Epidemiologic and biological data suggest a role for androgens and perhaps their receptor in hepatocellular carcinoma (HCC) development. However, few studies evaluated an association between HCC risk and androgen receptor (AR) cytosine, adenine, guanine (CAG) repeat length. To examine whether the relationship between the AR CAG repeats and HCC risk was also evident in Chinese, we conducted this large population-based, case-control study of 2,000 pathologically confirmed HCC patients and 2,000 frequency-matched controls. Two different approaches for AR CAG repeat length (analyses with continuous and categorized polymorphism variables) were conducted in the statistical analyses. For AR CAG longer allele (CAG_L), we found that subjects with longer AR CAG_L repeats had a decreased risk of developing HCC (OR?=?0.87 for per CAG_A increase, 95 % CI 0.82-0.96, P?=?5.33?×?10(-4)). Compared to those with the shorter (<23) CAG_L repeat length, subjects in the category of longer (?23) CAG_L repeats had a significant 20 % decreased HCC risk (OR?=?0.80, 95 % CI 0.71-0.91, P?=?6.16?×?10(-4)). These findings suggest that androgen signaling underlies the development of HCC.
Breast cancer is the most common cancer in women around the world. However, the molecular mechanisms underlying breast cancer pathogenesis are only partially understood. Here, in this study, we found that P2X7R was up-regulated and miR-216b was down-regulated in breast cancer cell lines and tissues. Using bioinformatic analysis and 3'UTR luciferase reporter assay, we determined P2X7R can be directly targeted by miR-216b, which can down-regulate endogenous P2X7R mRNA and protein levels. Ectopic expression of miR-216b mimics leads to inhibited cell growth and apoptosis, while blocking expression of the miR-216b results in increased cell proliferation. Furthermore, our findings demonstrate that knockdown of P2X7R promotes apoptosis in breast cancer cells through down-regulating Bcl-2 and increasing the cleavage caspase-3 protein level. Finally, we confirmed that down-regulation of miR-216b in breast cancer is inversely associated with P2X7R expression level. Together, these findings establish miR-216b as a novel regulator of P2X7R and a potential therapeutic target for breast cancer.
This paper investigates two sEMG-based control strategies developed for a power-assist exoskeleton arm. Different from most of the existing position control approaches, this paper develops force control methods to make the exoskeleton robot behave like humans in order to provide better assistance. The exoskeleton robot is directly attached to a users body and activated by the sEMG signals of the users muscles, which reflect the users motion intention. In the first proposed control method, the forces of agonist and antagonist muscles pair are estimated, and their difference is used to produce the torque of the corresponding joints. In the second method, Linear Discriminant Analysis (LDA) based classifiers are introduced as the indicator of the motion type of the joints. Then, the classifiers outputs together with the estimated force of corresponding active muscle determine the torque control signals. Different from conventional approaches, one classifier is assigned to each joint, which decreases the training time and largely simplifies the recognition process. Finally, the extensive experiments are conducted to illustrate the effectiveness of the proposed approaches.
This systematic review summarizes evidence on allotransplantation of donor kidneys after resection of a small renal cancer or contralateral healthy kidneys from cadaveric donors with unilateral renal cancer. Eligible studies were identified by screening four bibliographic databases, contacting key authors, and analyzing the bibliographies of included studies. Two reviewers independently assessed the reports for inclusion and extracted data, which were summarized as a narrative review. In the 20 case report or case series studies included in the analysis, there were 97 documented cases of donor kidney transplantation after resection of small renal cancer without pathologically confirmed recurrence, whereas 22 cases used contralateral healthy kidneys from cadaveric donors with unilateral renal cancer with one case of cancer recurrence. These results suggest that the use of donor kidneys after resection of small renal cancer is associated with a relatively low cancer recurrence rate.
