Analysis on gene level revealed that a set of 24 genes could clearly discriminate epithelial from mesenchymal cell lines. The Selleck HDAC inhibitor identified composite gene expression measure clearly subdivided expression data from clinical samples in 2 groups. Moreover, the composite gene expression measure showed a correlation with the pathological

grade available for the clinical samples. Conclusion: This 24-gene signature revealed that clinical samples consisted of two distinct subpopulations. This suggests that the composite gene measure Akt tumor may predict whether a patient biopsy is enriched with epithelial or with mesenchymal cells. It could also give an idea of pathological grade of the sample making this signature a potential biomarker for patient stratification allowing personalized therapy. Poster LY3039478 clinical trial No. 125 Loss of R-Cadherin Facilitates Mammary Tumor Progression and Metastasis Rachel Hazan 1 1 Pathology, Albert Einstein College of Medicine, Bronx, NY, USA The mammary epithelium is thought to be stabilized by cell-cell adhesion mediated mainly by E-cadherin. Here we show that another

cadherin, Retinal (R)-cadherin, is critical for maintenance of the epithelial phenotype. R-cadherin is expressed in non-transformed mammary epithelium but absent from tumorigenic cell lines. In vivo, R-cadherin was prominently expressed in the epithelium of both ducts and lobules. In human breast cancer, R-cadherin was downregulated with tumor progression, with high expression in ductal carcinoma in situ and reduced expression in invasive duct carcinomas. By comparison, E-cadherin expression persisted in invasive breast tumors and cell lines where R-cadherin

was lost. Consistent with these findings, R-cadherin knockdown in normal mammary epithelium stimulated invasiveness and disrupted formation of acini despite continued E-cadherin expression. Conversely, R-cadherin overexpression in aggressive cell lines induced glandular morphogenesis and inhibited invasiveness, tumor formation, and lung colonization. R-cadherin also suppressed the MMP1, MMP2, and Cox 2 gene expression, associated with Amobarbital pulmonary metastasis. The data suggest that R-cadherin is an adhesion molecule of the mammary epithelium that acts as a critical regulator of the normal phenotype. As a result, R-cadherin loss contributes to epithelial suppression and metastatic progression. Poster No. 126 Paradoxical Effect of MUC1/G-TRUNC Expression in Breast Cancer – Metastatic Phenotype Associated with Tumor Abrogation Galit Horn 1,2 , Avital Gaziel1,2, Daniel H. Wreschner1, Marcelo Ehrlich1, Nechama I. Smorodinsky1,2 1 Department of Cell Research and Immunology, Tel-Aviv University, Tel-Aviv, Israel, 2 The Alec and Myra Marmot Hybridoma Unit, Tel-Aviv University, Tel-Aviv, Israel MUC1 is a prominent marker of breast cancer cells endowed with signal transduction potential due to its cytoplasmic domain.

Some of the challenges of nanotechnology development in third world nations as reported by Babajide [25] include but not limited to the following:  Lack of proper legislation/regulatory

framework and the relevant political drive  Lower government spending on research and development (R&D)  Lack of infrastructure and human capacity  Lack of proper education relating to curriculum development matters  Lack of private enterprise participation in research and development  Lack of proper collaboration and network programs among agencies  Research institutes and industries that will translate basic research into applied research and end products  Poor industrialization status of the third world countries  Inadequate foreign linkage particularly with donor agencies in nanotechnology  Fear of health, PHA-848125 molecular weight environmental, and safety risks associated with nanotechnology Lessons for Africa and LDC – the nanotechnology way forward Various lessons can be learnt from this discussion

on nanotechnology initiatives for African nations and other CSF-1R inhibitor LDC, which they can adopt as practical steps to establish a robust nanotechnology program in their country. These lessons include but not limited to the following: 1. A OICR-9429 supplier ministry of nanotechnology or a department of nanotechnology should be created under the ministry of science and technology to focus on Cell Penetrating Peptide human capital development through students on researcher support program as well oversee the general activities of nanotechnology in the nation.   2. A strong collaboration link between African nations and nations like South Africa, India, and European Union which has strong nanotechnology capabilities should be established in order to help guide them on various areas of nanotechnology activities including funding.   3. The nation’s policy formulations and definite goals should favor nanoscience and nanotechnology such that inclusion of nanotechnology budget in relevant ministry

of government is guaranteed.   4. African nations and LDC can only make a headway in the activities of nanotechnology by making enormous budgetary allocations to research and development of nanotechnology and indeed launch the NNI formally like other nations that are already advanced in nanotechnology programs.   5. A wide campaign through seminars/symposiums should be carried out through universities/governmental agencies so as to recognize the importance of nanotechnology in the oncoming industrial revolution.   6. Private companies should be encouraged to partner with the public sector in funding nanotechnology programs with a view to develop nanotechnology and improve the nation’s economy.   7. Short- and long-term plans on nanotechnology should be set in motion to promote the development of new companies, new products, and advance materials.   8.

