Profiling Cancer Patients Based on Their Motives for Seeking Informational and Emotional Support Online.

Understanding why patients seek informational and/or emotional support online is fundamental to providing patients with accurate and reliable support that is tailored to their needs, preferences, and personal situation. Based on the stress and coping theory and uses and gratifications theory (UGT), this study aimed to identify theoretically-founded profiles of cancer patients differing in their motives for seeking informational and/or emotional support online, and to compare the profiles in terms of patients' psychological and background characteristics, and perception of health care services. Hierarchical cluster analysis was conducted, using questionnaire data from patients visiting a large Dutch health website (N = 181). This revealed three distinctive profiles, i.e., overall seekers (n = 83, 46.0%), occasional information seekers (n = 83, 46.0%), and contact exchangers (n = 15, 8.0%). Patients across these profiles differed in their eHealth literacy, with the contact exchangers being more eHealth literate than the overall seekers and occasional information seekers. The results can be used to create awareness among health care providers, web designers, and patient organizations on different types of cancer patients with different motives for seeking informational and/or emotional support online, and help them to tailor recommendations to and development of (online) sources that fit patients' needs. Future research could further investigate the integration of stress and coping theory with UGT by acknowledging the interplay of different coping strategies and different gratifications.

Correlations of mouse lymphoma xenografts with the expressions of MMP-9 and Bcl-2.

The article "Correlations of mouse lymphoma xenografts with the expressions of MMP-9 and Bcl-2, by C.-L. Shi, X.-Y. Zhang, Y. Li, L.-L. Song, L. Wang, published in Eur Rev Med Pharmacol Sci 2019; 23 (3): 1176-1183-DOI: 10.26355/eurrev_201902_17010-PMID: 30779087" has been retracted by the authors as they believe that they have not yet fully studied their work and have discovered some great new results. Therefore, they will rearrange the manuscript and try to provide a more accurate model. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/17010.

[Analysis on the incidence of new occupational diseases in Weihai City from 2009 to 2020].

Objective: To analyze the pattern and characteristics of occupational diseases in Weihai City from 2009 to 2020, and to provide scientific basis for the formulation of occupational disease prevention. Methods: In February 2021, retrospective analysis was performed on the cases of occupational diseases diagnosed from 2009 to 2020 in Weihai City. The relevant information and data were collected to analyze the types of occupational diseases, onset age, working age, diagnosis time, industry distribution, economic type and enterprise size distribution. Results: From 2009 to 2020, a total of 453 cases of new occupational diseases were reported in Weihai City. There were 431 males (95.14%) and 22 females (4.86%) . The average onset age was (49.16±8.51) years, and the average working age was (17.89±9.30) years. The incidence of pneumoconiosis and other respiratory diseases (322 cases, 71.08%) , occupational otolaryngology and oral diseases (71 cases, 15.67%) and occupational chemical poisoning (36 cases, 7.95%) were the top 3 cases, of which 313 cases were pneumoconiosis and 69 cases were noise deafness. The cases were mainly concentrated in the 40-59 years age group (357 cases, 78.81%) and the 10-19 years working age group (175 cases, 38.63%) . There were significant differences in the incidence of occupational diseases in different ages and different working ages (χ(2)=97.64, 80.74, P<0.001) . The new cases were mainly in mining industry (134 cases, 29.58%) , shipbuilding or maintenance industry (97 cases, 21.41%) , and private enterprises (350 cases, 77.26%) . Conclusion: Pneumoconiosis and noise deafness are the main emerging occupational diseases in Weihai City. Occupational disease prevention and control in private enterprises such as mining and shipbuilding or maintenance industry should be strengthened.

[Comparison of pulse pressure variation, stroke volume variation, and plethysmographic variability index in pediatric patients undergoing craniotomy].

