The top 100 most-cited papers in pheochromocytomas and paragangliomas: A bibliometric study.

Background: The purpose of this study was to define and analyze the characteristics of the top 100 most-cited articles and reviews on the topic of pheochromocytomas and paragangliomas (PPGLs) by using bibliometric methods. Methods: We explored the Web of Science Core Collection database to gather the 100 top-cited original articles and reviews of PPGL from 1985 to 20 December 2020. We conducted a bibliometric study to identify the most influential journals, authors, countries, and institutions in the PPGL field. Results: The 100 top-cited papers were cited a total number of 25,723 times, ranging from 131 to 1,144 (mean, 257.23 ± 173.64). All of these 100 top-cited papers were published between 1999 and 2017, and the number of top-cited papers published before 2008 (1999-2008) was significantly higher than that after 2008 (2009-2017) (p = 0.043). The journal with the highest number of published papers is the Journal of Clinical Endocrinology & Metabolism (n = 23). The United States was the most productive country in this topic, which published about half of these publications (n = 51). The National Institutes of Health (NIH) had the largest number of publications (n = 17). Genes or genetics is still the hottest topic in the field of PPGLs. Conclusions: We defined and analyzed the top 100 most-cited papers in the field of PPGLs by gathering detailed information. These data provided insights into the most influential studies related to PPGL. We hoped to inspire researchers and readers in this field to improve their understanding of PPGL research trends and provide ideas for future research from unique perspectives.

Microwave irradiation coupled with zero-valent iron that enhances the composite geopolymerization of chromite ore processing residue and its mechanisms.

In this work, microwave (MW) irradiation was employed to enhance the zero-valent iron (ZVI)-dominated de-contamination of chromite ore processing residue (COPR). A coupling system and the traditional two-step procedure were both conducted to evaluate the effects of MW irradiation on the reduction and the incorporation of COPR into the composite materials-based geopolymers. The factors including the ratios of liquid to solid, the mass ratios of ZVI to COPR, and the acid dosage had some obvious influence on the reduction of COPR in the MW system. The compressive strengths of 31.54 and 41.56 MPa were determined from the two-step procedure and the coupling system at the COPR dosage of 10% (mass ratio), respectively. The employment of MW irradiation not only strengthened the formation of the geopolymer matrices but also improved the chemical stabilization of Cr species in the solidified blocks. The coupled process was more conducive to incorporating the treated COPR into the geopolymer-based crystalline microstructures compared with the subsequent usage of ZVI reduction and MW irradiation.

ISYNA1 is overexpressed in bladder carcinoma and regulates cell proliferation and apoptosis.

BACKGROUND: Bladder cancer (BCa) is one of the most common urological malignancies. While Inositol-3-phosphate synthase 1 (ISYNA1) expression and function were largely unknown in BCa. We aimed to study the expression and role of ISYNA1 in bladder cancer and investigate its potential mechanisms via ingenuity pathway analysis (IPA). METHODS: ISYNA1 expression was quantified by qRT-PCR in bladder cancer cell lines as well as normal urothelial cell line. Knocking down ISYNA1 gene in BCa T24 cells was achieved by shRNA lentivirus transfection. MTT and Celigo assay were used to assess cell proliferation. Flow cytometry was applied to test cell cycle and apoptosis. In addition, IPA was performed using PrimeView™ Human Gene Expression Array. Imunohistochemistry (IHC) was performed in BCa patient tissue microarray to verify the association between ISYNA1 expression and patients' clinicopathological features. RESULTS: ISYNA1 was significantly upregulated in BCa samples vs. para-tumor tissues. Higher expression were significantly associated with tumor T stage and lymph node metastasis of bladder cancer patients. Similarly, it was elevated in BCa cell lines (5637 and T24) compared with SVHUC cells. Knocking down ISYNA1 significantly decreased proliferation, induced apoptosis and cell cycle arrest in T24 cells. Furthermore, IPA indicated that ISYNA1 was an important regulatory factors and related networks were involved in multiple functional processes. CONCLUSION: Taken together, current study suggest ISYNA1 promotes proliferation and inhibit apoptosis in bladder cancer cells, and its expression correlated with BCa patients' clinicopathological features. Thus, ISYNA1 may serve as a potential biomarker and therapeutic target for BCa patients.

Microarray expression profiles analysis revealed lncRNA OXCT1-AS1 promoted bladder cancer cell aggressiveness via miR-455-5p/JAK1 signaling.