Those that showed only partial restoration of a characteristic were scored as (+). Those showed restoration of motility are called class I mutants, those that did not show a full restoration of motility are class II mutants. A subset of class II mutants which include the surface mutants D52A

and T54A fail to localize correctly as identified using immunofluorescence microscopy. The remaining class II mutants localize correctly, but do not restore motility. The remaining nine point mutants failed to accumulate detectable amounts of MglA and are classified as class III mutants, which are mot- and dev-. Localization patterns are shown for each motility phenotype and mutant class. Mutations at one position, Thr78, yielded mutants in classes I and II. Thr78 is conserved in the MglA homologs found in bacteria, but it represents RG7420 solubility dmso a significant departure from the consensus found in all other prokaryotic and eukaryotic GTPases,

which use an aspartate in this position. MglA could tolerate serine in this position, but alanine and asparate abolished activity. Thr78 may represent a target for modification in MglA or may be essential for the interaction between MglA and critical effector proteins. Mutations in Ras that correspond with this region of the MglA protein are known to render Ras insensitive to GAP proteins [36, 40], thereby affecting click here the rate of GTP hydrolysis in vivo by interaction with a critical surface feature of Ras-GAP known as the “”arginine finger”" [41]. Thus, the change of Thr78 to Asp may affect the ability of MglA to interact with other proteins in vivo. Consistent with this idea, we found that T78D was dominant to WT MglA for motility and development. These results show that threonine is critical for Dorsomorphin ic50 activity and suggest that MglA and its homologs represent a novel subfamily of GTPases. Activating mutations are predicted to shift the balance to favor more of the GTP-bound (on) state of the GTPase. While it is not possible to make a global generalization, since some of the activating mutants failed to make protein, mutants with G21V and L22V made protein and were partially

motile. The phenotype of the L22V mutant was less severe than that of the G21V PR-171 chemical structure mutant, a result that is consistent with the phenotypes reported for eukaryotic GTPases [42]. G21V was a mutation based on G12V of Ras, which decreases the rate of hydrolysis, a fact confirmed in a bacterial MglA from Thermus thermophilus. kcat for a G21V mutant was 7 times lower than that of WT MglA [19]. They also reported individual movement on buffered 1.0% agar slabs. In contrast, we saw predominantly social motility in our microscopic assays, with few individually moving cells (<5%). As previously discussed, the differences in nutritional conditions as well as agar content may dictate which motility system is active. However, Leonardy et al. did not investigate the effect on motility under conditions where social motility was favored. Additionally, Leonardy et al.

It has been estimated that in the first 10 years after polypectomy, the risk of CRC is reduced to a level similar to that of individuals whose colonoscopy does not reveal the presence of polyps [4,5]. Different molecular mechanisms seem to be related to CRC development. The vast majority of tumors (about 50-80%), present chromosomal instability (CIN) [3,6,7], while a smaller fraction (10-15%) is characterized by microsatellite instability (MSI) [3,6,7]. In recent years, epigenetic alterations have gained recognition as a key mechanism in carcinogenesis. In particular, hypermethylation of CpG islands present in gene promoter sequences leads to the inactivation of tumor suppressor

genes, working Selleck CX-5461 in a different way with respect to genetic mutations [8,9]. This aberrant methylation status occurs at the same time as genetic alterations which drive the initiation and progression of colorectal cancer, suggesting that methylation plays an important role in many stages of tumor transformation [10-14]. The existence of a methylator phenotype could be related to distinctive biological and/or clinical characteristics [15]. CRCs that show hypermethylation changes in numerous different CpG-rich DNA regions are defined selleck chemicals as showing the CpG island methylator phenotype (CIMP) [16]. CIMP-positive cancers have distinct clinical pathological characteristics such as proximal

colon location, mucinous and poorly differentiated histology, female preponderance and older age [17]. This phenotype also seems to be associated with MSI and BRAF mutations [18,19]. Conversely, buy SBI-0206965 hypomethylation of specific sequences may decrease the fidelity of chromosomal segregation