OBJECTIVE: To compare well-known preload dynamic parameters intraoperatively including stroke volume variation (SVV), pulse pressure variation (PPV), and plethysmographic variability index (PVI) in children who underwent craniotomy for epileptogenic lesion excision. METHODS: A total of 30 children aged 0 to 14 years undergoing craniotomy for intracranial epileptogenic lesion excision were enrolled. During surgery, we measured PPV, SVV (measured by the Flotrac/Vigileo device), and PVI (measured by the Masimo Radical-7 monitor) simultaneously and continuously. Preload dynamic parameter measurements were collected at predefined steps: after induction of anesthesia, during opening the skull, intraoperative electroencephalogram monitoring, excision of epileptogenic lesion, skull closure, at the end of the operation. After exclusion of outliers, agreement among SVV, PPV, and PVI was assessed using repeated measures of Bland-Altman approach. The 4-quadrant and polar plot techniques were used to assess the trending ability among the changes in the three parameters. RESULTS: The mean SVV, PPV, and PVI were 8%±2%, 10%±3%, and 15%±7%, respectively during surgery. We analyzed a total of 834 paired measurements (3 to 8 data sets for each phase per patient). Repeated measures Bland-Altman analysis identified a bias of -2.3 and 95% confidence intervals between -1.9 and -2.7 (95% limits of agreement between -6.0 and 1.5) between PPV and SVV, showing significant correlation at all periods. The bias between PPV and PVI was -5.0 with 95% limits of agreement between -20.5 and 10.5, and that between SVV and PVI was -7.5 with 95% limits of agreement between -22.7 and 7.8, both not showing significant correlation. Reflected by 4-quadrant plots, the con-cordance rates showing the trending ability between the changes in PPV and SVV, PPV and PVI, SVV and PVI were 88.6%, 50.4%, and 50.1%, respectively. The concordance rate between PPV and SVV was higher (92.7%) in children aged less than 3 years compared with those aged 3 and more than 3 years. The mean angular bias, radial limits of agreement, and angular concordance rate in the polar analysis were not clinically acceptable in the changes between arterial pressure waveform-based parameters and volume-based PVI (PPV vs. PVI: angular mean bias 8.4°, angular concordance rate 29.9%; SVV vs. PVI: angular mean bias 2.4°, angular concordance rate 29.1%). There was a high concordance between the two arterial pressure waveform-based parameters reflected by the polar plot (angular mean bias -0.22°, angular concordance rate 86.6%). CONCLUSION: PPV can be viewed as a surrogate for SVV, especially in children aged less than 3 years. The agreement between arterial pressure waveform-based preload parameters (PPV and SVV) and PVI is poor and these two should not be considered interchangeable. Attempt to combine PVI and PPV for improving the anesthesiologist's ability to monitor cardiac preload in major pediatric surgery is warranted.

Circular RNA circHIPK3 modulates prostate cancer progression via targeting miR-448/MTDH signaling.

PURPOSE: Prostate cancer (PCa) is one of the most diagnosed cancers in men worldwide. Several studies have identified that circular RNAs (circRNAs) have a crucial impact on the biological processes in PCa. Therefore, it is necessary to study the molecular mechanism of circRNAs in tumor progression and metastasis. METHODS: RNA interference was used to decrease circHIPK3 and MTDH expression. Overexpression vector was used to increase circHIPK3 and MTDH expression. Luciferase reporter assay were used to detect the relationship between circHIPK3 and miR-448 or between miR-448 and MTDH. MTT assay, colony formation assay and transwell assay were used to measure proliferation and migration of PCa cells. RESULTS: Circular RNA circHIPK3 was significantly increased in PCa tissues and cell lines. And overexpression of circHIPK3 promoted the migration, proliferation, and invasion of PC-3 and 22Rv1 cells, while knockdown of circHIPK3 markedly repressed the above-mentioned series of biological processes. Furthermore, circHIPK3 promoted metadherin (MTDH) expression by sponging miR-448. In vivo experiments, it was also found that overexpression of circHIPK3 significantly promoted tumor growth. CONCLUSIONS: Our research shows that circHIPK3 plays a carcinogenic effect in PCa by regulating the miR-448/MTDH axis, indicating that circHIPK3 may be a potential therapeutic target for PCa.

Long noncoding RNA ROR1­AS1 overexpression predicts poor prognosis and promotes metastasis by activating Wnt/ß-catenin/EMT signaling cascade in cervical cancer.