Bladder cancer (BCa) is one of the most prevalent cancers of the urinary system worldwide. Accumulating evidence suggests that long noncoding RNAs (lncRNAs) perform a vital function in the pathogenesis and progression of BCa. In the current study, we identified a novel lncRNA OXCT1-AS1 and investigated its role and potential mechanisms in BCa. The microarray results showed the expression of lncRNAs, microRNAs, and messenger RNAs between BCa primary tumor tissues and metastatic lymph nodes were significantly different. The quantitative polymerase chain reaction verification was performed to ensure the reliability of the screening results. The Cell Counting Kit 8 and transwell assay were used to assess the tumor cell proliferation and invasion abilities in vitro, respectively. The dual-luciferase activity assay was performed to investigate the potential mechanism of competing endogenous RNA network. lncRNA OXCT1-AS1, which elevated in metastasis lymph node, was significantly upregulated in BCa cell lines compared with SVHUC-1. We demonstrated OXCT1-AS1 inhibited miR-455-5p to decrease its binding to the JAK1 3'-untranslated region, which could upregulate the expression of JAK1 at the protein level, thus promoting BCa proliferation and invasion. Therefore, lncRNA OXCT1-AS1 could act as a potential biomarker and therapeutic target for patients with BCa.

Association of the invasiveness of colon cancer with the expression of C/EBPα.

The present study aimed to investigate the association of the invasiveness of colon cancer (CC) with the expression of CCAAT/enhancer binding protein α (C/EBPα). Immunohistochemistry was performed to determine the expression of C/EBPα in the cancer and adjacent tissue samples from 48 patients with CC. A pCDGFP-C/EBPα eukaryotic expression vector was constructed, and a wound-healing assay was performed to observe the effect of transfection on the migration of SW480 cells. In addition, the expression levels of tumor invasion-associated proteins, including Kruppel-like factor 5 (KLF5), matrix metallopeptidase (MMP)-2, MMP-9, and E-cadherin (ECD) were detected subsequent to transfection. Immunohistochemistry analysis demonstrated that the rate of low C/EBPα expression in normal tissue was 6.25%, whereas the rate in CC tissues was 68.75%; this difference was statistically significant (P<0.05). The patients with lower C/EBPα expression exhibited statistically larger tumor diameters, more advanced tumor-node-metastasis (TMN) stages and a greater likelihood of lymph node metastasis. The overexpression of C/EBPα significantly reduced the mobility of SW480 cells, and the expression of KLF5, MMP-2 and MMP-9 was reduced, whereas the expression of ECD was increased. In conclusion, C/EBPα was downregulated in CC tissue samples, and associated with the TMN stage and metastasis of CC; in addition, the overexpression of C/EBPα significantly reduced the invasiveness of CC cells. This may be significant for the diagnosis and treatment of CC in the future.

Glucocorticoid-Inducible Kinase 2 Promotes Bladder Cancer Cell Proliferation, Migration and Invasion by Enhancing ß-catenin/c-Myc Signaling Pathway.

Background: Bladder cancer is one of the most common malignancies in urologic system. The glucocorticoid-inducible kinase 2 (SGK2) expression and function were largely unknown in cancers. Current study was aimed to investigate the role of SGK2 in bladder cancer and its potential mechanisms. Methods: SGK2 expression was quantified by western blot (WB) in multiple bladder cancer cell lines (T24, 5637, J82 and UMUC3) compared with normal urothelial cell line (SVHUC). SGK2 knocking down and overexpression model were established by lentivirus transfection. MTT, colony formation, wound healing and transwell assay were used to assess the tumor cell proliferation, migration and invasion abilities, respectively. In addition, molecular function analysis was performed using FunRich software V3. Immunoprecipitation (IP) assay was applied to investigate the interaction between SGK2 and ß-catenin at protein level. TCGA database was retrieved to verify the association between these genes and clinical tumor stage as well as prognosis among bladder cancer patients. Results: SGK2 expression was significantly upregulated in multiple bladder cancer cell lines compared with SVHUC at protein level. Cell proliferation, migration and invasion abilities were significantly decreased after knocking down SGK2 in J82 and UMUC3 cell lines. Inversely, cell aggressive phenotypes were significantly increased after overexpressing SGK2 in T24 cell line. Furthermore, functional analyses of SGK2 based on TCGA database showed that SGK2 related genes were involved in receptor activity, ATP binding, DNA repair protein, trans-membrane receptor activity and lipid binding. In addition, protein interaction analysis identified c-Myc was significantly enriched in SGK2 positively associated genes. The prediction was validated by WB and IP assay that SGK2 could directly bind with ß-catenin at protein level to regulate their downstream gene c-Myc expression in bladder cancer to influence tumor progression. And clinical data generated from TCGA database also identified these downstream genes were significantly associated with tumor stage and survival status of bladder cancer patients. Conclusion: Taken together, our findings suggest SGK2 promotes bladder cancer progression via mediating ß-catenin/c-Myc signaling pathway, which may serve as a potential therapeutic target for bladder cancer patients.

