[Show abstract][Hide abstract] ABSTRACT: Tumor necrosis factor receptor-associated protein 1 (TRAP1), an important member of mitochondrial heat shock protein 90 family, is involved in multiple biological processes in several types of tumors. However, its pathological role in esophageal squamous cell cancer (ESCC) remains unknown. Herein, we demonstrated the clinical value of TRAP1, and its role in apoptosis and motility in ESCC. The clinical potential of TRAP1 was investigated through immunohistochemical analysis in 328 ESCC samples, which revealed that strong TRAP1 expression was associated with increased risk of lymph node metastasis, while high TRAP1 expression correlated with poor prognosis. Expression of TRAP1 was found to be an independent prognostic factor for patients with ESCC. Additionally, TRAP1 upregulation antagonized cisplatin-induced apoptosis while its downregulation sensitized cells to cisplatin-induced apoptosis. As revealed by the transwell assay, TRAP1 overexpression promoted migration and invasion as compared to the control groups. In contrast, silencing of endogenous TRAP1 expression attenuated the ability of migration and invasion. Finally, the molecular mechanism investigated in the present study demonstrated that TRAP1-mediated migration and invasion occurred through STAT3/MMP2 signaling pathway. In conclusion, TRAP1 may be considered as a molecular predictive marker for prognosis and a novel molecular candidate for therapeutic target in ESCC.
Journal of Genetics and Genomics 09/2014; · 2.92 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Background & Aims
High-resolution microendoscopy is an optical imaging technique with the potential to improve the accuracy of endoscopic screening for esophageal squamous neoplasia. Although these microscopic images can readily be interpreted by trained personnel, quantitative image analysis software could facilitate the use of this technology in low-resource settings. In this study we developed and evaluated quantitative image analysis criteria for the evaluation of neoplastic and non-neoplastic squamous esophageal mucosa.
We performed image analysis of 177 patients undergoing standard upper endoscopy for screening or surveillance of esophageal squamous neoplasia, using high-resolution microendoscopy, at 2 hospitals in China and 1 in the United States from May 2010 to October 2012. Biopsies were collected from imaged sites (n=375); a consensus diagnosis was provided by 2 expert gastrointestinal pathologists and used as the standard.
Quantitative information from the high-resolution images was used to develop an algorithm to identify high-grade squamous dysplasia or invasive squamous cell cancer, based on histopathology findings. Optimal performance was obtained using mean nuclear area as the basis for classification, resulting in sensitivities and specificities of 93% and 92% in the training set, 87% and 97% in the test set, and 84% and 95% in an independent validation set, respectively.
High-resolution microendoscopy with quantitative image analysis can aid in the identification of esophageal squamous neoplasia. Use of software-based image guides may overcome issues of training and expertise in low-resource settings, allowing for widespread use of these optical biopsy technologies.
Clinical Gastroenterology and Hepatology 07/2014; · 6.53 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Lung adenocarcinoma is one of the most common histological subtypes of lung cancer. The incidence of this disease was continuously increased. This study aims to detect the expressions of Napsin A, TTF-1, ERCC1, RRM1, EGFR, HER2, ERα, ERβ, PR, and Bcl-2 in lung adenocarcinoma and to explore their correlations with clinicopathological characteristics and prognosis.
A total of 227 lung adenocarcinoma specimens were constructed in tissue microarrays. The expressions of the 10 tumor biomarkers were analyzed by immunohistochemistry on paraffin-embedded sections.
Among the 10 markers, Napsin A was gender-related (P=0.049). Napsin A, PR, and EGFR were significantly associated with smoking. TTF-1 and ERCC1 were closely associated with tumor size. Napsin A, TTF-1, ERα, and PR were remarkably associated with tumor differentiation. TTF-1, Bcl-2, and ERCC1 were closely associated with tumor stage (P<0.05). No marker was related to age. No correlations were observed between ERβ, HER2, and RRM1 expressions and clinicopathological parameters (P>0.05). Univariate analysis results showed that Napsin A, TTF-1, and ERCC1 were significantly associated with overall survival. TTF-1 was remarkably associated with disease-free survival (P<0.05). Stage I cases were further analyzed and revealed that only Napsin A expression was associated with overall survival (P<0.05). No marker was correlated with disease-free survival (P>0.05). Multivariate analysis results showed that pathological staging was significantly associated with overall survival and disease-free survival (P<0.05). No marker was identified as a predictor of patient outcome (P>0.05).
