were detected. Liver tissues were stained with HE, and steatosis score was measured. RESULTS: After 4-week treatments, H group showed more body mass loss than L group and D group ( P<0.05). The serum alanine aminotransferase (ALT) level of NG group was higher than that of H, L, M, and NS groups ( P<0.05). Serum cholesterol and triglyceride declined to normal levels by diet intervention or drug treatment. High-dose exenatide treatment ran a risk of increasing serum uric acid level. The serum levels of aspartate aminotransferase (AST), glucose, homeostasis model assessment-insulin resistance (HOMA-IR), lipase, and amylase had no significant differences between groups (P>0.05). Hepatic steatosis score was reduced by diet intervention or drug treatment. CONCLUSIONS: High-dose exenatide treatment can effectively reduce body mass of obese mice, but it has little difference when compared with dietary intervention in improving blood fat and liver steatosis.

[Preliminary Study on the Wnt5a Expression in Obese Mice with Hepatocellular Carcinoma].

OBJECTIVES: To investigate the Wnt5a expression in obese mice with hepatocellular carcinoma. METHODS: Two groups of 6-week C57BL/6J mice were fed with chow-diet and high-fat-diet for 8 weeks respectively, to establish obesity model in the latter group. Mice in Hepal-6 group (including normal-body mass mice and obese mice) were injected with Hepa1-6 hepatocarcinoma cell lines through caudal vein, while the controls were given NS. Serum and tissue samples were taken at the age of 18 weeks for serological and morphological study. The expression of Wnt5a and ß-catenin in liver were examined by immunohistochemistry. RESULTS: At the age of 18-week, tatty degeneration was observed in the livers of obese control mice. Tumor cell masses were found in the livers of both obese and (including normal-body mass mice and obese mice) control mice by inoculation with Hepal-6, while focal necrosis was only observed in the obese+Hepal-6 group. The levels of serum transaminases, cholesterol and alpha-fetoprotein (AFP) were significantly different between groups ( P<0.05). The immunohistochemistry showed that the highest expression of Wnt5a was observed in liver tissues of normal control group, followed in sequence by obese control group, normal+Hepal-6 group, and obese+Hepal-6 group ( P<0.05). The expression of ß-catenin was just opposite ( P<0.05). CONCLUSIONS: The expression of Wnt5a was decreased, and the ß-catenin was abnormal accumulation. It may be closely related to the formation and progression of hepatocellular carcinoma.

[Effects of VEGF on Proliferation, Apoptosis and Insulin Secretion in Rat Pancreatic Islet Cells].

OBJECTIVE: To investigate the effect of vascular endothelial growth factor (VEGF) on proliferation, apoptosis, insulin secretion and related gene expression in rat pancreatic islet cell (INS-1). METHODS: INS-1 cells were treated with different concentrations of VEGF. CCK-8 kit was used to detect the proliferation of INS-1 cells and the cell apoptosis were evaluated by using Annexin V and propidium iodide (PI) double staining kit. INS-1 cells were treated with VEGF and the standard glucose stimulated insulin secretion test with ELISA was conducted. The expression of related genes in pancreatic islets was detected by real-time quantitative PCR. The effect of VEGF on isulin protein expression was evaluated with Western blot. RESULTS: No significant changes (P > 0.05) in INS-1 cells were observed after treated with different concentrations of VEGF at 24 h, 48 h and 72 h. But when VEGF concentration were 80 ng/mL and 160 ng/mL, an inhibitory effect on cell apoptosis were noticed (P < 0.01). The addition of VEGF to the high-glucose media significantly reduced the release of insulin at the concentration of 40 ng/mL. A decreasing trends of the expression level of sulfonylurea receptor gene (Sur), inwardly rectifying potassium channel gene 6. 2 (Kir6. 2) as well as the release of insulin were noticed as the increasing of VEGF concentrations. The expression of glucokinase gene (GCK) first decreased and then increased, but the expression of glucose transporter gene 2 (Glut 2) were increased first and then decreased. CONCLUSION; VEGF inhibited the secretion of insulin from INS-1 cells in the high-glucose condition. Our study provides new clues to the function of VEGF on the glucose metabolism.

[Association Between Serum Uric Acid and Acute Cerebral Infarction: a Case Control Study].

