after transfection, cells were harvested at 36 hrs after transfe

after transfection, cells were harvested at 36 hrs. after transfection and lysates were analyzed for luciferase activity using the Dual Luciferase Reporter assay (Promega, U.S.A.) according to the manufacturer’s directions with this website a GloMax™ Microplate Luminometer (Promega, U.S.A.). The luciferase reporter plasmids were co-transfected with pRL-SV40 to correct for variations in transfection efficiency. The relative luciferase activity normalized to the value of pRL-SV40 activity. Results were expressed as fold induction of pCCD1-Luc activity in CNE1 cells, which was assigned a value of 1. WHI-P131, PD98059 and AG1478 inhibited

the activities of cyclin D1 induced by stable expression LMP1. CNE1-LMP1 cells were

transfected with cyclin D1 promoter-reporter construct and Renilla luciferase plasmid as an internal control. The data represent Temsirolimus concentration the mean ± SD of the three independent experiments performed in triplicate. To observe WHI-P131, PD98059 and AG1478 inhibiting the activities of cyclin D1 induced by stable expression LMP1, 24 hrs. after transfection, cells were treated with WHI-P131 (Calbiochem, U.S.A. ), PD98059 (Cell Signalling Technology, U.S.A. ), AG1478 (Cell Signalling Technolgoy, U.S.A.) or 0.1% DMSO for 2 hr. Cells were harvested at 26 h after transfection and subjected to the luciferase assay. Empty firefly reporter vector served as the negative control. Electrophoretic

mobility shift assay (EMSA) EMSA for EGFR/STAT3 binding to cyclin D1 was performed using the LightShift™ Chemiluminesent EMSA kit (Pierce, U.S.A ) and was conducted according to the manufacturer’s protocol. Briefly, Double-stranded oligonucleotides, were labeled using the biotin 3′end labeling (Invitrogen, U.S.A ). Ten μg of nuclear extracts were incubated with 2 μl biotin-labeled probes in binding buffer for 20 min. at room temperature. Additionally, increasing concentrations of 200- fold of excess of a cold competitive oligonucleotide (biotin- unlabeled probe) and NF-κB biotin-unlabeled probe (as a nonspecific competitive probe) were added to confirm specificity of the interaction. The reaction mixture was then loaded onto 10% non- denaturing polyacrylamide gel containing 0.5× Tris borate (TBE) and electro- 3-mercaptopyruvate sulfurtransferase phoresed in 0.5× TBE at 4°C prior to visualization according to the manufacturer; Followed by transferred to BiodyneR B Nylon membrane, avidin-HRP to probes, and visualized and quantitated with a PhosphorImager (Bio Rad, U.S.A). All the double-stranded probes were synthesized as follows: for the putative binding site of EGFR in the cyclin D1 promoter: 5′-TCGCTGAGATTCTTTGGCCGTCTG-3′ (wild type) and 5′-TCGCTGAGATACTCGGGCCGTCTG-3′ (mutated type). For the STAT3 binding site in cyclin D1 promoter: 5′-GTGGCGTTCTTGGAAATGCG- CCCA-3′ (wild type) and 5′-GTGGCGAGCTTGTGAATGCGCCCA-3′ (mutated type).


distributed continuous variables were expres

Normally distributed continuous variables were expressed as the mean ± SD and compared using the Student’s t test. Non-normally

distributed continuous variables were expressed as the median (interquartile range) and compared using the Mann–Whitney U test. Categorical variables were expressed as numbers (proportions) and analyzed PD0332991 supplier using the chi-squared test or Fisher’s exact test. The trend for each value was analyzed using the Jonckheere−Terpstra [26] test. All probability values were 2-tailed and all confidence intervals were computed at the 95 % level. Results Patient characteristics In this study,