Napsin A, TTF-1, and ERCC1 are the markers indicating good prognosis of lung adenocarcinoma.
Zhongguo fei ai za zhi = Chinese journal of lung cancer 03/2014; 17(3):243-53.
[Show abstract][Hide abstract] ABSTRACT: Cigarette smoking is an established risk factor for esophageal cancers. Yes-associated protein 1 (YAP1), the key transcription factor of the mammalian Hippo pathway, has been reported to be an oncogenic factor for many cancers. In this study, we find nicotine administration can induce nuclear translocation and activation of YAP1 in ESCC. Consistently, we observed nuclear translocation and activation of YAP1 by knockdown of CHRNA3, which is a negative regulator of nicotine signaling in bronchial and esophageal cancer cells. Nicotine administration or CHRNA3 depletion substantially increased proliferation and migration in esophageal cancer cells. Interestingly, we find that YAP1 physically interacts with nAChRs, and nAChRs-signaling dissociates YAP1 from its negative regulatory complex composed with α-catenin, β-catenin and 14-3-3 in the cytoplasm, leading to upregulation and nuclear translocation of YAP1. This process likely requires PKC activation, as PKC specific inhibitor Enzastaurin can block nicotine induced YAP1 activation. In addition, we find nicotine signaling also inhibits the interaction of YAP1 with P63, which contributes to the inhibitory effect of nicotine on apoptosis. Using immunohistochemistry analysis we observed upregulation of YAP1 in a significant portion of esophageal cancer samples. Consistently, we have found a significant association between YAP1 upregulation and cigarette smoking in the clinical esophageal cancer samples. Together, these findings suggest that the nicotine activated nAChRs signaling pathway which further activates YAP1 plays an important role in the development of esophageal cancer, and this mechanism may be of a general significance for the carcinogenesis of smoking related cancers.
PLoS ONE 03/2014; 9(3):e90836. · 3.53 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: OLC1 was recently identified to be a potential oncogene. However, the role of OLC1 in human esophageal cell carcinoma (ESCC) is unknown. The aim of this study was therefore to evaluate the expression of OLC1 in human ESCC from normal, premalignant, and malignant lesions, and to clarify the mechanisms by which OLC1 contributes to the progression of ESCC.
Two hundred and fourteen paired ESCC specimens, and an independent set from 28 ESCC patients, were used to analyze the correlation between OLC1 expression and the pathological characteristics of tumors using immunohistochemistry. Stable OLC1-overexpressing and OLC1-interfering esophageal cancer cells were established and a series of experimental methods were used to investigate the biological functions and mechanisms of action of OLC1.
We showed that OLC1 was overexpressed in 145 of 214 (67.8%) of human ESCC specimens, compared with in only 59 of 214 (27.57%) paired adjacent normal tissues (P<0.001). OLC1 overexpression occurred at a rate of 35% (10/28) at the stage of mild/moderate dysplasia, but was significantly upregulated to 66% (22/33) at the stages of severe dysplasia and in situ carcinoma, while 71% positive staining (22/28) was observed in invasive carcinoma tissues compared with normal tissues (P<0.05). We also provided evidence that OLC1 abnormalities significantly altered the cell proliferation and apoptosis induced by cytotoxic agents. OLC1 overexpression suppressed apoptosis, and was associated with attenuated caspase-3 activation and increased Bcl-2 stability.
Our study provides strong evidence suggesting OLC1 abnormalities may contribute to the development of human ESCC and have some important clinical significance.