OBJECTIVE: To determine the association between serum uric acid levels and acute cerebral infarction. METHODS: 700 patients with acute cerebral infarction were recruited in the study, with 700 healthy individuals serving as controls. Blood samples of the participants were collected to measure uric acid, triglyceride, cholesteral, blood glucose, urea and creatinine. Logistic regression model was established to examine the association between serum uric acid and acute cerebral infarction. RESULTS: The patients with acute cerebral infarction had lower levels of serum uric acid than the healthy controls (P <0. 05). The logistic regression model showed that decreased levels of serum uric acid were barely associated with acute cerebral infarction (odds ratio: 0. 998, 95% confidence interval: 0. 996-1. 000, P<0. 05), after controlling for other confounding factors. CONCLUSION: Association between serum uric acid and acute cerebral infarction is not confirmed.

[The Association Between Serum Uric Acid and Creatinine in Patients with Hypothyroidism].

OBJECTIVE: To determine the relationship between serum uric acid (SUA) and creatinine (SCr) in patients with hypothyroidism. METHODS: A total of 2 078 people who took physical examinations in the West China Hospital, Sichuan University in May 2014 participated in this study. Serum thyrotropin (TSH), free thyroxine (FT4) and free triiodothyronine (FT3) were detected by electrochemiluminescence. SUA was measured using uricase UV method. The participants were divided into three groups according to their thyroid function: hypothyroidism, subclinical hypothyroidism (SCH) and control. The prevalence of hyperuricemia in each group was Estimated. Correlation analyses were performed for the serum indicators. RESULTS: There were 1 685 participants in the control group, 38 in the hypothyroidism group, and 355 in the subclinical hypothyroidism group. Hypothyroidism patients had significantly higher levels of TSH than those in the control and SCH groups. Significant differences in serum levels of FT3 and FT4 were found between the three groups. Higher levels of SCr (P=0. 005) and SUA (P=0. 008) were also found in hypothyroidism patients compared with those in the control and SCH groups. In those younger than 60 years, men were more likely to catch hyperuricemia than women, with 50-59 year old men having the highest prevalence of hyperuricemia. Higher prevalence of hyperuricemia in men (compared to women) was also found in those older than 60 years, but without statistical significance (P=0. 09). After correcting for gender, TSH showed no correlations with SUA (r=-0. 01, P=0. 648) and SCr (r=-0. 02, P=0. 284); FT4 showed negative correlations with SUA (r= -0. 978, P=0. 001) and SCr (r= -0. 599, P= 5. 012); FT3 showed negative correlations with SUA (r= -0. 745, P=0. 007) and SCr (r -0. 457, P=0. 034). CONCLUSION: Reduced thyroid hormone levels may lead to elevated SCr levels. And elevated SCr levels may be issociated with elevated levels of SUA in patients with hypothyroidism.

[Effect of Serum Uric Acid on Renal Function of Patients with Abnormal Glucose Metabolism].

OBJECTIVE: To determine the effect of serum uric acid on renal function of patients with abnormal glucose metabolism. METHODS: A total of 1 495 people who took physical examinations in West China Hospital of Sichuan University in May 2014 were recruited in this study. Serum nitrogen (BUN), creatinine (SCr), triglycerides (TG), cholesterol (TC), high-density lipoprotein (HDL-C), low-density lipoprotein (LDL-C) and uric acid (SUA) of the participants were detected by an automatic biochemical analyzer. The glomerular filtration rate, (eGFR) was calculated with CKD-EPI. According to hyperuriceima (HUA), the participants were divided into groups with impaired fasting glucose (IFG), diabetes (DM), IFG with hyperuicimia, and DM with hyperuricemia. The participants with normal fasting plasma glucose served as controls. Renal dysfunction was detected using eGFR≤50 mL/(min . 1. 73 m2) and SCr≤1. 7 µg/mL. RESULTS: About 13. 18% (197/1 495) participants were identified as IFG with HUA: male (158)/female (39) ratio =4.05; 4.41% (66/1 495) as DM with HUA: male (58)/female (8) ratio = 7. 25. Participants with HUA in the control, IFG and DM groups had higher levels of BUN and SCr and lower levels of eGFR than those without HUA (P<0. 05). HUA was more likely to be associated with serum. lipid in the control and IFG groups (most P<0. 05) than in the DM group (P>0. 05). DM patients without HUA had better renal function and serum lipid levels than those who had HUA in their early stage of abnormal glucose metabolism (IFG with HUA) (P<0. 05). The prevalence of renal dysfunction of IFG patients with HUA was significantly higher than those without HUA, similar to the prevalence of renal dysfunction of DM patients with HIUA (P

[Changes of bone mineral density and bone metabolic marker in patients with subclinical hypothyroidism].