we enrolled 50 IgAN patients with complete or partial clinical remission after TSP. The basic characteristics of the enrolled patients (N = 50) whose clinical parameters could be collected are summarized in Table 1. The study population included 40 % males with a median age of 37 years. The average CCr and LY2109761 manufacturer urinary protein excretion levels were 98.2 ml/min and 0.54 g/day, respectively. A total of 52 % of the patients had complete clinical remission after TSP. Table 1 Clinical background of IgAN patients   Number of patients (N = 50) Age 37 (25–48) selleck chemicals llc Sex (male %) 20 (40.0 %) Onset to tonsillectomy (years) 2.0 (1.0–4.0) SBP (mmHg) 122.3 ± 20.5 TP (g/dl) 6.8 ± 0.57 Albumin (g/dl) 4.2 ± 0.41 BUN (mg/dl) 15 ± 5.8 S-Cre (mg/dl) 0.82 ± 0.34 CCr (ml/min) 98.2 ± 26.8 UP (dipstick) 3+; 13, 2+; 8, 1+; 19, ± or −: 10 UP (g/day) 0.54 (0.3–1.3) U-OB (dipstick) 3+; 27, 2+; 17,1+; 4, ±; 2 IGL score 1.47 (1.3–1.99) Gd-IgA1 (units/mg IgA) 117.3 ± 45.6 IgA/IgG-IC (OD) 0.81 ± 0.31 Continuous data are presented mean ± SD or median [IQR], and categorical data as number of patients (%) SBP systolic blood pressure, BUN blood urea nitrogen, Amoxicillin S-Cre serum creatinine, CCr creatinine clearance, UP urinary protein, U-OB urinary occult blood, IGL index of the glomerular

lesion, TP total protein Table 2 Clinical background and course of complete and partial remission groups   Complete remission (N = 26) Partial remission (N = 24) P Age 32.0 (24–43) 40.5 (28.5–50) 0.13 Sex (male %) 13 (50 %) 7 (29.2 %) 0.13 Onset to tonsillectomy (years) 1.0 (1.0–3.0) 3.0 (2.0–4.0) 0.02 SBP (mmHg) 122.4 ± 20.2 123.5 ± 21.4 0.85 TP (g/dl) 6.8 ± 0.51 6.8 ± 0.64 0.7 Albumin (g/dl) 4.3 ± 0.36 4.1 ± 0.44 0.13 BUN (mg/dl) 13.8 ± 3.7 16.1 ± 7.4 0.18 CCr (ml/min) 103.3 ± 24.2 92.8 ± 28.8 0.06 UP (g/day) 0.45 (0.3–1.0) 0.75 (0.36–1.45) 0.19 IGL score 1.40 (1.29–1.79) 1.62 (1.35–2.2) 0.18 S-Cre (mg/dl)  Baseline 0.77 ± 0.19 0.82 ± 0.41 0.87  1 year 0.78 ± 0.24 0.84 ± 0.43 0.56  3–5 year 0.77 ± 0.26 0.91 ± 0.70 0.

Open Access This article is distributed under the terms of the Cr

Open Access This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited. References 1. Black DM, Cummings SR, Karpf DB, Cauley JA, Thompson DE, Nevitt MC, Bauer DC, Genant HK, Haskell WL, Marcus R, Ott SM, Torner JC, Quandt SA, Reiss TF, Ensrud KE (1996) Randomised trial of effect of alendronate on risk of fracture in women with existing vertebral fractures. Fracture

Intervention Trial Research Group. Lancet 348:1535–1541CrossRefPubMed 2. Black DM, Schwartz AV, Ensrud KE, Cauley JA, Levis S, Quandt SA, CRT0066101 in vivo Satterfield S, Wallace RB, Bauer DC, Palermo L, Wehren LE, Lombardi A, Z-DEVD-FMK ic50 Santora AC, Cummings SR (2006) Effects of continuing or stopping

alendronate after 5 years of treatment: the Fracture Intervention Trial Long-term Extension (FLEX): a randomized trial. JAMA 296:2927–2938CrossRefPubMed 3. Black DM, Delmas PD, Eastell R, Reid IR, Boonen S, Cauley JA, Cosman F, Lakatos P, Leung PC, Man Z, Mautalen C, Mesenbrink P, Hu H, Caminis J, Tong K, Rosario-Jansen T, Krasnow J, Hue TF, Sellmeyer D, Eriksen EF, Cummings SR (2007) Once-yearly zoledronic acid for treatment of postmenopausal osteoporosis. N Engl J Med 356:1809–1822CrossRefPubMed PI3K inhibitor 4. Chesnut CH III, Skag P-type ATPase A, Christiansen C, Recker R, Stakkestad JA, Hoiseth A, Felsenberg D, Huss H, Gilbride J, Schimmer RC, Delmas PD (2004) Effects of oral ibandronate administered daily or intermittently on fracture risk in postmenopausal osteoporosis. J Bone Miner Res 19:1241–1249CrossRef 5. Cummings SR, Black DM, Thompson DE, Applegate WB, Barrett-Connor E, Musliner TA, Palermo L, Prineas R, Rubin SM, Scott JC, Vogt T, Wallace R, Yates AJ, LaCroix AZ (1998) Effect of alendronate on risk of fracture in women with low bone density but without vertebral fractures: results from the Fracture Intervention Trial. JAMA 280:2077–2082CrossRefPubMed