PLoS ONE 03/2014; 9(3):e90958. · 3.53 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Genomic changes affecting tumour suppressor genes are fundamental to cancer. We applied SNP array analysis to a panel of testicular germ cell tumours to search for novel tumour suppressor genes and identified a frequent small deletion on 6q25.3 affecting just one gene; ZDHHC14. The expression of ZDHHC14, a putative protein palmitoyltransferase with unknown cellular function, was decreased both at RNA and protein levels in testicular germ cell tumours. ZDHHC14 expression was also significantly decreased in a panel of prostate cancer samples and cell lines. Through next generation sequencing of the ZDHHC14 genomic locus we discovered several mutations in both cancer types. Inducible overexpression of ZDHHC14 led to reduced cell viability and increased apoptosis through the classic caspase-dependent pathway. Finally, we confirmed our in vitro findings of the tumour suppressor role of ZDHHC14 in a mouse xenograft model, showing that overexpression of ZDHHC14 inhibits tumourigenesis. Thus we have identified a novel tumour suppressor gene that is commonly downregulated in testicular germ cell tumours and prostate cancer, as well as given insight into the cellular functional role of ZDHHC14, a potential protein palmitoyltransferase that may play a key protective role in cancer.
The Journal of Pathology 01/2014; · 7.33 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: To evaluate PIK3CA gene mutations and PIK3CA expression status in Chinese esophageal squamous cell carcinoma (ESCC) patients, and their correlation with clinicopathological characteristics and clinical outcomes.
PLoS ONE 01/2014; 9(7):e103021. · 3.53 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Lung cancer has the highest mortality rate among malignant tumors. Proteomics is a powerful tool to identify protein biomarkers. The identification of protein biomarkers associated with lung adenocarcinoma would have significance for making prognoses and designing targeted therapies.
In our study, we applied a two-dimensional difference gel electrophoresis approach coupled to a matrix-assisted laser desorption/ionization time-of-flight mass spectrometric analysis for the identification of proteins differentially expressed between lung adenocarcinoma and the paired normal bronchial epithelial tissues derived from seven patients (four of them developed distant metastasis after operation). In addition, we chose two candidate proteins and examine their expression levels in lung adenocarcinoma and adjacent normal tissues using immunohistochemistry methods, and their expression levels in serum of patients and healthy donors by ELISA.
In this study, 173 proteins were found to be differentially expressed (ratio>1.5 or<-1.5, P≤0.05), and 22 of them were identified by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. Thirteen proteins were at lower levels in the lung adenocarcinoma group, while nine proteins were at higher abundance. Immunohistochemistry analysis confirmed the expression levels of the two candidate proteins. The differential expression of the candidate secreted protein in serum from lung adenocarcinoma samples and healthy controls was showed by ELISA.
Our results demonstrated a differential protein expression pattern for lung adenocarcinoma compared with the paired normal bronchial epithelial tissues. Further functional validation of candidate proteins is ongoing and might provide new insights in lung adenocarcinoma.
[Show abstract][Hide abstract] ABSTRACT: BACKGROUND: Long interspersed nuclear element-1 (LINE-1 or L1), the most abundant and only autonomously active family of non-LTR retrotransposons in the human genome, expressed not only in the germ lines but also in somatic tissues. It contributes to genetic instability, aging, and age-related diseases, such as cancer. Our previous study identified in human gastric adenocarcinoma an upregulated transcript GCRG213, which shared 88% homology with human LI sequence and contained a putative conserved apurinic/apyrimidinic endonucleas1 domain. METHODS: Immunohistochemistry was carried out by using a monoclonal mouse anti-human GCRG213 protein (GCRG213p) antibody produced in our laboratory, on tissue microarray constructed with specimens from 175 gastric adenocarcinoma patients. The correlation between GCRG213p expression and patient clinicopathological parameters was evaluated. GCRG213p expression in gastric cancer cell lines were studied using Western blotting analysis. L1 promoter methylation status of gastric cancer cells was tested using methylation-specific PCR. BLASTP was used at the NCBI Blast server to identify GCRG213p sequence to any alignments in the Protein Data Bank databases. RESULTS: Most primary gastric cancer, lymph node metastases and gastric intestinal metaplasia glands showed positive GCRG213p immunoreactivity. High GCRG213p immunostaining score in the primary gastric cancer was positively correlated with tumor differentiation (well differentiated, p = 0.001), Lauren's classification (intestinal type, p < 0.05) and a late age onset of gastric adenocarcinoma (>=65 yrs; p < 0.05). GCRG213p expression has no association with other clinicopathological parameters, including survival. Western blotting analysis of GCRG213p expression in gastric cancer cells indicated that GCRG213p level was higher in gastric cancer cell lines than in human normal gastric epithelium immortalized cell line GES-1. Partial methylation of L1 in gastric cancer cells was confirmed by methylation-specific PCR. BLASTP program analysis revealed that GCRG213p peptide shared 83.0% alignment with the C-terminal region of L1 endonuclease (L1-EN). GCRG213p sequence possesses the important residues that compose the conserved features of L1-EN. CONCLUSIONS: GCRG213p could be a variant of L1-EN, a functional member of L1-EN family. Overexpression of GCRG213p is common in both primary gastric cancer and lymph node metastasis. These findings provide evidence of somatic L1 expression in gastric cancer, and its potential consequences in the form of tumor.