Association of metformin intake with bladder cancer risk and oncologic outcomes in type 2 diabetes mellitus patients: A systematic review and meta-analysis.

BACKGROUND: Recent clinical trials indicated that metformin intake might play a protective role in the incidence and oncologic outcomes of various cancers. However, its protective effect on bladder cancer remains uncertain. METHODS: We performed a meta-analysis to investigate the association between metformin intake and bladder cancer risk as well as oncologic outcomes in diabetes mellitus (DM) patients. A comprehensive literature search was performed using PubMed, Embase, and the Cochrane Central Search Library in December 2017. Hazard ratio (HR) with 95% confidence interval (CI) was pooled. RESULTS: A total of 9 retrospective cohort studies with 1,270,179 patients were included. A meta-analysis revealed that metformin intake was associated with an increased recurrence-free survival (HR = 0.55, 95% confidence interval [CI] = 0.35-0.88; P = .01; I = 64%), improved progression-free survival (HR = 0.70, 95% CI = 0.51-0.96; P = .03; I = 33%), and prolonged cancer-specific survival (HR = 0.57, 95% CI = 0.40-0.81; P = .002; I = 0%). However, results demonstrated that metformin intake was not associated with a decreased incidence of bladder cancer (HR = 0.82, 95% CI = 0.61-1.09; P = .17; I = 85%) or an increased overall survival in bladder cancer patients (HR = 0.83, 95% CI = 0.47-1.44; P = .50; I = 64%). CONCLUSION: The present meta-analysis indicated that metformin intake could improve the prognosis of bladder cancer patients. Further prospective cohort studies and mechanistic studies are still required to determine the precise role of metformin in the initiation and progression of bladder cancer.

Association Between 12 Polymorphisms of VEGF/Hypoxia/Angiogenesis Pathway Genes and Risk of Urogenital Carcinomas: A Meta-Analysis Based on Case-Control Studies.

Objective: Previous studies indicated potential associations between polymorphisms in genes of VEGF/hypoxia/angiogenesis pathway and risk of urogenital carcinomas However, the results were controversial and inconclusive. Here, we conducted an in-depth meta-analysis to investigate the precise associations between polymorphisms in VEGF/hypoxia/angiogenesis related genes and risk of urogenital carcinomas. Methods: We searched PubMed, Web of Science, EMBASE, and Cochrane Library to identify all eligible publications. Pooled odds ratios (ORs) corresponding with the 95% confidence intervals (CIs) were calculated to evaluate their associations. Subgroup analysis was conducted to further ascertain such relationship and investigate sources of heterogeneity. Results: In the end, a total of 96 case-control studies fulfilled the inclusion criteria were enrolled for 12 polymorphisms in 4 VEGF/hypoxia/angiogenesis related genes. The pooled results showed eNOS-rs2070744 polymorphism conferred a significantly increased overall risk of urogenital carcinomas in allele, homozygote, and recessive models, respectively. In addition, eNOS-Intron 4a/b VNTR polymorphism was identified related to an increased risk of urogenital carcinomas in recessive model. And VEGF-rs699947 polymorphism was also identified an increased risk of renal cell carcinoma (RCC) in allelic, heterozygote, dominant, homozygote, and recessive models. Conclusion: To conclude, eNOS-rs2070744 and eNOS-Intron 4a/b VNTR polymorphisms are risk factors for urogenital carcinomas. VEGF-rs699947 polymorphism was also identified as an increased risk factor for renal carcinoma.

High Expression of Long Noncoding RNA MALAT1 Indicates a Poor Prognosis and Promotes Clinical Progression and Metastasis in Bladder Cancer.