6. Harris ST, Watts NB, Genant HK, McKeever CD, Hangartner T, Keller M, Chesnut CH III, Brown J, Eriksen EF, Hoseyni MS, Axelrod DW, Miller PD (1999) Effects of risedronate treatment on vertebral and nonvertebral fractures in women with postmenopausal osteoporosis: a randomized controlled trial. Vertebral Efficacy With Risedronate Therapy (VERT) Study Group. JAMA 282:1344–1352CrossRefPubMed 7. Lyles KW, Colon-Emeric CS, Magaziner JS, Adachi JD, Pieper CF, Mautalen C, Hyldstrup L, Recknor C, Nordsletten L, Moore KA, Lavecchia C, Zhang J, Mesenbrink P, Hodgson PK, Abrams K, Orloff JJ, Horowitz Z, Eriksen EF, Boonen S (2007) Zoledronic acid and clinical fractures and mortality after hip fracture. N Engl J Med 357:1799–1809CrossRefPubMed 8.

In previous studies we have shown that CcpA is a pleiotropic regu

In previous studies we have shown that CcpA is a pleiotropic regulator of S. suis carbon metabolism, virulence gene expression and the expression of

the arginine deiminase (AD) system [37–39]. The latter is crucial for bacterial survival in acidic environments and is most likely required for alternative ATP generation. Hence, we tested respective S. suis mutant strains 10ΔccpA and 10ΔAD for gentamicin tolerant persister cells. CFU of bacterial strains grown to the exponential growth phase were determined over time after treatment with 100-fold MIC gentamicin. The gentamicin MIC values of the mutant strains did not differ from those of the wild type strain. No JPH203 research buy change in persister levels was observed for exponential grown strain 10ΔccpA, whereas the AD mutant strain 10ΔAD showed an approximately two log-fold higher persister cell level over time compared to the wild type (Figure 4A). This difference was abrogated

when stationary VRT752271 growth phase cultures were challenged by gentamicin check details (Figure 4B). Interestingly, during the later growth phase the persister level of strain 10ΔccpA decreased as compared to the wild type and strain 10ΔAD. Figure 4 Effect of specific gene inactivation on S. suis persister formation. Exponential (A) or stationary (B) grown S. suis strains were treated with 100-fold MIC of gentamicin over time. Persister cell levels were determined for the wild type strain 10, and its knock-out mutant strains 10∆ccpA and 10∆AD, which lack the genes coding for the global transcriptional regulator CcpA and the catabolic arginine deiminase system, respectively. The values are means of three biological replicates and error bars indicate the standard deviation. Significant differences to wildtype persister levels were calculated by a

one-tailed t-test (*, P < 0.05; **, P < 0.01). Persister cell formation occurs in different S. suis strains and streptococcal species Next, we tested antibiotic tolerance and persister cell formation in other S. suis strains and Tyrosine-protein kinase BLK streptococcal species. For this, we analyzed a human serotype 2 isolate (strain 05ZYH33) originating from a S. suis outbreak in China and a serotype 9 strain (strain A3286/94) isolated from a pig with meningitis [40, 41]. The MIC values of gentamicin for strain 05ZYH33 and strain A3286/94 are given in Additional file 1: Table S1. In all strains, treatment with 100-fold MIC of gentamicin induced the characteristic biphasic killing curve and resulted in a complete killing of bacteria after 24 hours. No substantial differences could be observed between strains in the exponential growth phase (Figure 5). On the other hand, using stationary cultures strain 10 showed the highest degree of drug tolerance. Strains A3286/94 and 05ZYH33 were killed more efficiently, especially during the first hour of antibiotic treatment, with persister cell differences of up to two log-fold CFU.