BMC Cancer 05/2013; 13(1):265. · 3.32 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Tumor-to-tumor metastasis is a fairly rare phenomenon. The lung cancers are the most common donors, but are exceedingly rare as recipients. Here we report a case of a lung adenocarcinoma acting as the recipient of papillary thyroid carcinoma, with multiple spreading foci of the two cancers in the lung simultaneously. The morphology and immunohistochemisty (Napsin-A, Thyroglobulin) are very important in differential diagnosis of lung primary adenocarcinoma and metastatic papillary thyroid carcinoma. Virtual slides The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/2069496615891134.
[Show abstract][Hide abstract] ABSTRACT: Sporadic gastrointestinal stromal tumors (GISTs) usually form a well-circumscribed mass. In contrast, diffuse interstitial cell of Cajal (ICC) hyperplasia along the Auerbach plexus without a discrete mass may occur in patients with germline mutations in the NF1, c-KIT or PDGFRA genes. However, sporadic, diffuse ICC hyperplasia without c-KIT or PDGFRA mutations has not been reported. We describe herein one such case, forming a giant diverticulum. A 63-year-old woman with no features of Neurofibromatosis 1 (NF1) presented with increasing abdominal pain for more than 30 years. A large, diverticulum-like mass in the ileum was resected. Microscopically, a diffuse proliferation of bland spindle cells was seen extending for 12 cm, replacing the muscularis propria and lined by intact mucosa. The spindle cells were CD117+/CD34+/DOG1+/SMA+/Desmin-/S100-. Mutation analyses did not reveal any mutations in c-KIT or PDGFRA. The lesion had two silent mutations in the NF1 gene. It is rare of the diffuse form of sporadic ICC hyperplasia showing diffuse longitudinal microscopic growth completely replacing the muscularis propria, mimicking diffuse ICC hyperplasia in hereditary GIST syndromes, but without solid components and no c-KIT or PDGFRA gene mutations. This peculiar form of sporadic ICC hyperplasia may be related to intestinal dysmotility in this ileal segment and giant diverticulum formation.
International journal of clinical and experimental pathology 01/2013; 6(12):2989-96. · 1.78 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Esophageal squamous cell carcinoma (ESCC) is a leading cause of cancer-related death in China and has limited effective therapeutic options except for early surgery, since the underlying molecular mechanism driving its precursor lesions towards invasive ESCC is not fully understood. Cellular senescence is the state of the permanent growth arrest of a cell, and is considered as the initial barrier of tumor development. Human differentiated embryo chondrocyte expressed gene 1 (Dec1) is an important transcription factor that related to senescence. In this study, DEC1 immunohistochemical analysis was performed on tissue microarray blocks constructed from ESCC combined with adjacent precursor tissues of 241 patients. Compared with normal epithelia, DEC1 expression was significantly increased in intraepithelial neoplasia and DEC1 expression was significantly decreased in ESCC in comparison with intraepithelial neoplasia. In vitro, DEC1 overexpression induced cellular senescence, and it inhibited cell growth and colony formation in ESCC cell line EC9706. Fresh esophagectomy tissue sections from five ESCC patients were detected by immunohistochemistry of DEC1 and senescence-associated β-galactosidase (SA-β-Gal) activity, and strongly positive expression of DEC1 was correlated to more senescent cells in these fresh tissue sections. Kaplan-Meier method analysis of the 241 patients revealed that DEC1 expression levels were significantly correlated with the survival of ESCC patients after surgery. The expression levels of DEC1 were also correlated with age, tumor embolus, depth of invasion of ESCC, lymph metastasis status and pTNMs. These results suggest that DEC1 overexpression in precursor lesions of ESCC is a protective mechanism by inducing cellular senescence in ESCC initiation, and DEC1 may be a potential prognostic marker of ESCC.
