Eventually, the voids will reach such a big size to cause a lift-off of the layers with the formation of surface blisters, as observed by AFM. The blisters correspond therefore to bubbles containing PD-1/PD-L1 mutation molecular H2. They have developed from microscopic cavities, decorated by clustered mono-hydrides and (Si-H2) n , n ≥ 1, complexes, which have increased their volume because of the increase of the inside pressure due to the thermal expansion of the H2 gas upon annealing. It was seen in previous works on a-Si, a-Ge layers and a-Si/a-Ge multilayers that

for annealing time and/or temperature higher than those considered here, further degradation of the layer surface occurs by explosion of the blisters [19, 20]. Table 2 Total integrated intensity (cm −1 ) of the IR stretching mode Annealing time (h) I SM(cm−1)   H = 0.4 ml/min H = 0.8 ml/min H = 1.5 ml/min    0 12.8 30.8 72.1    1 11.4 26.8 52.5    4 10.5 24.2 45.1 Total integrated intensity (cm−1) of the IR stretching mode, I SM, as a function of annealing time for the different hydrogenation rates. Conclusions The origin of surface blisters that form in hydrogenated

RF-sputtered a-Si layers submitted to annealing has been investigated by studying the evolution of the Si-hydrogen bonds by means of IR spectroscopy. By increasing the annealing time and/or H content, the blister size increased. Correspondingly, IR spectroscopy showed that the density of the isolated Si-H mono-hydrides decreased, while selleck compound the concentration of the clustered (Si-H) n groups and (Si-H2) n , n ≥ 1, polymers increased. As both these complexes

reside on the inner surfaces of voids, it is concluded that their accumulation at such surfaces favours the void size increase. It was also seen that the total amount of bonded H decreased upon annealing, suggesting that some H is released from its bonds to Si. The H liberated from the (Si-H) n groups and (Si-H2) n polymers decorating C-X-C chemokine receptor type 7 (CXCR-7) the void surfaces is expected to form molecular H2 within the voids. The expansion of the H2 gas would cause further growth of the voids up to a size able to produce surface blistering. Authors’ information MS is a scientific adviser at the Institute of Technical Physics and Materials Science, Research Centre for Natural Sciences, GANT61 in vivo Hungarian Academy of Sciences, Budapest, Hungary. CF is a senior scientist at the IMEM Institute of the Consiglio Nazionale delle Ricerche, Parma, Italy. ZS is a PhD student and young researcher at the Institute for Solid State Physics and Optics, Wigner Research Centre for Physics, Hungarian Academy of Sciences, Budapest, Hungary. KK is a research professor at the Institute for Solid State Physics and Optics, Wigner Research Centre for Physics, Hungarian Academy of Sciences, Budapest, Hungary. LN is a researcher at the IMEM Institute of the Consiglio Nazionale delle Ricerche, Parma, Italy.

Transfectants were selected with 90 μg/ml hygromycin

for 48 hours before harvesting. The scrambled control EhC2A (363–391 scrambled) shRNA transfectant was used as a control for EhC2A Cell Cycle inhibitor protein levels. HM1:IMSS nontransfected amebae were not included. The level of EhC2A protein in the EhC2A (363–391 scrambled) control shRNA transfectant was defined as 100 ± 5.0% (± SE). The EhC2A (363–391) shRNA transfectant yielded a knockdown of EhC2A protein to a level of 3.0 ± 0.4% (P < 0.0001). The EhC2A (502–530) shRNA transfectant Saracatinib cost had no knockdown effect on EhC2A levels (106.1 ± 7.3%) and was statistically the same (P = 0.3141) as the EhC2A (363–391 scrambled) shRNA control transfectant (Figure 4). Student’s t test was used for statistical analysis. qRT-PCR was not performed for these samples. Figure 4 Western blot for EhC2A transfectants. A representative Western blot is shown with three biological replicates each for EhC2A (363–391), EhC2A (502–530), and ABT263 EhC2A (363–391 scrambled control) shRNA transfectants. Results are representative of three biological replicates per shRNA transfectant

with each sample run in triplicate. Each sample was also serially diluted 1:2, 1:4, and 1:8. Each membrane was probed anti-EhC2A and with anti-actin antibody as a loading control. The level of EhC2A protein in the scrambled control transfectant was defined as 100% (± 5%). The EhC2A (363–391) shRNA transfectant had strongly reduced levels of EhC2A protein: it was only 3.0 ± 0.4% of the scrambled control. The EhC2A (502–530) shRNA transfectant had no knockdown effect on EhC2A levels (106.1 ± 7.3%). Northern blots of small RNAs Since the E. histolytica U6 promoter had never been characterized, we tested if shRNAs or other small RNAs were being produced by the U6 promoter. The PATMK samples were included because they had been shown to have significant