OBJECTIVE: Several long noncoding RNAs (lncRNAs) display functional effects in the tumorigenesis and progression of cervical cancer (CC). We aimed to investigate the roles of lncRNA tyrosine protein kinase transmembrane receptor 1 antisense RNA 1 (ROR1­AS1) in the development of CC patients. PATIENTS AND METHODS: Reverse Transcription-Polymerase Chain Reaction (RT-PCR) was performed for the determination of ROR1­AS1 levels in both CC tissues and cell lines. The clinical value of ROR1­AS1 expression in CC patients was statistically analyzed. After transfection with si-ROR1­AS1 in SiHa and HeLa cells, cellular growth and apoptosis were examined by Cell Counting Kit (CCK-8) assay, cell colony formation, and flow cytometry. Then, wound-healing assays and transwell assays were performed to evaluate cell migration and invasion, respectively. The related proteins of epithelial-mesenchymal transition (EMT) markers and Wnt/ß-catenin signaling pathway was assessed using Western blot assays. RESULTS: We found that that the expressions of ROR1­AS1 were distinctly increased in CC tissues and cell lines. Clinical study revealed that high ROR1­AS1 expression was associated with distant metastasis, FIGO stage, and shorter five-year survival. Functional assays by performing in vitro assays revealed that inhibition of ROR1­AS1 distinctly suppressed CC cell proliferation, colony formation, migration and invasion, and promoted apoptosis. Based on results of Western blot, we showed that the downregulation of ROR1­AS1 inhibited the levels of N-cadherin and vimentin. In addition, the distinctly decreased levels of c-myc, ß-catenin, and cyclin D1 were observed in CC cells transfected with si-ROR1­AS1. CONCLUSIONS: Our results suggest that ROR1­AS1 is likely to serve as an efficient therapeutic approach in respect of CC treatment. Our results suggest that KLF5 may be a potential therapeutic target in laryngeal carcinoma.

Theacrine attenuates myocardial fibrosis after myocardial infarction via the SIRT3/ß-catenin/PPARγ pathway in estrogen-deficient mice.

OBJECTIVE: To investigate the role of theacrine in the protection of ventricular remodeling and chronic heart failure after myocardial infarction in the estrogen-deficient mice. MATERIALS AND METHODS: Female C57BL/6 mice aged 8 weeks old were selected and then subjected to bilateral oophorectomy. At 7 days after surgery, the models of the myocardial infarction were established by ligating the anterior descending coronary artery. On the first day after myocardial infarction, Theacrine (20 mg/kg) was administered via gavage for continuous 28 days. Thereafter, the cardiac function in each group of mice was detected via cardiac ultrasonography for small animals at 7, 14, and 28 days after surgery. The mice were sacrificed after 28 days. The infarct size of mice was determined through 2,3,5-triphenyltetrazolium chloride (TTC) and Evan blue double staining assay, while the myocardial fibrosis was assessed via Masson staining assay. The expression levels of collagen-related proteins Collagen I, Collagen III, alpha-smooth muscle actin (α-SMA), and the transforming growth factor-ß (TGF-ß) were measured by Western blotting (WB). The terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) staining assay was applied to evaluate the myocardial apoptosis, and the WB was employed to detect apoptosis-associated proteins. The expression level of silent information regulator 2 homologue 3 (SIRT3) protein was detected by immunohistochemistry, and the expression levels of SIRT3, ß-catenin and peroxisome proliferator-activated receptor gamma (PPARγ) protein were measured via WB. RESULTS: Compared with those in the Sham group, the ejection fraction (EF) and fractional shortening (FS) in estrogen-deficient mice were significantly lowered, the myocardial fibrosis and myocardial apoptosis were clearly aggravated, and the SIRT3 expression was decreased at 28 days after myocardial infarction. The theacrine could improve the cardiac function after the myocardial infarction in estrogen-deficient mice and relieve both myocardial fibrosis and myocardial apoptosis during chronic remodeling after myocardial infarction in estrogen-deficient mice. After the intervention with theacrine, the estrogen-deficient mice with myocardial infarction had up-regulated SIRT3 and PPARγ levels and a reduced ß-catenin level in the heart. CONCLUSIONS: Theacrine is able to activate SIRT3 and repress myocardial fibrosis and apoptosis after myocardial infarction in ovariectomized mice, thereby improving the cardiac function of ovariectomized mice with myocardial infarction through the possible downstream signal pathway ß-catenin/PPARγ.

[Study of iron overload assessment by T2* magnetic resonance imaging in patients with myelodysplastic syndromes].