PLoS ONE 07/2012; 7(7):e41862. · 3.53 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Esophageal squamous cell carcinoma (ESCC) is highly prevalent in China and other Asian countries, as a major cause of cancer-related mortality. ESCC displays complex chromosomal abnormalities, including multiple structural and numerical aberrations. Chromosomal abnormalities, such as recurrent amplifications and homozygous deletions, directly contribute to tumorigenesis through altering the expression of key oncogenes and tumor suppressor genes.
To understand the role of genetic alterations in ESCC pathogenesis and identify critical amplification/deletion targets, we performed genome-wide 1-Mb array comparative genomic hybridization (aCGH) analysis for 10 commonly used ESCC cell lines. Recurrent chromosomal gains were frequently detected on 3q26-27, 5p15-14, 8p12, 8p22-24, 11q13, 13q21-31, 18p11 and 20q11-13, with frequent losses also found on 8p23-22, 11q22, 14q32 and 18q11-23. Gain of 11q13.3-13.4 was the most frequent alteration in ESCC. Within this region, CCND1 oncogene was identified with high level of amplification and overexpression in ESCC, while FGF19 and SHANK2 was also remarkably over-expressed. Moreover, a high concordance (91.5%) of gene amplification and protein overexpression of CCND1 was observed in primary ESCC tumors. CCND1 amplification/overexpression was also significantly correlated with the lymph node metastasis of ESCC.
These findings suggest that genomic gain of 11q13 is the major mechanism contributing to the amplification. Novel oncogenes identified within the 11q13 amplicon including FGF19 and SHANK2 may play important roles in ESCC tumorigenesis.
PLoS ONE 06/2012; 7(6):e39797. · 3.53 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Endoscopic resection is a less invasive treatment than esophagectomy for superficial esophageal squamous cell carcinoma, but patients with lymph node metastasis need additional treatment after endoscopic resection. The purpose of this study was to establish a set of indicators to identify superficial esophageal squamous cell carcinoma patients at a high risk of metastasis. In all, 271 superficial esophageal squamous cell carcinoma esophagectomy cases were reviewed retrospectively. The relationships between clinicopathological parameters and immunohistochemical findings (p53, cyclin D1, EGFR and VEGF) on tissue microarrays, on the one hand, and lymph node metastasis were assessed by univariate and multivariate logistic regression analyses. Patients with intraluminal masses and ulcerated masses had a high risk of lymph node metastasis. Patients with superficial esophageal squamous cell carcinoma (1) thinner than 1200 μm; (2) confined to the mucosa; (3) with submucosal invasion <250 μm; (4) with submucosal invasion ≥250 μm but with negative VEGF expression and well/moderately differentiated or basaloid histology; or (5) with submucosal invasion ≥250 μm but with weak VEGF expression and well-differentiated histology had almost no risk of lymph node metastasis. We recommend endoscopic resection for all erosive, papillary and plaque-like superficial esophageal squamous cell carcinomas where endoscopic resection is clinically feasible, and esophagectomy for all other erosive, papillary and plaque-like cases and all intraluminal masses and ulcerated tumors. No additional treatment is needed for endoscopic resection cases with superficial esophageal squamous cell carcinoma (1) thinner than 1200 μm; (2) confined to the mucosa; (3) with submucosal invasion <250 μm; (4) with submucosal invasion ≥250 μm but with negative VEGF expression and well/moderately differentiated or basaloid histology; or (5) with submucosal invasion ≥250 μm but with weak VEGF expression and well-differentiated histology. These clinical and pathological criteria should enable more accurate selection of patients for these procedures.