knockdown of PATMK protein levels as compared to the scrambled PATMK shRNA control transfectant [39], and therefore would be good candidates for expressing the shRNAs. Northern blotting of the PATMK [39] and Igl shRNA transfectant small RNAs was performed. Transfected trophozoites were selected with GBA3 30 μg/ml hygromycin for 48 hours before harvesting, since we had seen protein knockdown previously at that level of selection [39]. Non-transfected HM1:IMSS amebae were included as a negative control. Fifty μg of small RNAs from PATMK shRNA transfectants [39] and the Igl shRNA transfectants were probed with oligo probes targeting the respective sense and antisense strands of the shRNAs (Figure 5). The PATMK (3552–3580) [39] and Igl (2777–2805) shRNA samples had substantial expression of ~70 and ~30 nucleotide small RNAs, the expected sizes for the unprocessed hairpin and the processed siRNA respectively.

Prognosis is known to be dramatically influenced

by cytoreductive surgery and response to adjuvant platinum/taxane-based chemotherapy. However, even good responders to initial treatment often have a poor PF 01367338 prognosis due to secondary relapse. Such relapses are generally chemoresistant and remain the major cause of death. Thus, it may be useful to treat chemosensitive patients in order to kill residual clones and avoid the chemoresistant relapse. Different consolidation therapies have been considered: conventional maintenance chemotherapy, intraperitoneal treatment with chemotherapy and/or hyperthermia, and HDC with HSCS. The latter has been widely used in the context of poor risk hematological malignancies and sometimes in chemosensitive solid tumors such as metastatic breast cancer [21–25] or germ cell tumors [26] with controversial results. The main toxicity of high-dose alkylating

agents is hematological. Stem cell transplantation is needed in such treatment strategies to limit the duration and consequences of aplasia. Nevertheless, severe infection can always occur during grade 4 neutropenia and MK-1775 nmr remains the major potential risk during severe aplasia. However we observed no toxic death after HDC in this study. Several promising but preliminary studies have reported that HDS plus HSCS may improve ovarian cancer outcome in first-line therapy. These results were observed when HDC was used either as front-line treatment [19, www.selleckchem.com/products/qnz-evp4593.html 27], or as consolidation therapy [17, 28–32]. However published randomized phase III trials did not confirm these results. In a single center small-sized study from Papadimitriou et al.[19], although PFS was numerically improved by HDC (85.2 months versus 18 months),

the difference was not significant (p=0.059). Moreover, no significant difference was observed in OS (not reached after 75 months of follow-up versus 75 months, p=0.38). The authors attributed PFS gain to the higher rates of stages IV (14% vs. 8.1%) and larger post-operative enough residue (32.6% vs. 21.6%) in the conventional therapy arm. Mobus et al. reported similar findings in their relatively large phase III trial published in 2007 [20]. Median PFS was 29.5 months in the HDC arm versus 20.5 in the control arm (p=0.40). There was also no difference regarding OS (54.4 vs. 62.8 months, p=0.54). Conclusions of these studies were that HDC does not improve outcome in advanced ovarian cancer. Nevertheless a question that could be asked is: are these conclusions relevant for all patients or is there a subset of patients who may benefit from HDC? In this retrospective study, we tried to address this issue using a subgroup analysis approach in a large population of more than 160 patients.

Vaccine 28(41):6704–6713. 25. Laban A, Cohen A: Interplasmidic and intraplasmidic recombination in Escherichia coli K12. Mol Gen Genet 1981,184(2):200–207.PubMed 26. Cohen A, Laban A: Plasmidic recombination in Escherichia coli K12: the role VE-822 ic50 of recF gene function. Mol Gen Genet 1983,189(3):471–474.PubMedCrossRef 27. Fishel RA, James AA, BMN 673 clinical trial Kolodner R: recA -independent general genetic recombination of plasmids. Nature 1981,294(5837):184–186.PubMedCrossRef 28. Matfield M, Badawi R, Brammar WJ: Rec-dependent

and Rec-independent recombination of plasmid-borne duplications in Escherichia coli K12. Mol Gen Genet 1985,199(3):518–523.PubMedCrossRef 29. James AA, Morrison PT, Kolodner R: Genetic recombination of bacterial plasmid DNA. Analysis of the effect of recombination-deficient mutations on plasmid recombination. J Mol Biol 1982,160(3):411–430.PubMedCrossRef