Objectives: To analyze the cardiac T2* value, liver iron concentration (LIC) , and related laboratory parameters in myelodysplastic syndrome (MDS) with iron overload and evaluate the changes of organ functions after iron chelation therapy. To explore the value of magnetic resonance imaging (MRI) T2* in making early diagnosis and assessing organs iron overload. Methods: Retrospective investigation was used to observe the cardiac T2* value, LIC, iron metabolism parameters and related laboratory parameters of 85 MDS patients from Nov 2014 to Jan 2018. Among them, 7 MDS patients with Low/Int-1 have received iron chelation therapy for 6 months during two MRI examinations. The above parameters were collected before and after iron chelation therapy for comparison. Results: Correlations were found between heart T2* value and age (rs=-0.290, P=0.007) and left ventricular ejection fraction (LVEF) (rs=0.265, P=0.009) . There was a significant negative correlation between heart T2* value and blood transfusion units (rs=-0.701, P<0.001) . There was a significant positive correlation between LIC and serum ferritin (SF) (rs=0.577, P<0.001) . There was also a correlation between LIC and ALT (rs=0.268, P=0.014) and blood transfusion units (rs=0.244, P=0.034) . There was no correlation between heart T2* and pro-BNP, SF (all P>0.05) , and no correlation between LIC and age (P>0.05) . The increase of heart T2* between the normal and abnormal groups was statistically significant (P=0.005) , but the iron overload ratio of the heart T2*<20 ms was not significant between the two groups. There was statistical significance in the proportion of severe liver iron overload (LIC>15 mg/g DW) (P=0.045) . After iron chelation therapy, the values of SF, transferrin saturation, ALT, AST, pro-BNP and LIC of 7 patients were decreased compared with values before iron chelation therapy, and the peripheral blood cell level was increased. However, the changes of LVEF and T2* values after iron chelation were not obvious. Conclusion: MRI T2* may be a predictor of iron overload in patients with MDS in early stage, and may be more valuable compare with LVEF, SF and other laboratory indicators. The safety and repeatability of MRI cardiac T2* examination are recognized, and it can be used as an ideal detection for patients with iron overload.

Correlations of mouse lymphoma xenografts with the expressions of MMP-9 and Bcl-2.

OBJECTIVE: To establish a mouse lymphoma xenograft model so as to investigate the correlation between the expression of matrix metallopeptidase-9 (MMP-9) and that of B-cell lymphoma 2 (Bcl-2) in lymphomas. MATERIALS AND METHODS: Diffuse large Bcl (DLBCL) cells were cultured, and a mouse lymphoma xenograft model was established via the subcutaneous injection. Mouse lymphoma tissues were extracted, and the expressions of MMP-9 and Bcl-2 messenger ribonucleic acids (mRNAs) in the xenograft tumor were detected using Real-time polymerase chain reaction (PCR). Immunohistochemistry was used to detect the expression levels of MMP-9 and Bcl-2 proteins in lymphoma tissues and tumor-adjacent tissues. The consistency of MMP-9 expression and Bcl-2 expression was analyzed via Spearman's rank correlation analysis. RESULTS: The expressions of MMP-9 and Bcl-2 in lymphoma tissues were increased. The expression levels of MMP-9 and Bcl-2 proteins in lymphoma tissues were higher than those in tumor-adjacent tissues. The expression levels of MMP-9 and Bcl-2 were correlated with the body weight loss degree of mice, and the expression of MMP-9 was positively associated with that of BCL-2 in lymphomas. CONCLUSIONS: MMP-9 and Bcl-2 are associated with the onset of DLBCL, and they are potential impact factors affecting the prognosis.

LncRNA SNHG8 participates in the development of endometrial carcinoma through regulating c-MET expression by miR-152.

OBJECTIVE: To investigate the possible function and mechanism of lncRNA SNHG8 in the pathogenesis of endometrial carcinoma. PATIENTS AND METHODS: We utilized qRT-PCR to detect the expression of SNHG8 in 60 cases of endometrial carcinoma and 25 cases of normal endometrium; after that, the endometrial carcinoma cell lines were screened. SNHG8 was transfected into endometrial carcinoma cells by Lipofectamine and the proliferative activity of cells was detected by cell counting kit-8 (CCK-8) assay. Bioinformatics methods were used to detect the target microRNA. miR-152 is predicted to bind to SNHG8 and target genes of c-MET. Luciferase reporter assay was performed to detect the relative luciferase activity between miR-152 and c-MET, SNHG8. The interactions between SNHG8, miR-152, and c-MET were further verified by transfection of miR-152 mimics, miR-152 mimics + OE-SNHG8, SNHG8 siRNA, and SNHG8 siRNA + miR-152 inhibitor. RESULTS: SNHG8 expression in endometrial carcinoma tissue was significantly higher than that in normal endometrium. After transfection with SNHG8 siRNA, the cell viability of AN3CA cells decreased, whereas the activity of Ishikawa was increased after transfection with SNHG8 overexpression plasmid. Bioinformatics predictions and dual luciferase reporter assay illustrated that SNHG8 was bound to miR-152 and miR-152 targeted on c-MET. In addition, miR-152 mimics inhibited the expression of c-MET, and the inhibitory effect was reversed after SNHG8 overexpression. Silencing SNHG8 reduced c-MET expression, and c-MET expression was reversed after addition of miR-152 inhibitor. CONCLUSIONS: SNHG8 is highly expressed in endometrial carcinoma, and SNHG8 targets c-MET through miR-152 to regulate the proliferation of endometrial cancer cells.