[20], suggesting that it may be involved in the chromosomal instability phenotype [21]. Calpain DNA methylation changes probably lead adenomatous precursor lesions to progress into malignant tumors. In fact, sessile serrated adenomas, considered important precursors of cancer, are often CIMP-positive. Taking the above considerations into account, a better understanding of the epigenetic mechanisms associated with adenoma-carcinoma transition could represent an important tool for CRC prevention. In accordance with international guidelines, pre-neoplastic lesions of the colon and rectum are classified according to pathological parameters (size, histology, number of polyps and dysplasia) as having high or low risk of recurrence. In high risk patients a new colonoscopy is performed after 3 years, while in low risk subjects the time interval is extended to 5 years. However, this type of subdivision is unable to predict the real risk of developing a new lesion. In fact, it has been seen that patients who are classified as high risk may not experience any further problems, while those who are classed as low risk may relapse after a short time.

GO profiling demonstrated a prominent differential effect related to rRNA processing and ribosomal biogenesis, which were repressed AZD7762 research buy by PAF26 but induced by melittin. A high number of genes from these annotations showed this marked differential response with extremely significant p-values (Additional File 4), including the group of seven genes induced by melittin and repressed by PAF26 (Figure 2), and was also confirmed by quantitative RT-PCR in

selected genes (Figure 3A, CGR1 and NOP16). The repression behavior is shared in the response to other AMP, antimicrobial compounds and additional stress conditions [35, 38, 61]. mRNAs from ribosomal proteins and rRNA processing enzymes are predicted to destabilize under stress conditions [71]. It is assumed Bioactive Compound Library manufacturer that shutdown of ribosome biogenesis and thus SN-38 nmr protein translation will free cell resources to cope with a hostile environment.

However, our study opens additional questions as to the significance of the induction (rather than repression) of this response in the case of melittin, or of the increased resistance to PAF26 in some of the corresponding deletion strains such as that of the nucleolar protein NOP16 (Figure 5A). The gene BTN2 has been reported to modulate arginine uptake through down-regulation of the CAN1p arginine permease [59]. Our study shows that BTN2 was one of the most repressed gene by both peptides (Additional File 3), suggesting that the cell is sensing the high arginine levels caused by peptide internalization and mounts an active response to deal with it. GO profiling indicated the specific involvement of the “”nonprotein amino acid metabolic process”" Methamphetamine in the response to PAF26, including genes from the biosynthesis or arginine, metabolism

of amino groups and urea cycle (ARG1, ARG3, ARG5,6 and ARG7), which were induced by PAF26 but not by melittin. ARG1 was the gene with the highest PAF26-specific induction identified in our macroarray study, and such strong expression change was confirmed through qRT-PCR analysis (Figure 3). ARG1 codes for the argininosuccinate synthase and is known to be transcriptionally repressed in the presence of arginine. Induction of these genes is indicative of attempt of metabolization of the high concentration of amino groups of cationic AMP such as PAF26. In fact, their induction could lead to accumulation of derived metabolites in the cell. Although the question of ammonium toxicity in yeast is still controversial [72], we speculate that this could be the case given the higher resistance to PAF26 of the deletion mutants assayed. In any case the high resistance to PAF26 of a number of ARG gene deletants confirms the involvement of these pathways in the peptide killing mechanism (Figure 5B). Importantly, susceptibility to PAF26 did not correlate with peptide interaction/internalization into cells in Δarg1 (Figure 7).

Conclusions This study for the first time directly demonstrates that PpiD functions as a chaperone and that its previous classification as a folding factor for OMPs

must be revised. PpiD appears to belong to the SurA-like family of chaperones but different from SurA it plays no major role in the maturation of OMPs. A biochemical capability of PpiD to also assist the folding of OMPs becomes relevant only in the absence of both chaperones for unfolded OMPs, SurA and Skp. In addition, the role of PpiD in the periplasm appears to be restricted to folding events that take place in close proximity to the inner membrane, as only membrane-anchored PpiD functions in vivo. Taken together, our data are in line with the recently proposed role of PpiD as a periplasmic gatekeeper of the Sec translocon [24], as they suggest that it acts as a chaperone for initial folding events of Selleckchem MLN2238 many newly exported proteins. We speculate that PpiD may have a role at the periplasmic exit site of the Sec translocon similar to that