30. Kolodner R, Fishel RA, Howard M: Genetic recombination of bacterial plasmid DNA: effect of RecF pathway mutations on plasmid recombination in Escherichia coli . J Bacteriol Selleckchem SN-38 1985,163(3):1060–1066.PubMed 31. Smith GR: Homologous recombination in procaryotes. Microbiol Rev 1988,52(1):1–28.PubMed 32. Kolodner R, Fishel RA, Howard M: Genetic recombination of bacterial plasmid DNA: effect of RecF pathway mutations on plasmid recombination in Escherichia coli . J Bacterio 1985,163(3):1060–1066. 33. Cox MM: A broadening view of recombinational DNA repair in bacteria. Genes Cells 1998,3(2):65–78.PubMedCrossRef

34. McClelland M, Sanderson KE, Spieth J, Clifton SW, Latreille P, Courtney L, Porwollik S, Ali J, Dante M, Du F, et al.: GPX6 Complete genome sequence of Salmonella enterica serovar Typhimurium LT2. Nature 2001,413(6858):852–856.PubMedCrossRef 35. Bi X, Liu LF: recA -independent and recA -dependent intramolecular plasmid recombination. Differential homology requirement and distance effect. J Mol Biol 1994,235(2):414–423.PubMedCrossRef 36. Kato T, Rothman RH, Clark AJ: Analysis of the role of recombination and repair in mutagenesis of Escherichia coli by UV irradiation. Genetics 1977,87(1):1–18.PubMed 37. Mahan MJ, Casadesus J, Roth JR: The Salmonella Typhimurium RecJ function permits growth of P22 abc phage on recBCD + hosts. Mol Gen Genet 1992,232(3):470–478.PubMedCrossRef 38. Clark AJ: rec genes and homologous recombination proteins in Escherichia coli . Biochimie 1991,73(4):523–532.PubMedCrossRef 39. Kowalczykowski SC, Dixon DA, Eggleston AK, Lauder SD, Rehrauer WM: Biochemistry of homologous recombination in Escherichia coli . Microbiol Rev 1994,58(3):401–465.PubMed 40. Zaman MM, Boles TC: Plasmid recombination by the RecBCD pathway of Escherichia coli . J Bacteriol 1996,178(13):3840–3845.PubMed 41. Persky NS, Lovett ST: Mechanisms of recombination: lessons from E. coli . Crit Rev Biochem Mol Biol 2008,43(6):347–370.PubMedCrossRef 42.

On the basis of the jackknife validation, MHS performs poorly on several organisms. M. genitalium represents a unique case; nearly 80% of its genes are essential. There is little difference between the AUC for the ideal sorting, the MHS sorting, and the random assortment. Even so, MHS produced a 38.8% sorting, with a p-value of 2 × 10-9 compared to random. It is unclear why H. influenzae and H. pylori and to a lesser extent E. coli performed poorly. This result suggests that these organisms may contain species specific essential genes. For H. pylori the authors of the initial essentiality screen note a surprising lack of overlap with the essential gene sets from

other organisms [44]. As the number of essential genes in H. pylori is in the same range as most of the other organisms in DEG, this could suggest an alternative set of essential Belinostat manufacturer genes. In the case of E. coli, we note that the number of essential genes is nearly double the average for the other DEG organisms, which likely reflects its status as one of the most well-studied bacteria. This larger set may confound the E. Semaxanib datasheet coli jackknifing validation. Somewhat paradoxically, these features may be beneficial for this analysis. The

outlier organisms may incorporate more diversity in our reference set of essential genes, increasing the likelihood of identification of diverse essential genes within wBm. This does come with the trade-off of increasing the false positive rate, however, this is mitigated by two factors. First, the design of the MHS assigns more confidence to genes conserved across multiple organisms, moving well supported essential gene predictions towards the top. Second, the pipeline for the rational drug design process utilizes the predictions of essential wBm genes to inform a manual selection of drug targets. A moderate false positive rate can be screened out based on manual analysis and pathway information. As an additional experiment, it could be informative to examine non-DEG genes predicted as essential in the jackknifing validation to identify essential genes missed by the knockout experiments. A gene conserved nearly universally across DEG but missing in a small number

of organisms may be useful to investigate under alternative experimental conditions. Genes identified by MHS are predicted Prostatic acid phosphatase to belong to a set of genes which are essential and broadly conserved across bacterial life. This set includes many targets of modern broad-spectrum antibiotics. A compound targeting genes from this class is more likely to produce antibiotics effective across a broad range of bacterial species. Though gene orthology does not specifically indicate drug cross-reactivity, the distribution of the targeted gene NVP-BEZ235 solubility dmso should be considered. While developing a novel broad-spectrum antibiotic would be advantageous, for this specific application such a compound may also come with negative side-effects. Ideally, a mass drug administration protocol against B.