OBJECTIVE: To investigate the change of bone mineral density and bone metabolism biochemical markers in subclinical hypothyroidism. METHODS: This study included total 122 patients with subclinical hypothyroidism and 153 healthy age and gender matched people as control. All the patients and controls were subjected to the measurements of bone density by dual energy X-ray absorptiometry (DEXA), and serum free triiodothyronine (FT3), free thyroxine (FT4), thyroid stimulating hormone (TSH), Ca2+, PO4(3+), alkaline phosphatase (ALP) levels. All the data was analyzed statistically with the stratification of gender and menopause status. RESULTS: Compared to the control, the patients with subclinical hypothyroidism had significantly higher incidence of bone mass loss (P < 0.005) and lower level of Serum Ca2+ (P < 0.05) and higher levels of serum PO4(3+), T-value and Z-value (P < 0.05). Furthermore, premenopausal women had higher Z-value (P < 0.01) , but no significantly differences of T-value, serum PO4(3+) was found either in pre-menopause or post-menopause women when compared to the control. Multiple linear regression analysis showed gender (B = 0.543, P < 0.0001) was positive correlation with T value, female had lower T values. Moreover, T value was negative correlated to menopausal status (B = -0.274, P = 0.001), age (B = -0.161, P < 0.0001) and TSH (B = -0.108, P < 0.0001). CONCLUSION: Subclinical hypothyroism appears decreased serum calcium and low bone density.

[Blood lipid, glucose and uric acid in people with subclinical hypothyroidism].

OBJECTIVE: To investigate the changes of blood lipid, fasting blood glucose and blood uric acid and its clinical significance in people with subclinical hypothyroidism. METHODS: Body mass index (BMI), thyroid stimulating hormone (TSH), free triiodothyronine (FT3), free tetraiodothyronine (FT4), total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), fasting blood glucose (FBG) and uric acid (UA) were measured and compared in 356 people with subclinical hypothyroidism and 331 health people (controls). RESULTS: Compared to the control group, people with subclinical hypothyroidism had higher levels of BMI, TSH, TC, LDL-C, TG, FBG, UA (P < 0.05) and non-significant decrease of HDL-C (P > 0.05). The level of TSH was positively correlated with TC (r = 0.254), LDL-C (r = 0.110), TG (r = 0.218), BMI (r = 0.119) and FBG (r = 0.210) (P < 0.05). The level of HDL-C was not correlated with TSH (P > 0.05). CONCLUSION: Thyroid dysfunction may have an effect on the metabolism of blood lipid, FBG and UA.

[Preliminary study on the expression of cystatin C in primary liver cancer].

OBJECTIVE: To preliminarily investigate the expression of cysteine proteinase inhibitors C (cystatin C) in primary hepatic carcinoma. METHODS: Hepatic tissue samples and peripheral blood samples were collected from 41 cases of primary hepatic carcinoma, 24 cases of cirrhosis and 40 cases of normal control. To primary hepatic carcinoma, three kinds of hepatic tissue samples were harvested, including carcinoma tissue, adjacent non-tumor tissue, and distant normal tissue. The expression levels of cystatin C in hepatic samples and blood samples were measured by immunohistochemistry method and latex enhanced immune turbidimetric method respectively, and the differences of cystatin C expressions were compared in primary hepatic cancer, cirrhosis, and normal control. Furthermore, the relationships of cystatin C expression with tumor size, intrahepatic metastasis, serum AFP level were studied with correlation analysis. RESULTS: The expression of cystatin C was positive, in primary hepatic carcinoma. Part of adjacent non-tumor tissue, and distant normal tissue and cirrhosis tissues had some degree of cyctatin C expression. Wilcoxon test showed that the differences of cyctatin C expression in different hepatic tissues were statistics significance (P < 0.01). The proportion of positive cell, staining intensity, and the product of these two was: carcinoma tissues > adjacent non-tumor tissues> cirrhosis tissues > distant normal tissue. Compared with normal control, primary hepatic carcinoma and cirrhosis both had higher serum cystatin C level (P < 0.001), but there was no difference between hepatic carcinoma and cirrhosis (P = 0.769). The correlation analysis showed that the level of serum cystatin C was not related to serum AFP, tumor size, or intrahepatic metastasis. CONCLUSION: The expression of cystatin C in primary hepatic carcinoma is higher than that of adjacent non-tumor tissue, distant normal tissue, and cirrohsis tissue. The serum cystatin C level of primary hepatic carcinoma is higher than that of normal control.