Modern Pathology 05/2012; 25(10):1364-77. · 6.36 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Caveolin-1 (CAV-1), one component of caveolae, involves in multiple cellular processes and signal transductions. We previously showed that the expression of CAV-1 gene in NCI-H446 cells inhibited cell proliferation and promoted cell metastasis. Here we explore the function of CAV-1 on tumor growth and metastasis by using NCI-H460 in vitro. First, we established NCI-H460 cell line, which CAV-1 was stably knockdown. Then we investigated the effects of CAV-1 on the morphology, proliferation, cell cycle and metastasis potential for NCI-H460 cell by crystal violet stains, CCK-8, colony formation, flow cytometry, scratch-wound assay and transwell assay. Western blot was used to examine the expression changes of cyclin D1, PCNA, E-cadherin and β-catenin. Our results showed stable knockdown of CAV-1 inhibited the proliferation of NCI-H460 cells. Cell cycle of the transfected cells was arrested in G1/S phase and the expressions of cyclin D1 and PCNA protein were downregulated. Downregulation of CAV-1 promoted the migration and invasion abilities of NCI-H460 cells in vitro. The expression of β-catenin increased and the level of E-cadherin decreased. In summary, our findings provide experimental evidence that CAV-1 may function as a proproliferative and antimetastatic gene in NCI-H460 cell line.
[Show abstract][Hide abstract] ABSTRACT: Many human cancers present as multifocal lesions. Understanding the clonal origin of multifocal cancers is of both etiological and clinical importance. The molecular basis of multifocal prostate cancer has previously been explored using a limited number of isolated markers and, although independent origin is widely believed, the clonal origin of multifocal prostate cancer is still debatable. We attempted to address clonal origin using a genome-wide copy-number analysis of individual cancer and high-grade prostatic intraepithelial neoplasia (HGPIN) lesions. Using Affymetrix array 6.0 copy-number analysis, we compared the genomic changes detected in 48 individual cancer and HGPIN lesions, isolated from 18 clinically localized prostate cancer cases. Identical genomic copy-number changes, shared by all same-case cancer foci, were detected in all 13 informative cases displaying multiple tumor foci. In addition, individual HGPIN lesions in the two multifocal-HGPIN cases available shared identical genomic changes. Commonly known genomic alterations, including losses at 6q15, 8p21.3-8p21.2, 10q23.2-10q23.31, 16q22.3, 16q23.2-16q23.3 and 21q22.2-21q22.3 regions and gain of 8q24.3 were the most frequently detected changes in this study and each was detected in all same-case foci in at least one case. Microarray data were confirmed by fluorescence in situ hybridization in selected foci. Our high-resolution genome-wide copy-number data suggest that many multifocal cases derive from a single prostate cancer precursor clone and that this precursor may give rise to separate HGPIN foci and may further progress to multifocal invasive prostate cancer. These findings, which demonstrate the monoclonal origin of multifocal prostate cancer, should significantly enhance our understanding of prostate carcinogenesis.
Genes Chromosomes and Cancer 02/2012; 51(6):579-89. · 3.84 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: We have previously reported genetic differences between Western and Chinese prostate cancers, including different frequencies of ERG rearrangements. We investigated further ERG expression and rearrangements in prostate cancers and high-grade prostatic intraepithelial neoplasia (HGPIN) from the UK and China to determine differences between these two populations by tissue microarray based immunohistochemistry and fluorescence in situ hybridization. In keeping with our previous observation, that ERG was rearranged at a higher frequency in UK prostate cancer samples (38%, 58/155) than Chinese ones (8%, 7/93), ERG rearrangements were also found in 21% (4/19) and 0% (0/19) foci of HGPIN in UK and Chinese samples respectively. ERG nuclear expression in UK cancers (34%, 54/160) was significantly higher than that in Chinese ones (10%, 9/88) (p<0.001). ERG nuclear expression in UK HGPIN (28%, 11/39) was higher than that in Chinese HGPIN (0%, 0/9), but without statistical significance (p=0.193). ERG nuclear expression was correlated to ERG rearrangements in both UK (Kappa=0.686) and Chinese (Kappa=0.565) cancers. These data demonstrate that ERG rearrangement and expression frequencies are different in prostate cancers from UK and China as early as the precursor lesion, HGPIN. The nuclear expression is associated with ERG rearrangements which mainly occur in the Western samples. UK and Chinese prostate cancers may be the result of different genetic mechanisms.
American Journal of Cancer Research 01/2012; 2(6):736-44. · 3.97 Impact Factor