of TF at the exit site of the translating ribosome. Methods Media and growth conditions Luria-Bertani (LB) media were check details prepared as described [51]. Ampicillin (Ap), chloramphenicol (Cm), kanamycin (Kan), spectinomycin (Spec), and tetracycline (Tc) were used at final concentrations of 100, 20, 30, 50 and 10 μg ml-1, respectively. For assaying β-galactosidase activity in cpxP-lacZ reporter strains the medium was buffered with 100 mM sodium phosphate to a pH of 7.0, at which cpxP transcription, which is affected by extracellular alkaline pH, is induced to a medium level [57]. Strains were grown at 37°C with aeration GSK2399872A mw unless noted otherwise. Strains Strains used in this work are listed in Table 2. Mutant alleles were moved into the appropriate strains either by general transduction using phage T4-GT7 [52] or by P1

CHIR-99021 research buy transduction [53]. The presence of the mutant alleles in recombinants was verified by PCR. To generate SurA-depletion strains the chromosomal surA gene was placed under the control of the IPTG-inducible promoter P Llac-O1 [23] by gene replacement as described previously [54]. A ~3.1 kb DNA fragment bearing an Ω:: spectinomycin-P Llac-O1 fusion flanked by approximately 500 bp of imp and surA sequence, respectively, was obtained from pΩSurA by cleavage with EcoRI and partial digest with HindIII. E. coli KM22 was electroporated with the purified fragment. Recombinants were selected on LB/Spec and used as donors for transduction of the Ω::spec-P Llac-O1 -surA locus into the appropriate strains. The final Ω::spec-P Llac-O1 -surA strains were transformed with pPLT13 to provide the LacI repressor protein. Table 2 Strains used in this study Strain Genotype Source, reference, donor strain CAG16037 MC1061 ϕλ[rpoH P3::lacZ] [56] CAG24029 CAG16037 surA::Tn10dCm [6] CAG33398 MC1061 λRS88(cpxP-lacZ) C.A. Gross laboratory CAG37057 CAG16037 Δskp zae-502::Tn10 C.A.

Fig. 4 Polymerase chain reaction for ECT2. To confirm deletions, PCR was carried out by using primers specific for human ECT2 based on previously published sequence data. In patients 1 and 2, no amplification band was detected, confirming the CGH results Immunohistological evaluation for ECT2 protein in these two patients revealed no expression of this molecule in renal tubular epithelium (Fig. 5). Fig. 5 ECT2 protein expression in renal specimens from our patients compared with a normal renal specimen by immunofluorescence using anti-ECT2 antibody. Histologically normal portions of specimens obtained from patients Vorinostat with renal trauma served as normal

kidney tissue. In the normal kidney specimen, ECT2 protein was localized in the renal tubules (a), which was confirmed by phase-contrast microscopy high throughput screening (b), while in the two patients, expression was absent at these sites (c patient 1, d patient 2) Discussion FSGS includes primary

and secondary forms. In primary FSGS, aberrant CD2AP and Wilms’ antioncogene (WT1), which encode proteins constituting the slit membrane responsible for the filtration function of glomerular epithelial cells, have been reported, suggesting glomerular epithelial cell impairment [1, 2, 9]. Familial or hereditary development of FSGS has also been reported in association with gene aberration of inverted formin 2, ACTN4, and MYH9 [10–13]. However, no abnormality was noted in these reported genes in many patients with FSGS. Secondary FSGS may occur when glomerular epithelial cells are impaired by drugs such as heroin, HIV infection, or conditions with reduced numbers of nephrons such as congenital renal disease, low birth weight, oligomeganephronia, and renal dysplasia [1, 3]. Reduction in the number of nephrons can cause hyperfiltration-induced

renal circulatory dynamics abnormalities that impair glomerular epithelial cells. Secondary glomerulosclerosis also develops from congenital or acquired renal tubulointerstitial disorders such as Dent’s disease, Lowe syndrome, and reflux nephropathy, an EVP4593 nmr important causative disease of terminal renal failure; NADPH-cytochrome-c2 reductase FSGS lesions have been observed in the course of these diseases [2, 3]. Tight junctions function as an intercellular barrier regulating paracellular permeability in vertebrate epithelial and endothelial cells [14]. They also provide physical “fences” within the membrane bilayer that prevent intermixing of membrane proteins, thus maintaining cell surface asymmetry. Furthermore, they provide essential structures and serve as specific sites for vesicle targeting to establish and maintain epithelial polarity of the cell membrane [14]. Tight junctions are composed of large complexes of cytoplasmic and membrane proteins. Adapters such as tight junction protein ZO-1 and signaling molecules such as small GTPases are components of the complexes [15].