In both patients, after treatment with in vitro active antimicrob

In both patients, after treatment with in vitro active antimicrobial agents (colistin and nitrofurantoin), clinical improvement was observed and in subsequent urine samples of patient 1 E. coli NDM-4 was

no longer isolated. Patient 2 was discharged without further microbiological investigation. Patient 1 was previously hospitalized in India, a geographical region with high prevalence of NDM-producing isolates. This is the first example of importation of an Indian NDM-4-producing isolate in Italy following a hospital transfer, confirming the recent observations suggesting that the Indian subcontinent may represent an important reservoir of NDM producers. Because patient 2 had not a history of travel to NDM endemical areas and GDC-0973 ic50 PFGE profile of the strains was identical, it is plausible that a spread of NDM-4 -producing E.coli from patient 1 to patient 2

occurred. According to the hospital microbiology laboratory records, no further isolation Idasanutlin mouse of NDM-4-positive bacteria was reported to date in our hospital. To our knowledge, we report here the first NDM-4 producing E.coli detected in Italy and the fourth worldwide [2, 3, 23] . NDM-4 producing E.coli strains have been previously described in patients from India, Cameroon and Denmark. In this last case, the Danish patient was previously hospitalizes in Vietnam. In three cases (Cameroon, Denmark and Italy), isolates belonged to the ST405 sequence type. This finding

is alarming because, ST405, has been previously identified as a successful Selleck GSK2118436 international sequence type and it could favor the RVX-208 spread of NDM producers. Conclusions This is the first report on the emergence of an MDR strain of E.coli producing the NDM-4 MBL in Italy as the result of importation of an Indian NDM-4-producing isolate following a hospital transfer. The isolate belonged to a well-known international sequence type (ST405) able to spread and cause outbreak. Our data confirms the need for a systematic screening to rapidly detect NDM-producing strains especially among patients previously hospitalized in the endemic geographic areas to avoid dissemination of carbapenemase-producing Enterobacteriaceae. Authors’ information Erika Coppo is a Microbiology PhD student working at the Microbiology Unit, DISC, University of Genoa, Italy. Valerio Del Bono, MD, has been working since 1994 in Infectious Disease department in Genoa as attending physician in chief. He is a member, as a responsible for Infectious Disease, of the healthcare-associated infection control team of San Martino-IST Hospital. He acts as a referee for several international journals. He is author or co-author of more 40 internationally published papers.

Figure 1 Evolution of the PSi optical thickness nd as a function

Figure 1 Evolution of the PSi optical thickness nd as a function of the doping current. The red circles are the ratio of the nd values (n is the refractive index and d the physical thickness) before and after the doping process. The transferred charge is the same for all samples. The line fit is to be intended as a guide for the eyes. If the doping process were independent on the doping current, the data should follow a horizontal

line, since no evolution would be expected. However, our results, even with the large spread, indicate that there is a clear trend, although a fully quantitative determination cannot be obtained. It must be noted that a spread in the data is expected because there are several small parameters that can affect the results. For instance, the minute differences in the surface/bulk properties of the starting 3-Methyladenine purchase Si wafer will affect the shape of the pore openings VX-661 mouse and, in turn, the diffusion of the Er solution within the pores. This effect is also expected for samples coming from different parts of the starting Si wafer (32 samples are obtained for each 4-in. wafer). The line fit is shown as a guide for the eyes to evidence the trend. Given the correlation of the samples optical properties with their Er content [14, 15], based on the data of Figure 1, we can get a first

hint that this evolution indicates a current intensity-dependent Er content. selleckchem Electrochemical characterization Figures 2 and 3 show the measured voltage transients for applied currents with low and high densities, mafosfamide respectively, in two nominally identical PSi samples (2.5-μm thick). The total transferred charge is the same for both transients. The inset of Figure 3 shows an enlargement of the plot of Figure 3 (red dots) superposed to its first derivative (blue dots). The same effect has been observed for several other thicknesses.The results of Figures 2 and 3 demonstrate the existence of two different transient shapes: at low currents, a single transitory (ST) is evidenced by the regular increase of the voltage absolute value (Figure 2),

while a double transitory (DT) is evidenced for higher currents (Figure 3), where a variation in the slope during the voltage evolution is clearly visible also as a clear peak in its first derivative (inset of Figure 3). The presence for higher currents of a slope change indicates that two different Er deposition processes are involved, while a single regime is present for lower currents. Although to date the onset of the transition between the two regimes as a function of the doping parameters is not clearly definite, we observed that all higher current density doping processes exhibit a DT, while all lower current ones exhibit a ST. We also observed that the DT shape depends on the current intensity and that there is a correlation of the shape with the current density (not shown). Figure 2 Voltage evolution in PSi Er doping using a low constant current intensity.