In due course, negative wound pressure therapy was performed with wound dressing changes at intervals of four days. It was possible to cover the abdomen and to bridge the fascia defect using a Vicryl mesh; thereafter, a definite closure could be performed. Following the operation the selleck screening library patient needed a bowel rest, nasogastric suction and intravenous fluid

therapy. We were able to initiate a light diet after the complete resolution of abdominal pain and eventually return the patient to a normal diet. The bridging of nutritional support was required. The patient could be mobilized and will perform postdischarge rehabilitation. Discussion IDSMA remains a rare condition, with postmortem investigations showing an incidence of about 0.06% [14]. However, to date, an agreement on the standardized treatment for this condition has not been reached. Within the past five years, reports featuring a small series of cases of patients with IDSMA can be found in the literature; prior to this period, only case reports are predominantly available. Based on a PubMed search, we identified 14 studies that fulfill the search criteria, which consisted of 323 cases altogether. Table 1 provides an overview of these publications.

Table 1 Summary of small case series on patients with IDSMA Year of publication Author Total number of cases Medical treatment Open surgery Endovascular therapy 2014 Kim HK et al. [15] 27 27 – - 2014 Ahn HY et al. [16] 13 12 1 0 2014 Li DL et al. [17] 42 24 7 11 2013 Dong Z et al. [7] 14 4 1 9 2013 Jia ZZ et al. buy AZD9291 [18] 17 14 0 MX69 3 2013 Li N et al. [19] 24 0 0 24 2013 Luan JY et al. [20] 18 7 0 11 2013 Choi JY et al. [21] 12 10 0 2 2012 Pang P [22] 12 3 0 9 2012 Zhang X [23] 10 6 2 2 2011 Min SI et al. [24] 14 7 1 6 2011 Park YJ et

al. [25] 58 53 4 1 2011 Cho BS [26] 30 23 1 6 2009 Yun WS [9] 32 28 3 1 Sum   323 218 20 85 The investigation period was from January 1, 2009 to June 1, 2014. Cases are subdivided due to treatment strategies. Medical treatment seems to be effective in IDSMA. During a follow-up of 18 months a reduction of occlusion in the true lumen could be seen in up to 89% and progressive resolution of false lumen thrombosis in all patients [15]. Nevertheless, a fail rate of roughly 34% among conservative therapy approaches that includes the administration of effective anticoagulation through intravenous heparin makes such an approach 4SC-202 appear questionable [27–29]. Endovascular therapy offers safe and quick therapy for patients with IDSMA. The first description of this approach by Leung et al. was followed by multiple reports of successful treatments by several authors describing complete resolution of the pain in most cases [30–33]. In a follow-up of 6 months stent patency could be found in 100%, a false lumen patency in 22% and new development of dissection in the SMA distal to the stent in 4% of all cases [19].

As shown PF-6463922 in Figure 1, the adhesion to fibronectin was differentially modulated by the antibiotics. Oxacillin-, moxifloxacin-, clindamycin- and linezolid-treated bacteria displayed increased binding to fibronectin. This effect was GS-9973 order observed for all strains tested except fnbA/B-negative DU5883. The increase in amplitude of fibronectin binding was strain-dependent. Oxacillin treatment increased fibronectin binding from 1.8- to 2.7-fold relative to the untreated control; moxifloxacin treatment increased binding from 1.4- to 2.3-fold; clindamycin

treatment increased binding from 1.5- to 1.8-fold; and linezolid treatment increased binding from 1.6- to 2.3-fold, depending on the tested strain. By contrast, fibronectin binding was significantly reduced after rifampicin treatment. The decrease was strain-dependent and ranged from 1.5- to 3.5-fold compared to the untreated control. Vancomycin and gentamicin had no effect on bacterial adhesion to fibronectin-coated plates (data not shown). Antibiotics-induced reduction in bacterial density had no significant confounding effect on fibronectin binding in our model, as demonstrated by the absence of correlation between n-fold changes in bacterial density and fibronectin binding in antibiotics-treated GF120918 cell line strain 8325-4 (Additional File 1). The DU5883 strain, defective for fnbA and fnbB genes [9], did not adhere to fibronectin-coated