Breast cancer (BC) remains one of the most common cancers among women. The human X-ray repair cross-complementing 1 (XRCC1) gene plays key roles in base excision repair, and genetic polymorphisms of XRCC1 may be associated with the susceptibility to BC. This study aimed to evaluate the relationship between the XRCC1 genetic polymorphisms and BC susceptibility. A total of 354 BC patients and 366 cancer-free controls were enrolled in this study. Data about the risk factors of BC were collected using questionnaires. The XRCC1 genetic polymorphism was determined using created restriction site-polymerase chain reaction (CRS-PCR) and DNA sequencing methods. No significant differences in the allelic and genotypic frequencies of c.1804C>A genetic polymorphism were detected between cases and controls. The distributions of BC patients risk factors were not significantly different between CC, CA, and AA genotypes. These findings indicate that the c.1804C>A genetic polymorphism of XRCC1 gene is not significantly associated with BC susceptibility in the Chinese women.
Cytoplasmic HuR is associated with reduced survival in invasive breast cancer. We designed this study to determine the predictive and prognostic value of HuR expression in women with breast cancer who underwent neoadjuvant chemotherapy followed by surgical resection. We immunohistochemically analyzed cytoplasmic HuR expression in tumor biopsy cores obtained from 139 patients with invasive breast cancers who received paclitaxel and anthracycline-based neoadjuvant chemotherapy. We evaluated the relationship of HuR expression level with pathologic complete response (pCR), local recurrence-free survival (LRFS), distant recurrence-free survival (DRFS), recurrence-free survival (RFS), and overall survival (OS). Cytoplasmic HuR expression was present in 60 cases (43.2 %). The expression of cytoplasmic HuR was significantly associated with high nuclear grade (P < 0.0001) and ER (P = 0.001) and PR (P = 0.005) status. Multivariate regression analysis further revealed that high nuclear grade (P = 0.023), negative ER status (P = 0.043), and human epidermal growth factor receptor 2 (HER2) overexpression (P < 0.0001), but not cytoplasmic HuR expression, were significant independent predictors of pCR. Interestingly, multivariate Cox analysis revealed that cytoplasmic HuR expression was a strong independent predictor of reduced LRFS (P = 0.014), DRFS (P = 0.001), RFS (P < 0.0001), and OS (P = 0.019) irrespective of pCR. Furthermore, the patient group with tumors showing both expression of cytoplasmic HuR and non-pCR had a worse prognosis in LRFS (P = 0.048), DRFS (P < 0.0001), RFS (P < 0.0001), and OS (P = 0.001) than did other patient groups; patients with tumors showing negative cytoplasmic expression of HuR and pCR had the best prognosis in all RFS and OS. Cytoplasmic expression of HuR is an independent prognostic marker in breast cancer patients undergoing chemotherapy. Combination analyses of HuR expression and pCR, compared with pCR alone, can better predict clinical outcome in patients with primary breast cancer.
The expression level of Nrf2 is increased in series of tumors and it plays a vital role in proliferation of cancer cells. However, little is known about the clinical implications and biological functions of Nrf2 in endometrial carcinoma. The aim of this study is to study whether up-regulation of Nrf2 expression can promote growth of endometrial carcinoma cells. Using immunohistochemistry, Nrf2 protein expression was analyzed in endometrial carcinoma patients. A series of assays was performed to elucidate the role of Nrf2 in growth of endometrial carcinoma. Positive rate of Nrf2 was 64.3 % (45/70) in endometrial carcinoma patients, and it was associated with FIGO stage and histological grade (P < 0.05). In addition, ectopic overexpression of Nrf2 promoted the growth of endometrial carcinoma cells in vitro and in vivo. Interestingly, Nrf2 protein translocation from cytoplasm to nucleus may influence differentiation of endometrial carcinoma cells. These results suggest that Nrf2 participates in progression of endometrial carcinoma by influencing the growth and differentiation of endometrial carcinoma cells, and it could be used as a novel and potential therapeutic target for endometrial carcinoma.