This article reviews our 10 years of clinical experience in perfo

This article reviews our 10 years of clinical experience in performing rotary gamma knife in patients with secretory pituitary MI-503 solubility dmso adenomas. The focus of this research is to define accurately the efficacy, safety, complications, and role of rotary gamma knife for treatment of secretory pituitary adenomas. Methods Characteristic of the patients Between 1997 and 2007, 1681 patients with a diagnosis

of secretory pituitary adenoma were treated with MASEP rotary gamma knife(MASEP instruments, Inc., Shenzhen, P.R. China) in our medical center. The patients with secretory pituitary adenoma treated in our studies are those loss convenience, intolerant of or resistant to medical therapies. Some of them were evaluated Nutlin-3 ic50 ineligible for neurosurgery because of body health and the others rejected to surgery on private choice or economic condition. 347 patients under medical therapies irregularly less than 3 months after

MASEP GKRS and getting follow-up with at least 60 months were taken in our study, and those with follow-up less than 60 months or taken medical therapies regularly after MASEP GKRS were excluded. Our study population comprised 162 men (46.7%) and 185 women (53.3%). Their age ranged from 17 to 86 years (mean 41.8). The patients presented with a 1- to 19-year history (mean 2.7). In 47 of these patients some form of prior treatment such as transsphenoidal resection, or craniotomy and resection had been conducted. The others were deemed ineligible for microsurgery because of body health or private choice, and MASEP GKRS served as the primary treatment modality. Endocrinological, ophthalmological, and neuroradiological exams were taken for all of them. The diagnosis was made on the basis of magnetic resonance imaging (MRI) findings, endocrinological exam findings, pathological findings (available for postoperative patients), and their clinic history. Of these patients treated, not 68(19.6%) had a diagnosis of adrenocorticotropic hormone-secreting adenomas, 176(50.7%) had a diagnosis of prolactinomas, and 103(29.7%) had growth hormone-secreting adenomas. The mean follow-up period

was 67.3 months (range 60~90 months) (Table 1). Table 1 Characteristics of patients with pituitary adenomas treated with MASEP GKRS Characteristic Value(%) The statistics of the population      Sex   male 162(46.7) female 185(53.3)    Mean age(yrs) 41.8 (range17~86)    Mean history(yrs) 2.7(range1 to 19) No. of previous treatments   transsphenoidal resection 27* craniotomy and resection 23 Mean follow-up after GKRS(mos) 67.3 (range 60~90) Type of adenomas      ACTH adenomas 68(19.6) microadenoma(size, cm3) 21 (0.8~1.1) macroadenoma(size, cm3) 47 (1.2~6.4)    Prolactinomas 176(50.7) microadenoma(size, cm3) 0 macroadenoma(size, cm3) 176(1.2~17.9)    GH adenomas 103(29.7) microadenoma(size, cm3) 0 macroadenoma(size, cm3) 103(2.3~21.

However, the role of miRNAs in SCLC pathogenesis has not been ext

However, the role of miRNAs in SCLC pathogenesis has not been extensively studied. Our investigation identified a group of miRNAs that show a progressive differential expression from HBECs to NSCLC and SCLC cells. Several of the miRNAs identified in this study have been shown to be associated with various cancer types in previous studies. GSK2118436 nmr For BI-D1870 example, we found significant overexpression of miR-103, miR-107, miR-301 and miR-338 in lung cancer cells as compared to HBECs. These miRNAs have been shown to be over-expressed in several types of cancers including

lung cancers [17, 50, 51], and high expression of miR-103 and miR-107 were correlated with poor survival in cancer patients (esophageal squamous and pancreatic tumors) [51, 52]. These miRNAs might contribute to common pathways during the transformation of normal cells to tumor cells during lung cancer pathogenesis, and the greater extent of aberrant expression of these miRNAs in SCLCs relative to NSCLCs might contribute to the more aggressive phenotype of the former. Our study also identified a group of miRNAs that might contribute to the establishment of SCLC features and the specific phenotypes that differentiate SCLC from NSCLC. PF-02341066 order For example, we found over-expression of miR-17-5p in SCLCs compared to NSCLCs. This miRNA was recently shown to target Rbl2,