BACKGROUND: Recent studies have demonstrated that the expression of long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) promotes cancer cell proliferation, invasion, and metastasis in many tumor types, but the association between bladder cancer and MALAT1 remains unknown. MATERIALS: The expression of MALAT1 was tested by in situ hybridization (ISH) in 120 bladder cancer specimens. The association between MALAT1 expression and clinicopathological features and prognosis of the patients with bladder cancer was analyzed. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to verify the relationship between the expression of MALAT1 and progression and metastasis of bladder cancer. RESULTS: ISH showed that high MALAT1 expression was associated with advanced histological grade, high tumor stage, and positive lymph nodes. Kaplan-Meier survival analysis and Cox regression analysis indicated that high tumor stage, positive lymph nodes, and high MALAT1 expression were independent prognostic indicators for overall survival (OS) of patients with bladder cancer. qRT-PCR showed that the expression of MALAT1 in bladder cancer tissues was 2.85 times higher than those measured in adjacent normal tissues (P < .001). The expression of MALAT1 was 2.673 ± 0.254 in non-muscle-invasive bladder cancer and 2.987 ± 0.381 in muscle-invasive bladder cancer (P = .018). In bladder cancer specimens with positive lymph nodes, MALAT1 expression was 3.167 ± 0.297 versus 2.896 ± 0.329 in bladder cancer specimens with negative lymph nodes (P = .020). CONCLUSION: High MALAT1 expression could serve as an independent prognostic factor for OS of patients with bladder cancer and could be considered as a potential therapeutic target of bladder cancer.

Metadherin regulates epithelial-mesenchymal transition in carcinoma.

Metadherin (MTDH) was first identified in primary human fetal astrocytes exposed to HIV-1 in 2002 and then recognized as an important oncogene mediating tumorigenesis, progression, invasiveness, and metastasis of carcinomas. Epithelial-mesenchymal transition (EMT) is a vital process in embryonic development, organ repair, and cancer progression. MTDH and EMT have also been proved to be related to the prognosis of patients with cancers. Recent studies reveal a relationship between MTDH overexpression and EMT in some malignancies. This review highlights the overexpression of MTDH and EMT in cancers and their correlations in clinical studies. Positive correlations have been established between MTDH and mesenchymal biomarkers, and negative correlations between MTDH and epithelial biomarkers have also been established. Furthermore, experiments reveal EMT regulated by MTDH, and some signal pathways have been established. Some anticancer drugs targeting MTDH and EMT are introduced in this review. Some perspectives concerning EMT regulation by MTDH are also presented in this review.

CCL21/CCR7 enhances the proliferation, migration, and invasion of human bladder cancer T24 cells.

OBJECTIVE: To investigate the effects of CCL21/CCR7 on the proliferation, migration, and invasion of T24 cells and the possible associated mechanisms: expression of MMP-2 and MMP-9, and regulation of BCL-2 and BAX proteins. METHODS: T24 cells received corresponding treatments including vehicle control, antibody (20 ng/mL CCR7 antibody and 50 ng/ml CCL21), and 50, 100, and 200 ng/ml CCL21. Proliferation was evaluated by MTT assay; cell migration and invasion were assayed using a transwell chamber. Cell apoptosis was induced by Adriamycin (ADM). The rate of cell apoptosis was examined by flow cytometry using annexin V-FITC/PI staining. Western-blot was used to analyze MMP-2 and MMP-9 and BCL-2 and BAX proteins. RESULTS: CCL21 promoted T24 cell proliferation in concentration-dependent manner with that 200 ng/mL induced the largest amount of proliferation. Significant differences of cell migration were found between CCL21treatment groups and the control group in both the migration and invasion studies (P < 0.001 for all). The expressions of MMP-2 and MMP-9 proteins were significantly increased after CCL21 treatment (p < 0.05 for all). Protein expression of Bcl-21 follows an ascending trend while the expression of Bax follows a descending trend as the concentration of CCL21 increases. No difference was found between the control group and antibody group for all assessments. CONCLUSION: CCL21/CCR7 promoted T24 cell proliferation and enhanced its migration and invasion via the increased expression of MMP-2 and MMP-9. CCL21/CCR7 had antiapoptotic activities on T24 cells via regulation of Bcl-2 and Bax proteins. CCL21/CCR7 may promote bladder cancer development and metastasis.

Preservation of the saphenous vein during laparoendoscopic single-site inguinal lymphadenectomy: comparison with the conventional laparoscopic technique.