[Selective myelo-protection by MDR1 and MnSOD genes regulated by a specific promoter].

OBJECTIVE: To study the specific protection of myeloid cells from chemotherapeutic agents and radiation. METHODS: The recombinant retroviral vectors containing MDR1 gene and MnSOD gene regulated by APN myeloid promoter were constructed and introduced into myeloblastic cell line KG1a and hepatoma cell line BEL7402. The resistance of the cells to antitumor drugs and radiation were analyzed by cell survival assay. In vivo, the murine bone marrow cells were isolated and infected by the retroviral particles, which were transplanted into recipient mouse treated with paclitaxel or X-ray. The murine white blood cell (WBC) was counted in order to assay the effects of MDR1 or MnSOD gene on hematopoiesis in the course of chemotherapy and radiotherapy. RESULTS: The resistance to chemotherapeutic agents such as cochicine, Vp-16, vincristine, doxorubcin and paclitaxel were elevated markedly by 10.6, 10.4, 11.2, 4.2 and 14.2 folds in KG1a cell line transduced with MDR1 gene. The resistance to radiation increased 3.7 folds at the dose of 10 Gy compared with parental cells in KGla cell line transduced with MnSOD gene derived by APN promoter. In contrast, the chemosensitivity and the radiosensitivity showed no significant change in BEL 7402 cell line transduced with MDR1 gene and MnSOD gene. In vivo, the WBC counts in the mouse introduced with MDR1 gene or MnSOD gene were higher than those in the control mouse (P < 0.01). CONCLUSION: The expression of MDR1 gene and MnSOD gene regulated by APN myeloid promoter is effective on myelo-specific protection without enhancing the resistance of tumor cells in vitro. The hematopoiesis can be reconstituted in vivo during anticancer drug or radiation treatment. This study may provide experimental evidence and new clues for myeloprotection of cancer patients being treated with chemotherapy and/or radiotherapy.

[MnSOD gene regulated by aminopeptidase N promoter specifically protects bone marrow from radiation].

BACKGROUND & OBJECTIVE: It is an effective way to induce radio-tolerant gene into hematopoietic cells in bone marrow for overcoming the suppression of radiotherapy on hematopoietic system. However, this also increases the radiation tolerance of tumor cells. This study was designed to investigate a method to specifically protect bone marrow cell from being damaged by radiation, along without increasing resistance of tumor cell to radiation. METHODS: The retrovirus vector of manganese superoxide dismutase (MnSOD) gene regulated by aminopeptidase N (APN) bone marrow-specific gene promoter was constructed and induced into myeloblastic KG1a and cancer cell BEL7402. MnSOD mRNA level was analyzed by PT-PCR; MnSOD activity in the cells was determined; the sensitivity of bone marrow cell and hepatic carcinoma cell to x-ray was detected by cell survival test; the cell apoptosis was analyzed with flow cytometry and fractural DNA electrophoresis. RESULTS: The MnSOD mRNA level and enzyme activity in KG1a cells transferred with the gene was obviously increased. Expression of MnSOD mRNA drove by APN myelo-specific promoter effectively inhibited apoptosis of KG1a cells induced by radiation and endowed KG1a cell line with the enhancement of tolerance to radiation, which increased by 3.7 folds compared to parental cells at the dose of 10 Gy. In contrast, the level of MnSOD mRNA, the enyme activity of MnSOD and the radiosensitivity had no significant change in BEL 7402 cells transduced with MnSOD gene. CONCLUSION: APN bone marrow-specific promoter could control MnSOD gene expression highly in myeloid cell and lower in cancer cell. In the process of killing of cancer cell by x-ray, MnSOD gene regulated by APN bone marrow-specific promoter could specifically protect myeloid cell. This study provides a new clue to solve the bone marrow suppression in high dose radiotherapy.