Hepatocellular carcinoma (HCC) is one of the most frequently causing cancer-related deaths worldwide. Previous evidence suggests that the X-ray repair cross-complementing group 1 gene (XRCC1) is an important candidate gene for influencing the risk of HCC. The aim of this study was to assess the association of XRCC1 genetic polymorphisms with the risk of HCC in Chinese Han population. A total of 1314 subjects, including 651 HCC patients and 663 healthy controls, were enrolled in this case-control study. Two genetic variants (c.1254C>T and c.1517G>C) in XRCC1 gene were genotyped by created restriction site-polymerase chain reaction (CRS-PCR) and PCR-restriction fragment length polymorphism (PCR-RFLP) methods. Our data indicated that the allele and genotype frequencies of these two genetic variants were statistical difference in HCC cases and healthy controls. Association analyses suggested that these two genetic variants were statistically associated with the increased risk of HCC in all genetic models (for c.1254C>T, TT versus CC: OR = 2.30, 95% CI 1.61-3.28; CT versus CC: OR = 1.32, 95% CI 1.05-1.67; TT/CT versus CC: OR = 1.50, 95% CI 1.20-1.86; TT versus CT/CC: OR = 2.00, 95% CI 1.43-2.80; T versus C: OR = 1.47, 95% CI 1.25-1.73; for c.1517G>C, CC versus GG: OR = 1.90, 95% CI 1.34-2.69; GC versus GG: OR = 1.56, 95% CI 1.24-1.97; CC/GC versus GG: OR = 1.63, 95% CI 1.31-2.03; CC versus GC/GG: OR = 1.52, 95% CI 1.10-2.11; C versus G: OR = 1.45, 95% CI 1.23-1.70). The allele-T of c.1254C>T and allele-C of c.1517G>C genetic variants may contribute to HCC susceptibility in Chinese Han population.
Esophageal squamous cell carcinoma (ESCC) is one of the most frequent cancers and a leading cause of death from cancer in China. The human ELAV-like protein HuR has been found to contribute to cancer development and progression through stabilizing a group of cellular mRNAs of cancer-related genes. In this study, we investigated the expression of HuR in a cohort of ESCC patients using immunohistochemical staining. HuR detected in the cytoplasm of cancer cells was positive in 46.6 % of 58 ESCC specimens; 75.9 % of these specimens had nuclear immunoreactivity for HuR. Cytoplasmic HuR expression was higher in cancer tissues compared to 20 matched adjacent noncancerous tissues. A clinicopathological study showed that cytoplasmic HuR expression was positively associated with lymph node metastasis, depth of tumor invasion, and advanced stage, whereas nuclear HuR expression was not correlated with any clinicopathological factors. Patients positive for cytoplasmic HuR expression had a cumulative 5-year survival rate of 25.3 %, whereas it was 43.8 % for patients negative for cytoplasmic HuR expression. In a multivariate analysis, cytoplasmic HuR expression was an independent prognostic factor, whereas nuclear positivity for HuR was not. Our results indicate that high cytoplasmic HuR expression is associated with positive lymph node metastasis, deep tumor invasion, high stage, and poor survival in ESCC. Thus, HuR is the first mRNA stability protein whose expression is associated with poor survival in esophageal cancer.
MiR-222 in glioma can regulate cell cycle progression and apoptosis. However, the relationship between miR-222 and Wnt/?-catenin signaling pathway in glioma remains unknown. Here, we found that the Dickkopf-2 gene (DKK2) was a direct target of miR-222 by target prediction analysis and dual luciferase reporter assay. RNA interference silencing of DKK2 proved that miR-222 overexpression led to constitutive activation of ?-catenin through inhibition of DKK2 expression in glioma cells. Furthermore, miR-222 siRNA significantly inhibited tumorigenesis in vivo. Finally, Western blot analysis showed that miR-222 could regulate the expression of ?-catenin and the downstream genes of Wnt/?-catenin signaling pathway. Taken together, our findings reveal a new regulatory mechanism of miR-222 and suggest that miR-222 might be a potential target in glioma therapy.
The human embryonic lethal abnormal vision-like protein, HuR, is a member of the Hu family of RNA-binding proteins. Over the past decade, this ubiquitously expressed protein has been extensively investigated in cancer research because it is involved in the regulation of mRNA stability and translation in many cell types. HuR activity and function is associated with its subcellular distribution, transcriptional regulation, translational and post-translational modifications. HuR regulation of target mRNAs is based on the interaction between the three specific domains of HuR protein and one or several U- or AU-rich elements (AREs) in the untranslated region of target mRNAs. A number of cancer-related transcripts containing AREs, including mRNAs for proto-oncogenes, cytokines, growth factors, and invasion factors, have been characterized as HuR targets. It has been proposed that HuR has a central tumorigenic activity by enabling multiple cancer phenotypes. In this review, we comprehensively survey the existing evidence with regard to the diverse functions of HuR in caner development and progression. The current data also suggest that HuR might be a novel and promising therapeutic target and a marker for treatment response and prognostic evaluation.