OBJECTIVE: To prospectively study the surgical strategies and clinical efficacy of laparoendoscopic single-site (LESS) inguinal lymphadenectomy compared with conventional endoscopic inguinal lymphadenectomy for the management of inguinal nodes. PATIENTS AND METHODS: A total of 12 patients with squamous cell carcinoma of the penis who underwent penectomy between February and July 2013 were enrolled in the study. All 12 patients underwent bilateral inguinal lymphadenectomy (LESS inguinal lymphadenectomy in one limb and conventional endoscopic inguinal lymphadenectomy in the other) with preservation of the saphenous vein. All lymphatic tissue in the boundaries of the adductor longus muscle (medially), the sartorius muscle (laterally), 2 cm above the inguinal ligament (superiorly), the Scarpa fascia (superficially) and femoral vessels (deeply) was removed in both surgical techniques. All 24 procedures were performed by one experienced surgeon. RESULTS: All 24 procedures (12 LESS and 12 conventional endoscopic inguinal lymphadenectomies) were completed successfully without conversion to open surgery. For LESS inguinal lymphadenectomy and conventional endoscopic inguinal lymphadenectomy groups, the mean ± sd operating time was 94.6 ± 14.8 min and 90.8 ± 10.6 min, respectively (P = 0.145). No significant differences in the incidence of postoperative complications (skin-related problems, hecatomb, lower extremity oedema, lymphatic complications and overall complications) were noted between the two groups (P > 0.05). No lower extremity oedema occurred in any limbs of the two groups. No significant differences were observed in either lymph node clearance rate or detection rate of histologically positive lymph nodes (P > 0.05). The patient satisfaction rate with scar appearance and cosmetic results was significantly better in the LESS inguinal lymphadenectomy group than in the conventional endoscopic inguinal lymphadenectomy group of (75 vs 25%; P = 0.039). CONCLUSIONS: This preliminary study suggests that both LESS inguinal lymphadenectomy and conventional endoscopic inguinal lymphadenectomy are safe and feasible procedures for inguinal lymphadenectomy. Preservation of the saphenous vein during LESS inguinal lymphadenectomy/conventional endoscopic inguinal lymphadenectomy can effectively reduce the incidence of postoperative lower extremity oedema. LESS inguinal lymphadenectomy seems to provide better cosmetic results than conventional endoscopic inguinal lymphadenectomy.

miRNA-205 is a candidate tumor suppressor that targets ZEB2 in renal cell carcinoma.

BACKGROUND: This study aims to characterize the function of downregulated MicroRNA miR-205 in renal cell carcinoma (RCC), and show how the downstream zinc finger E-box-binding homeobox 2 (ZEB2) is negatively regulated by miR-205. MATERIALS AND METHODS: The expression of miR-205 was detected in RCC and adjacent non-tumor tissues using real-time polymerase chain reaction (PCR). The expression of miR-205 and ZEB2 was detected in RCC cell lines using real-time PCR. The luciferase reporter assay was used to assess ZEB2 as a target of miR-205. Protein levels of ZEB2, E-cadherin, and vimentin were measured by western blot after overexpression of miR-205 in ACHN cells. In vivo functions of miR-205 in ACHN cells were measured by MTT assays, migration and invasion assays, and flow cytometry. RESULTS: MiR-205 was significantly downregulated in RCC samples and cell lines compared with matched non-tumor tissues and HK-2 cells, respectively. No significant difference was found in miR-205 expression between well differentiated and poorly to moderately differentiated groups or between phase I and phase II-III. ZEB2 was upregulated in RCC cell lines compared with expression in HK-2 cells. Upregulation of miR-205 expression caused the downregulation of ZEB2 and vimentin, and the upregulation of E-cadherin in ACHN cells. miR-205 also inhibited proliferation, migration, and invasion, and induced apoptosis of ACHN cells. CONCLUSION: miR-205 is a candidate tumor suppressor that targets ZEB2 in RCC.

Retroperitoneoscopic dismembered pyeloplasty for ureteropelvic junction obstruction: modification of the procedure and our experience.