[Predict response to decitabine in patients with myelodysplastic syndrome and related neoplasms].

Objective: To identify clinical and molecular signatures for predicting response to decitabine (DAC) in patients with myelodysplastic syndrome (MDS) and related neoplasms. Methods: The clinical characteristics of 109 patients with MDS and related neoplasms who were treated with DAC were analyzed retrospectively and the next target sequencing was performed to define recurrently mutated genes in these disease samples, to examine the association of the clinical and molecular signatures with response to DAC treatment. Results: Of 109 MDS and related neoplasms patients, there were 70 males and 39 females, the median age was 61 years old (ranges: 17-85 years old) . According to the international prognostic scoring system (IPSS) , 46 cases were included in the relatively low risk group (low risk and intermediate-1 risk) , 63 in the relative high risk group (intermediate-2 and high risk) . There were 21 cases with complex karyotype, 17 chromosome 7 abnormality and 17 monosomal karyotype. The median courses of DAC treatment was 4 (2-11) . A total of 74 patients achieved response (67.9%) and 30 (27.5%) achieved complete response (CR) . Univariate analysis found that CR was higher in patients with high risk of IPSS, complex karyotypes, monosomal karyotypes, chromosome 7 abnormality, and platelet doubling after one cycle of DAC treatment. Patients with TP53 gene mutation were more likely to receive CR, 10 of 15 patients with TP53 mutations achieved CR. (66.7%) , which was significantly higher than that of the patients without TP53 gene mutation (21.3%) (P=0.001) . Multivariate analysis showed that TP53 gene mutation, platelet doubling after one cycle of DAC treatment and the complex karyotype were independent prognostic factors for CR. Of them, TP53 gene mutation is the strongest predictor (OR=4.39, 95%CI, 1.20-16.06, P=0.026) . Conclusion: TP53 mutation, platelet doubling after one cycle of DAC treatment and complex karyotypes could predict CR to DAC.

[Expression and clinical significance of HMGA2 in renal carcinoma].

Objective: To detect the high mobility group A2 (HMGA2) expression in renal carcinoma, and to explore the relationship with clinicopathological features and its significance for prognosis. Methods: 50 renal carcinoma specimens, 50 corresponding adjacent normal kidney tissue samples, and 40 benign renal tumor specimens were used in this study. The expressions of HMGA2 mRNA and protein were detected by RT-PCR, Western blot and immunohistochemical assays, and its relationship with clinicopathological features and prognosis in the renal carcinoma patients was analyzed. Results: The RT-PCR results showed that the relative expression levels of HMGA2 mRNA in the renal carcinoma, benign renal tumor tissues, and adjacent normal renal tissues were 0.84±0.23, 0.19± 0.06 and 0.08±0.04, respectively, and the expression in renal carcinoma tissue was significantly higher than those of the other 2 groups (P<0.01). The Western blot results showed that the relative expression levels of HMGA2 protein in the renal carcinoma, benign renal tumor tissues, and adjacent normal renal tissues were 0.91±0.24, 0.12±0.04 and 0.03±0.01, respectively, and the expression in renal carcinoma tissue was significantly higher than those of the other 2 groups (P<0.01). Immunohistochemical results showed that the expression of HMGA2 protein exhibited brown and tan granular, which mainly distributed in the cell nuclei. Among the 50 cases of renal carcinoma, 34 cases exhibited positive expression, with a positive rate of 68.0%. Among the 40 cases of benign tumor tissues, 3 cases had positive expression, with a positive rate of 7.5%, while among the 50 cases of adjacent normal renal tissues, there was only 1 case exhibiting positive expression of HMGA2 protein, with a positive rate of 2.0%. The protein expression of HMGA2 was significantly higher in the renal carcinoma than in the benign tumors and normal renal tissues (P=0.004). There was no statistically significant difference in the association of HMGA2 protein expressions with age, sex, tumor size and histological type (P>0.05), while significant difference did exist in the association with different statuses of TNM staging and lymph node metastasis (P<0.05). The median time to progression (TTP) in 34 HMGA2 protein-positive patients was (22.36±1.48) months and that of 16 HMGA2 protein-negative patients was (34.55±1.87) months (P<0.05). Conclusions: HMGA2 plays an important role in the tumorigenesis and development of renal carcinoma, and may be used as an important predictor for estimating the prognosis of renal carcinoma. HMGA2 might become a new diagnostic and prognostic marker for renal carcinoma.