HuR is an ubiquitously expressed RNA-binding protein that stabilizes messenger RNA and regulates translation. This protein has been shown to play an important role in carcinogenesis and cancer progression. P-glycoprotein (P-gp) is the product of the multidrug resistance 1 gene, and the overexpression of P-gp induces multidrug resistance and represents a major obstacle in cancer chemotherapy. The purpose of this study was to determine the expression of HuR and P-gp in human breast cancer tissues and analyze the relationship between HuR or P-gp expression and the clinical-pathological variables and patient outcomes. Immunohistochemistry was used to determine HuR and P-gp expression in 82 human breast cancer tissues and 20 matched adjacent noncancerous tissues. Additionally, 16 benign breast tumor samples were used as controls. The overexpression of cytoplasmic HuR was found in breast cancer but not in the matched adjacent noncancerous tissues or benign breast tumors. The expression levels of cytoplasmic HuR were significantly associated with increased age, high nuclear grade, and the positive expression of the ER, PR, and HER-2/neu. HuR was also associated with the expression of P-gp protein. Furthermore, univariate analysis indicates that patients with high expression levels of cytoplasmic HuR or P-gp had significantly reduced survival compared to patients with low expression levels. A multivariate analysis showed that age at diagnosis, nuclear grade, and cytoplasmic HuR positivity were independent indicators for disease-free survival and overall survival in patients with breast cancer. In conclusion, cytoplasmic HuR expression detected by immunohistochemical staining is a negative prognostic indicator for survival in patients with breast cancer.
The worry of potential residual renal cancer cells in donor kidney after resection of small renal cancer impedes the extensive use of such controversial donor source. To explore the impacts of organ preservation process on the survival of renal cancer cells, we detected cell proliferation and viability of benign and malignant renal cell lines and clinical renal samples after treated with simulated organ preservation process. It was found that the viability and proliferation of malignant renal cells are inhibited much more than that of benign renal cells during prolonged organ preservation. The inhibition of proliferation in benign renal cells is fully reversible, while in malignant renal cancer cells is not fully reversible after a certain time. So potential residual renal cancer cells could be partly inhibited and eliminated by organ preservation process.
Blood vessel invasion plays a very important role in the progression and metastasis of cancer. However, blood vessel invasion as a prognostic factor for survival in non-small cell lung cancer (NSCLC) remains controversial. The aim of this study is to explore the relationship between blood vessel invasion and outcome in patients with NSCLC using meta-analysis.
The role of lymphatic microvessel density (LVD) as a prognostic factor for survival of patients with non-small cell lung carcinoma (NSCLC) remains controversial. To evaluate this potential role, we performed a systematic review of the electronic databases PubMed and EMBASE for relevant literature to review and compile available survival results. To be eligible, a study had to assess LVD in patients with NSCLC and to compare survival based on LVD stratification. Among 12 eligible trials, all dealt with NSCLC, and 10 trials provided results for the meta-analysis of survival data (evaluable trials). In terms of survival, high LVD was reported to be an unfavorable prognostic factor for overall survival in 8 studies, whereas it was not in 4 studies. The overall survival hazard ratio for the 10 evaluable studies (1,426 patients) was calculated to be 1.41 (95% CI: 1.14-1.75) using a random effects model, indicating a poorer survival for NSCLC patients with high LVD. The hazard ratio was 1.52 (95% CI: 1.10-2.11) in 5 NSCLC studies where LVD was assessed based on D2-40 and 1.31 (95% CI: 1.08-1.60) in 4 studies where LVD was measured based on vascular endothelial growth factor receptor-3. This study supports the hypothesis that the lymphatic microvessel count or LVD, which reflects levels of lymphangiogenesis, is a poor prognostic factor for patient survival in surgically treated NSCLC. However, the present findings may overestimate the prognostic capacity of LVD because of publication and report bias. In addition, the standardization of lymphangiogenesis assessment by the lymphatic microvessel count is necessary.
Melanomas harbor aberrations in the c-Kit gene. We tested the efficiency of the tyrosine kinase inhibitor imatinib in selected patients with metastatic melanoma harboring c-Kit mutations or amplifications.