In this group of urban, South African women, pre-ARV women were significantly lighter than Crenolanib HIV-negative and ATM Kinase Inhibitor nmr non-ARV subjects and had lower fat mass than expected for their lean mass, raising the possibility that women with advancing HIV disease preferentially lose fat rather

than lean mass. There were no significant differences between groups in BMC or BMD at any site before or after adjustment for age, BA, weight and height and the observed smaller BA in the HIV-negative women disappeared after adjustment for age, height and weight. There was no significant difference in vitamin D status between groups with the majority of subjects having a serum concentration >50 nmol/l. The assessment of ‘optimal’ vitamin D status is problematic because varying cut offs are used to define sufficiency, insufficiency and deficiency [22]. A concentration below 25 nmol/l is generally recognised as indicating an increased risk of rickets and osteomalacia [23]. The 2010 Institute of Medicine report considered

that a blood 25(OH)D concentration of 20 ng/mL (50 nmol/l) to be sufficient for good bone health in ‘practically all individuals’ [24]. However, it noted that evidence was lacking to make a similar statement regarding non-skeletal health. In the context of HIV infection and ARV use, the optimal vitamin D status remains undefined because there may be different requirements for maximal bone health and immune functioning compared with HIV-negative populations. EPZ-6438 nmr However, in contrast to other reports

[4, 25], in our study, there were no indications that HIV infection was associated with inferior vitamin D status because there were no significant differences in vitamin D status between the three groups, the distributions of 25(OH)D concentration were similar, and vitamin D status appeared to be generally adequate with very few women having a concentration <25 nmol/l. Contrary to previous reports [9], we found no significant differences in BMD between selleck compound either group of HIV-positive and HIV-negative women. Full adjustment for bone and body size did not alter these results. This lack of any differences is surprising as HIV-positive women with low CD4 counts, requiring ARV initiation, were significantly lighter, with lower fat and lean mass, than the other women. However, it may reflect the selection criteria for this study because despite recruiting women with low CD4 counts, of clinical concern, women with severe clinical disease received immediate ARV therapy and were thus excluded from the study. It may also be influenced by the fact that the subjects were not intravenous drug users and thus not exposed to the additional effect on BMD that this poses. Another limitation may be that the groups were different in terms of duration of hormonal contraception use, parity and total duration of lactation; however, at the time of the study, no women were pregnant or lactating.

Biol Invasion 8:1495–1500CrossRef Xu HG, Qiang S, Han ZM, Guo JY, Huang ZG et al (2006b) The status and causes of alien species invasion

in China. Biodivers Conserv 15:2893–2904CrossRef Yan YH, He ZX, Gong Q, Chen HF, Xing FW (2007) The alien plant species in Guangzhou, check details China. Guihaia 27:570–575 Zerbe S, Choi IK, Kowarik I (2004) Characteristics and habits of non-native plant species in the city of Chonju, southern Korea. Ecol Res 19:91–98CrossRef Zheng YQ, Zhang CH (2006) Current status and progress of studies in biological invasion of exotic trees. Sci Silv Sin 42:115–122″
“Introduction Most species are rare (Brown et al. 1996) and almost all species are rare at some point during their existence. Rarity usually precedes extinction and new species often begin as rare Eltanexor manufacturer individuals in the landscape (Brown 1984). Some species maintain this rarity over the course of their existence while a few species become common (Murray and Lepschi 2004). Species abundance and distribution is a foundational discipline within ecology (Andrewartha 1961; Brown 1984; Krebs 1985), thus the causes and consequences of rarity fundamentally affect many ecological theories. While it is obvious how common species can persist, it is less obvious how rare species can maintain their population sizes when demographic challenges