a member of the Rb family [53]. Rb is a tumor suppressor that induces arrest of the cell cycle at G1 [54]. SCLCs have been shown to exhibit loss of Rb expression in 87-100% of tumors compared to less than 15% in NSCLC [55–57]. SCLC cells were also previously shown to be addicted to continued over-expression of miR-17-5p [58], and forced over-expression of the miRNA cluster that includes miR-17-5p (miR-17-92)

was shown to induce embryonic lung epithelial cell proliferation [59]. Coupled with these data, our results suggest that dysregulation of this miRNA could be an important distinction that defines the pathogenesis and phenotypic characteristics of SCLC compared to NSCLC. We also observed a significant increase in miR-135 expression in SCLC cells compared to NSCLC cells. miR-135 has recently been shown to inhibit expression of the tumor suppressor gene Adenomatous Polyposis Resveratrol Coli (APC) in colorectal cancer [60]. Loss of heterozygosity of APC has been shown in both small cell and non-small cell lung cancers, but appears to be more frequent in SCLC [61]. Silencing of this gene by CpG hypermethylation, however, is more frequent in NSCLC compared to SCLC [62], suggesting that various lung tumor subtypes could use different means to down-regulate this tumor suppressor. These findings suggest that SCLC preferentially utilizes microRNA-based regulatory mechanisms to reduce APC expression. miR-29a, -29b and -29c expression was shown be significantly down-regulated in SCLC cells compared to HBECs, whereas these reductions were not seen in NSCLC cells.

In transwell co-cultures, the mean percentage of MCF10AT cells la

In selleck chemical transwell co-cultures, the mean percentage of MCF10AT cells labeled by BrdU (i.e., BrdU labeling index) was decreased by 20% in co-culture with NAF (p = 0.011). The NAF utilized

were derived from three different individuals. In direct co-cultures, the mean reduction in BrdU labeling by the same three NAF was 46% (p < 0.001) (Fig. 1). There was variability among the three NAF in their ability to inhibit proliferation of MCF10AT, particularly learn more in direct contact co-cultures. The greater reduction in proliferation of MCF10AT in direct versus transwell co-culture was significant (p = 0.04) (Fig. 1). These results indicate that inhibition of epithelial growth by NAF is mediated by a mixture of direct-contact/insoluble and soluble factors.

Therefore, we selected differentially expressed genes from the microarray analysis encoding both soluble and matrix-bound, insoluble molecules for validation by quantitative, real-time PCR (QRT). Fig. 1 Proliferation of MCF10AT in 3D selleck chemicals direct and transwell co-cultures with NAF. Direct and transwell 3D (i.e., in Matrigel) co-cultures of MCF10AT cells with each of three NAF from different individuals were prepared. BrdU labeling of MCF10AT cells was counted by flow cytometry. Each NAF (i.e., NAF1, NAF2 and NAF3) suppressed proliferation of co-cultured MCF10AT cells to some extent in transwell co-cultures, and two of the three NAF (i.e., NAF1 and NAF3) suppressed proliferation of MCF10AT in direct co-cultures. When comparing the overall reduction in proliferation of Methisazone MCF10AT induced by the three NAF in all transwell

co-cultures combined (n = 10, checkered bar) to MCF10AT grown without co-cultured NAF (black bar), the decrease in proliferation was significant (p = 0.011). Similarly, the overall decrease in proliferation induced by the three NAF in all direct co-cultures combined (n = 14, checkered bar) compared to MCF10AT monocultures (black bar) was significant (p < 0.001). However, the degree of suppression was significantly greater in direct than transwell co-cultures (p = 0.04). Data are normalized to corresponding MCF10AT monocultures. Mean and standard error are shown Expression of a Subset of Differentially Expressed Genes was Confirmed by Real-Time PCR We selected eight genes from the list of 420 differentially expressed genes in NAF and CAF for validation by QRT (Fig. 2a, Supplemental Tables 1 and 2). The primary criterion for selecting genes for validation was that they encoded a secreted protein, either soluble or matrix-bound, that was known to regulate cell growth, migration, invasion and/or ECM remodeling.

Pilz S, Tomaschitz A,

Pilz S, Tomaschitz A, GSK2245840 concentration Ritz

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