Epidemiological studies have evaluated the association between has-miR-146a polymorphism (rs2910164) and cancer risk. However, published data are still inconclusive. Here, we performed a meta-analysis to assess the relationship between has-miR-146a polymorphism (rs2910164) and cancer susceptibility until May 8, 2010. Nineteen published case-control studies including a total of 10,496 cases and 12,885 controls were acquired. Overall, Increased cancer risk was found in domain model (OR = 1.18, 95% CI: 1.03-1.35) rather than in other genetic models when all studies were pooled into the meta-analysis. Stratified analysis shown that significant association between rs2910164 polymorphism and cancer susceptibility was present in Asians (OR = 1.14, 95% CI: 1.01-1.29 for CG vs. CC; OR = 1.19, 95% CI: 1.03-1.39 for GG + CG vs. CC), but not in Caucasian populations. In the subgroup analysis by cancer types, no significantly increased risk of breast, gastric, prostate or bladder cancer were found in any of the genetic models. In summary, this meta-analysis suggests that has-miR-146a polymorphism (rs2910164) is associated with increased cancer susceptibility in Asians. However, further well-designed studies with large sample size will be necessary to validate the risk identified in the current meta-analysis.
Inactivation of the tumor suppressor gene RASSF1A through methylation of the CpG islands within its promoter region as a prognostic factor for survival in non-small cell lung carcinoma (NSCLC) remains controversial. A meta-analysis of published studies investigating the effects of RASSF1A methylation on both relapse-free survival (RFS) and overall survival (OS) among NSCLC patients was performed. A total of 2802 patients from 19 eligible studies were included in the systematic review and 17 studies were included in the meta-analysis. In all, 32.6% of NSCLC patients had the methylated RASSF1A allele. Four of these studies investigated the correlation between RASSF1A methylation and RFS using univariate analysis. The univariate estimate for RFS was 1.87 [95% confidence interval (CI): 1.41-2.49; P < 0.0001] with no evidence of significant heterogeneity. Thirteen studies undertook univariate analyses of RASSF1A methylation and OS and 12 undertook multivariate analyses of RASSF1A methylation and OS. The pooled hazard ratio (HR) estimate for OS was 1.52 (95% CI: 1.33-1.74; P < 0.0001) by univariate analysis and 1.34 (95% CI: 1.15-1.57; P < 0.0001) by multivariate analysis. No significant heterogeneity was detected. For stages I-II NSCLC, the meta-risk remained highly significant by both univariate (HR = 1.94; 95% CI: 1.54-2.44; P < 0.0001) and multivariate analysis (HR = 1.39; 95% CI: 1.02-1.90; P = 0.039). This study shows that RASSF1A methylation appears to be an independent prognostic factor for poor survival in surgically treated NSCLC. However, the present findings require confirmation though adequately designed prospective studies.
HuR is a ubiquitously expressed RNA-binding protein that stabilizes the mRNAs of certain genes and regulates the translation to proteins. Elevated cytoplasmic expression of HuR has been suggested to be associated with reduced survival in a wide variety of human carcinomas. However, the clinical significance of HuR expression in lung cancer remains unknown. In this study, we examined HuR expression in 132 patients with non-small cell lung carcinoma (NSCLC) by means of immunohistochemistry and correlated clinicopathologic data, lymphatic microvessel density (LVD), or microvessel density (MVD) with HuR immunostaining. HuR was expressed in 80.3% (106/132) of cases and was predominantly localized in the nucleus. Cytoplasmic HuR expression occurred in 40.9% (54/132) of NSCLC specimens and was associated with high MVD and LVD. In univariate analysis, cytoplasmic HuR, but not nuclear HuR expression was found to significantly influence the relapse-free survival and overall survival. In addition, cytoplasmic expression of HuR was identified as an independent prognostic factor for survival in multivariate analysis. Our data provide evidence for a clinically prognostic role of HuR in NSCLC and demonstrate an association between HuR expression, and angiogenesis and lymphangiogenesis.