are so apparent. In order to gain a more mechanistic view of these challenges, Rabinowitz (1981) proposed a more specific classification AZD7762 of rarity in order to accurately describe species distribution and abundance patterns. She pointed out that species with specific habitat requirements (specialists) Masitinib (AB1010) might have different ecological and biological properties

than uncommon but generalist species and that local abundance (LA) (dense populations vs. sparse populations) and geographic range (GR) (large vs. small) might also shed light on the causes and consequences of rarity. This identification matrix yields eight categories (23 = 8), with seven of these categories reflecting some sort of rarity. The eighth species type in this matrix (Fig. 1), wide-ranging generalist species with dense populations, is a type that is not rare but common. The seven types of rarity have been widely utilized to describe patterns of species distribution: in a Web of Science search in June of 2009, 365 research papers cited this matrix. Fig. 1 Distribution of rarity types within the dataset of 101 species. Numbers indicate number of species per category included in the meta-analysis. Black areas of pie charts indicate the percent of the dataset each rarity type represents. Common species were not included (N = 0). Species identified on only two of the three rarity axes (N = 6, Appendix 1) are not included in this figure Investigation of species distribution and abundance patterns is a primary concern of ecological research, yet the majority of papers citing the Rabinowitz rarity matrix comes from the conservation literature.

021, HR=2.599; 95% CI=1.151-5.867), a low expression level of miR-375 (p=0.034, HR=2.451; 95% CI=1.429-5.135) and margin involvement (p=0.030, HR=2.543; 95% CI=1.093-5.918) were identified as significant unfavourable selleck kinase inhibitor prognostic factors (Table 10). Table 10 PD0332991 cost Univariate and multivariate survival analysis of the clinicopathological and molecular features of PDAC Factor   Univariate analysis Multivariate analysis HR (95% CI) p-value HR (95% CI) p-value Histology Well or moderate vs. poor 1.342 (0.621–2.901) 0.454     T category T 1/2 VS. T 3/4 2.282 (1.043–4.994) 0.039 1.518 (0.666–3.460) 0.320

Lymph node metastasis Negative vs. positive 1.935 (0.867–4.317) 0.107     Tumour size <2 cm vs. ≥2 cm 1.736 (0.790–3.814) 0.170     Perineural invasion None or slight vs. prominent 1.244 (0.563–2.752) 0.589     Margin involvement R0 vs. R1 2.550 (1.120–5.805) 0.026 2.543 (1.093–5.918) 0.030 Vascular invasion None or slight vs.

prominent 2.542 (1.154–5.601) 0.021 1.940 (0.819–4.597) 0.132 miR-155 expression High vs. low 2.414 (1.064–5.478) 0.035 1.365 (0.520–3.579) 0.538 miR-100 expression High vs. low 1.480 (0.683–3.205) 0.321     miR-21 expression High vs. low 2.610 (1.179–5.777) 0.018 2.599 (1.151–5.867) 0.021 miR-221 Selleck Tariquidar expression High vs. low 2.001 (0.868–4.617) 0.104     miR-31 expression High vs. low 2.735 (1.317-6.426) 0.039 2.637 (1.298-6.635) 0.048 miR-143 expression High vs. low 1.516 (1.211–4.429) 0.257     miR-23a expression High vs. low 1.639 (0.709–3.788) 0.248     miR-217 expression Low vs. high 1.419 (1.045-4.021) 0.205     miR-148a expression Low vs. high 1.739 (1.385-4.481) 0.093     miR-375 expression Low vs. high 2.337 (1.431-5.066) 0.022 2.451 (1.429-5.135) 0.034 Discussion The common drawback of miRNA expression profiling studies is the lack of agreement among several studies. Differences in measurement platforms and lab protocols as well as

small sample sizes can render gene expression levels incomparable. [33] systematically analysed representative miRNA profiling platforms and revealed that each platform is relatively stable in terms of its own intra-reproducibility; however, Isotretinoin the inter-platform reproducibility among different platforms is low. Although the ideal method involves the analysis the raw miRNA expression datasets that are pooled together, such a rigorous approach is often impossible due to the unavailability of raw data and the low inter-platform concordance of results among different studies would bring difficulties to the analysis. To overcome these limitations, it might be better to analyse datasets separately and then aggregate the resulting gene lists. In this study, we used a meta-analysis approach to analyse PDAC-specific miRNAs derived from independent profiling experiments. The well-known vote-counting strategy [12, 13] and the recently published Robust Rank Aggregation method [16, 17] were employed.