[Study of abnormal iron metabolism parameters and iron overload in patients with myelodysplastic syndromes].

Objective: To investigate the abnormalities of iron metabolism parameters, the prevalence and risk factors of iron overload and clinical characteristics of patients with myelodysplastic syndromes(MDS). Methods: Retrospective investigation was used to observe abnormal iron metabolism parameters and clinical characteristics of newly diagnosed 94 MDS patients in our center from June 2015 to March 2016. Results: Of 94 patients, 71(75.53%)had a hemoglobin level of less than 100 g/L at diagnosis. Iron overload was observed in 52(55.32%)of 94 MDS patients, in which a higher prevalence of iron overload was observed in low risk groups(IPSS low/Int-1 risk groups)than higher risk groups(Int-2/high risk groups). Higher levels of serum iron(SI)[36.5(8.5-64.7)mmol/L vs 25.2(3.7-45.3)mmol/L, P<0.01], transferrin saturation(TSAT)[43.5(12.2-77.2)% vs 53.4(14.8-97.5)%, P <0.01]and serum ferritin(SF)were observed in iron overload group. No differences of labile cellular iron(LCI)and reactive oxygen species(ROS)were observed between two groups(P=0.88, P=0.06). As the results of clinical complication of iron overload, alanine aminotransferase(ALT)[25(3-158)U/L vs 16(5-80)U/L, P=0.03]and type B natriuretic peptide precursor(proBNP)[190(6-4281)ng/L vs 84(12-2 275)ng/L, P= 0.05]levels were increased in iron overload group. There was no significant difference in iron metabolism parameters between patients with refractory anemia(RARS)and non RARS patients(P>0.05). Both frequency and volume of RBC transfusion had a significant effect on all iron metabolism parameters(SI, TSAT and SF)(P <0.01)except LCI and ROS. Excluded the patients with history of blood transfusion and SF levels over 1 000 µg/L, higher levels of LCI were mainly observed in dysplastic erythropoiesis and increased bone marrow erythroblasts ratio groups(P<0.01, P<0.05). Conclusion: The main cause of iron overload in MDS is chronic transfusion therapy. Both frequency and intensity of transfusion regimen have a main effect on iron metabolism parameters. LCI levels are mainly increased in newly diagnosed patients with the abnormalities of iron metabolism and have a stronger association with dysplastic erythropoiesis and increased bone marrow erythroblasts ratio. As the toxic fraction of iron and its negative impact on MDS, iron overload monitoring and chelation treatment decision can also be supported by LCI.

IMPDH2 mediate radioresistance and chemoresistance in osteosarcoma cells.

OBJECTIVE: Osteosarcoma (OS) is the most common primary malignant bone tumour in children and adolescents. Despite aggressive therapy, survival outcomes remain unsatisfactory, especially for patients with metastatic disease or patients with a poor chemotherapy response. Previous study founds inosine 5'-monophosphate dehydrogenase type II (IMPDH2) was an independent prognostic factor and observed frequent IMPDH2 overexpression in osteosarcoma patients with poor response to chemotherapy. In the present work, we provide evidence for direct involvement of IMPDH2 in the development of radioresistance and chemoresistance. MATERIALS AND METHODS: The expression of IMPDH2 was examined in OS cells. Stable cell lines overexpressing IMPDH2 and IMPDH2 knock-down cells were generated using the osteosarcoma cell line. The stable transfected cells, alone or in combination with cisplatin or γ-irradiation, was used to treat OS cells. The growth inhibitory and apoptotic effects of IMPDH2 in vitro and in vivo were examined. RESULTS: Overexpression of IMPDH2 in IMPDH2 poor-expressed U2OS cells induced strong cisplatin chemoresistance and γ-irradiation radioresistance through inhibition of apoptosis in vitro and in vivo. Knockdown of IMPDH2 in IMPDH2 rich-expressed Saos-2 cells resulted in significant chemosensitivity and γ-irradiation radiosensitivity through inducing of apoptosis in vitro and in vivo. CONCLUSIONS: IMPDH2 is directly involved in the development of chemoresistance and radioresistance in osteosarcoma cells, suggesting that targeting of IMPDH2 by shRNA in combination with chemotherapy and γ-irradiation might be a promising means of overcoming chemoresistance and radioresistance in osteosarcomas with high IMPDH2 expression.