Thymidylate synthase (TYMS), which catalyzes the conversion of deoxyuridine monophosphate to deoxythymidine monophosphate, is a central enzyme in the folate metabolic pathway. Epidemiological studies have evaluated the association between TYMS gene polymorphisms and breast cancer susceptibility; however, the published data are still inconclusive. To derive a more precise assessment of this relationship, we performed a meta-analysis based on currently available data by searching PubMed, EMBASE databases, and the Cochrane Library. A total of 10 eligible studies were identified for the TYMS TSER polymorphism (six studies with 2,718 cases and 3,423 controls) and for the TYMS TS3-UTR polymorphism (five studies with 1,969 cases and 2,290 controls). The overall odds ratio (OR) and the corresponding 95% confidence interval (CI) showed a statistical association between the TSER polymorphism and breast cancer risk under homozygote comparison (2R/2R vs. non-2R/non-2R; OR 1.25; 95% CI 1.04-1.50), allele contrast (2R vs. non-2R; OR 1.09; 95% CI 1.01-1.19) and the recessive model (OR 1.19; 95% CI 1.01-1.39). In the subgroup analysis by ethnicity, a statistically significant increase in cancer risk was found among Caucasians for homozygote comparison (OR 1.31; 95% CI 1.10-1.57), the allele contrast model (OR 1.12; 95% CI 1.02-1.23) and the dominant model (OR 1.40; 95% CI 1.00-1.95). For the TS3-UTR polymorphism, significant effects were shown using the allele contrast model (OR 1.33; 95% CI 1.03-1.73). However, the TS3-UTR polymorphism increased breast cancer risk among Asian women (del6 vs. ins6; OR 1.41; 95% CI 1.01-1.98) but not Caucasian women using the homozygote comparison. In conclusion, our meta-analysis suggests that the TSER polymorphism may increase susceptibility to breast cancer in the Caucasian population and the TS3-UTR polymorphism may be a genetic determinant for developing breast cancer in the Asian population; therefore, ethnic background should be carefully considered in further studies.
Tumor-associated macrophages (TAMs) have been implicated in promoting tumor progression and invasion. The onset and maintenance of tumor angiogenesis and lymphangiogenesis also seem to be partly driven by a group of polarized alternatively activated macrophages (aaMphi) in lung adenocarcinoma. Here, the aaMphi and classically activated macrophages (caMphi) were obtained using RAW264.7 cells via IL-4 and IFN-gamma + LPS treatment, respectively. Co-inoculation of aaMphi with Lewis lung carcinoma (LLC) cells promoted tumor growth, increased lymph node metastasis, and reduced the survival in C57BL/6 mice bearing LLC. Furthermore, the effects of the activated macrophages on the lymphangiogenesis-related properties of lymphatic endothelial cells (LECs) were investigated in vitro. When LECs were cultured in macrophages conditioned medium or in a co-culture system of macrophages and LECs, aaMphi significantly promoted proliferation, migration, and tube-like formation of LECs. We identified high VEGF-C expression in aaMphi and low expression in caMphi as well as unactivated macrophages by ELISA and Western blotting. In LECs, co-culture with aaMphi resulted in a significant increase of mRNA levels of specific lymphatic marker VEGF receptor-3 and the homeobox gene Prox-1, as well as lymphangiogenic factor VEGF-C rather than VEGF-D by quantitative RT-PCR. Furthermore, enhanced LECs migration and capillary formation by co-culture with aaMphi were significantly inhibited by rVEGF receptor-3/Fc chimera. In conclusion, these data show that aaMphi play a critical role in tumor-induced lymphangiogenesis through up-regulating VEGF-C and increasing lymphangiogenesis-related behavior of LECs, which may contribute to lymphatic invasion in lung adenocarcinoma.
The expression levels of the RNA-binding protein Hu antigen (HuR) and vascular endothelial growth factor-C (VEGF-C) were examined immunohistochemically in 81 non-small cell lung cancers (NSCLC) and 15 benign human lung tissues. HuR showed a nuclear overexpression in 82.7% (67/81) of NSCLC specimens. Cytoplasmic immunoreactivity for HuR was observed in 45.7% (37/81) of NSCLC, while only nuclear expression of HuR was observed in 13.3% (2/15) of benign lung tissues. The expression of VEGF-C was present in a subgroup of 70.4% (57/81) of tumor cases. In the human NSCLC samples, cytoplasmic but not nuclear HuR expression was significantly associated with increased levels of VEGF-C and with clinicopathological variables, including high tumor grade, poor differentiation and lymph node metastasis. In vitro, HuR showed a predominantly nuclear staining in Lewis lung cancer cells, as seen by confocal microscopy. When lung cancer cells were treated with siRNA targeted against HuR, expression levels of the HuR and VEGF-C proteins were significantly reduced, as seen by Western blotting. Our findings indicate that there is a dysregulation of the cellular distribution of the mRNA stability factor HuR in a subset of NSCLC. Examination of cytoplasmic HuR in NSCLC tissues will allow for valuable prognostic diagnosis of lymph node metastasis, as HuR might be an important mediator regulating the expression of VEGF-C.