PURPOSE: To report a modified retroperitoneoscopic dismembered pyeloplasty technique and its application in the treatment of ureteropelvic junction obstruction (UPJO). MATERIALS AND METHODS: From June 2010 to March 2012, retroperitoneoscopic dismembered pyeloplasty was performed in 46 patients with UPJO. Briefly, the renal pelvis was incised in the anterior aspect instead of the lateral aspect, and proximal ureter was spatulated with incision on its posterior wall. After adequately trim­ming, two layers of ureteropelvic anastomosis respectively lay on left and right side of one laparoscopic plane other than two different planes. In our refined procedure, the difficulty of intracorporeal suturing was greatly decreased. Data from 19 months mean follow-up were analyzed to evaluate the surgical outcomes. RESULTS: All operations were completed without open conversion. The mean operative time, estimated blood loss, and postoperative hospitalization stay were 108 min (75 to 155 min), 30 mL (15 to 60 mL) and 4 days (2 to 9 days), respectively. No intraoperative complications were occurred. Postoperative complications included 2 cases of minor abdominal wall hematoma and 1 case of transient postoperative anastomotic leakage for 8 days, which all were successfully treated by conservative management. A mean follow-up of 19 months (12 to 36 months) was performed which showed a success rate of 97.8%. One case (2.2%) underwent open surgery for persistence UPJO two months later. CONCLUSION: Our modification to the retroperitoneoscopic dismembered pyeloplasty procedure is technically feasible and reliable with low complications. It could be implemented as a useful alternative technique to great­ly decrease the difficulty of this procedure.

Transforming growth factor­ß1 induces epithelial­mesenchymal transition and increased expression of matrix metalloproteinase­16 via miR­200b downregulation in bladder cancer cells.

Transforming growth factor­ß1 (TGF­ß1) is involved in the migration and metastases of bladder cancer. The present study was designed to investigate whether TGF­ß1 is able to induce epithelial­mesenchymal transition (EMT) and the upregulation of matrix metalloproteinase­16 (MMP­16), and to identify an association between EMT and MMP­16 in bladder cancer. Following TGF­ß1 treatment, samples of HTB9 and T24 bladder cancer cells were collected at various time points. Western blotting and quantitative polymerase chain reaction (qPCR) confirmed that TGF­ß1 induced EMT in HTB9 and T24 cells at the protein and mRNA levels. The expression levels of the miR­200 family were determined by qPCR, which indicated that TGF­ß1 treatment significantly reduced the expression of miR­200b. Bioinformatic analysis indicated that MMP­16 may be the target of miR­200b. Reporter luciferase assay confirmed that MMP­16 is a direct downstream functional target of miR­200b. A Matrigel migration assay demonstrated that miR­200b overexpression inhibited the migration of bladder cancer cells. In summary, the current study demonstrated that exogenous TGF­ß1 leads to the induction of EMT and the downregulation of miR­200b in bladder cancer cells. To the best of our knowledge, this is the first evidence that MMP­16 is a direct target of miR­200b.

Recurrence of inflammatory myofibroblastic tumor in bladder secondary to prostate treated with laparoscopic radical cystectomy.

BACKGROUND: Inflammatory myofibroblastic tumor (IMT) is a rare borderline tumor. The nomenclature of this disease is confused in the literature. CASE REPORT: In this report, the case of a 62-year-old man with IMT recurrence of bladder secondary to prostate is presented. The possible etiology of IMT is discussed, along with its clinical manifestation and pathological features. The patient received a laparoscopic bladder radical resection. The pathology finding demonstrated the diagnosis of IMT and no regional lymph node involvement. CONCLUSIONS: IMT is a borderline tumor and unlikely to metastasize to regional lymph nodes. The patient has been observed for 2 years without recurrence.

[Expression of Ki-67, Bcl-2,Bax and caspase-3 in benign prostatic hyperplasia combined with prostatitis and their significances].

OBJECTIVE: To detect the expression of Ki-67, Bcl-2, Bax and caspase-3 in simple benign prostatic hyperplasia (BPH) and BPH combined with prostatitis,and to evaluate the effect of inflammation on the development and progression of BPH. METHODS: All specimens were obtained from patients undergoing surgical resection of the prostate. The paraffin section of the specimens was stained with hemotoxyline and eosin, and observed under light microscope to examine the inflammation hispathological changes. Sixteen patients with simple BPH (Group A) and 42 patients with BPH combined with prostatitis (Group B) were included. Immunohistochemical analysis and Western blot were used to examine the expression of Ki-67, Bcl-2, Bax and caspase-3. RESULTS: The expression of Ki-67 and Bcl-2 was significantly higher in Group B than that in Group A (P<0.05), and caspase-3 expression was significantly lower (P<0.05). There was no difference in Bax expression between the 2 groups (P>0.05). CONCLUSION: Prostatitis can up-regulate Ki-67, Bcl-2 expression, and down-regulate the expression of caspase-3 in BPH. Prostatitis appeared to play an important role in the development of BPH by affecting the proliferation and apoptosis of the prostatic cells.