Lymphatic vessel invasion (LVI) exerts an important process in the progression and local spread of cancer cells. However, LVI as a prognostic factor for survival in non-small cell lung cancer (NSCLC) remains controversial.
Aggressive fibromatosis (AF) is characterized by a nonmetastatic fibroblastic proliferative lesion that is histologically benign with infiltrative growth and frequent recurrence. To our knowledge, infantile AF is rarely reported. There are no clear guidelines regarding the management and treatment strategies for intracranial infantile AF because of its rarity. In China, there are few reports in the clinical literature concerning intracranial infantile AF. We describe 2 cases of intracranial infantile AF and review the relevant literature to better understand the pathological features, differential diagnosis and treatment of this condition.
The use of lymphatic microvessel density (LVD) and pro-lymphangiogenic mediators as prognostic factors for survival in breast cancer remains controversial. We searched the electronic databases PubMed and EMBASE without language restrictions for relevant literature to aggregate the survival results. To be eligible, every study had to include the assessment of the LVD or the expression of vascular endothelial growth factor (VEGF)-C or -D in patients with breast cancer and provide a survival comparison, including disease-free survival (DFS) or overall survival (OS), according to the LVD, VEGF-C or VEGF-D status. Across all studies, 56.64 % of patients were considered to have a VEGF-C-positive tumor, and 65.54 % of patients had VEGF-D-positive tumors. High LVD had an unfavorable impact on DFS, with a pooled hazard ratio (HR) of 2.222 (95 % CI 1.579-3.126) and an OS with a HR of 2.493 (95 % CI 1.183-5.25). According to the different lymphatic makers, the subgroup HR in the D2-40 studies was 2.431 (95 % CI 1.622-3.644) for DFS and 4.085 (95 % CI 1.896-8.799) for OS. VEGF-C overexpression, as assessed by immunochemistry, was a prognostic factor for decreased DFS (HR 2.164; 95 % CI 1.256-3.729) and for decreased OS (HR 2.613; 95 % CI 1.637-4.170). VEGF-D overexpression was a significant although weak prognostic factor for DFS only when assessed by immunochemistry, with a HR of 2.108 (95 % CI 1.014-4.384). Our meta-analysis demonstrated that LVD, VEGF-C and VEGF-D could predict poor prognosis in patients with breast cancer. However, standardization of the assessment of LVD and for the expression of lymphangiogenesis factors is needed.
This study demonstrates the dependence of non-local susceptibility effects on object orientation in gradient echo MRI and the reduction of non-local effects by deconvolution using quantitative susceptibility mapping. Imaging experiments were performed on a 3T MRI system using a spoiled 3D multi-echo GRE sequence on phantoms of known susceptibilities, and on human brains of healthy subjects and patients with intracerebral hemorrhages. Magnetic field measurements were determined from multiple echo phase data. To determine the quantitative susceptibility mapping, these field measurements were deconvolved through a dipole inversion kernel under a constraint of consistency with the magnitude images. Phantom and human data demonstrated that the hypointense region in GRE magnitude image corresponding to a susceptibility source increased in volume with TE and varied with the source orientation. The induced magnetic field extended beyond the susceptibility source and varied with its orientation. In quantitative susceptibility mapping, these blooming artifacts, including their dependence on object orientation, were reduced, and the material susceptibilities were quantified.
P-glycoprotein, the product of the MDR1 gene, is a transmembrane active efflux pump for a variety of environmental toxins and xenobiotics. Epidemiological studies have evaluated the association between MDR1 C3435T polymorphism and cancer susceptibility. However, published data are still inconclusive.
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