plates in any condition (with or without antibiotics). Clindamycin could not be tested with the DU5883 strain as it harbours the ermB gene and therefore is resistant to clindamycin (Table 3). Figure 1 Effect of antibiotics on the adhesion to human fibronectin. Exponential growth

many cultures of S. aureus laboratory strains 8325-4 and DU5883 and clinical isolates ST2008 1028, ST2008 0563, HT2000 0594 and HT2001 0390 were treated or not treated with 1/2 of the MIC of antibiotics (oxacillin, moxifloxacin, clindamycin, linezolid or rifampicin) and assayed for adhesion to fibronectin-coated microplates, as described in Methods section. The results are OD570 nm values reflecting bacterial adhesion to fibronectin. The values were obtained from 3 different wells previously incubated with the same bacterial suspension, and adhesion is expressed as the mean ± standard deviation (dark bars for untreated cultures and white bars for antibiotic treated cultures; results from three different experiments). Asterisk = significantly different from the control (corresponding isolate grown without antibiotic), with a P value of 0.05 by one-way analysis of variance followed by a posteriori Dunnett’s test. Effect of antibiotics on fnbA and fnbB mRNA levels We explored the effect of antibiotics on mRNA expression levels of the fnbA and fnbB genes which encode FnBPA/B. The fnbA and fnbB mRNA levels in exponential phase cultures of S.

Upon reopening the right chest there was immediate improvement in ventilation and blood pressure with approximately 1 L of clot present. Exploration of the chest cavity did not demonstrate surgical bleeding, though all dissection planes were oozing. The chest was repacked, and due to the prior episode of life-threatening ventilatory and hemodynamic

compromise, the decision was made to manage OSI-027 datasheet the patient with an open chest cavity to allow for respiratory and hemodynamic stabilization while correcting the hypothermia and coagulopathy. An adhesive plastic drape was folded over (to remove the adhesive surface) and placed over the right lung and a second adhesive plastic drape was placed over the entire trap-door incision to close the pleural space. The plastic drape was then vented medially to

prevent the development of a tension pneumothorax. The patient stabilized and responded to rewarming and BTSA1 mouse correction of his coagulopathy. At ~POT + 30 hours the patient was returned to the operating room for removal of chest packing and chest closure. Figure 2 demonstrates the status of the patient’s Cilengitide chemical structure wounds at time if initial return to the operating room. The chest was too tight to undergo a definitive sternal and pericostal closure, so soft-tissue closure was once again obtained by running the skin closed along the perimeter of the trap-door. Abdominal closure was deferred to the time of definitive chest closure, both of which were performed five days later. Figure 2 Status of patient’s wounds upon return to the operating room after 24 hours of open-chest management. The development of thoracic compartment syndrome necessitated therapeutic re-opening of the chest and open-chest management. A) Open trap-door thoracotomy. Comprised of connecting anterolateral thoracotomy in the 6th intercostal space, partial sternotomy, and supraclavicular incisions. The reflection edge for the trap-door is shown by the black hatched lines: the ribs along this edge were fractured by the reflection of the trap-door. B) Open midline

laparotomy with Bogota bag sewn onto the skin. The patient had an extensive treatment course in the surgical intensive care unit, manifesting severe acute respiratory distress syndrome, aminophylline requiring inhaled nitric oxide and prone-positioning ventilation. The patient also developed acute renal failure and severe deconditioning. The patient was eventually discharged to a long-term ventilatory care facility on post-trauma day 68, and returned to his home approximately 2 months thereafter. Discussion Thoracic compartment syndrome (TCS) has been reported predominantly in the pediatric and adult cardiac surgery populations, where this phenomenon has been described as a syndrome of “”mediastinal tightness”" following prolonged cardiac surgery [2–5].

Whereas the EcoSim analysis suggests an overall signature of negative co-occurrence, Fisher’s Exact test indicates negative and positive co-occurrences for certain species pairings. It is noteworthy that none of the three additional species exhibited negative co-occurrence with M. bolleyi and M. phragmitis in the total data set. Instead, M. bolleyi generally co-occurred significantly more frequently with Ms7Mb4 and Ms43Mb21 than expected

by chance. Such a positive co-occurrence may appear when the conditions that are conducive for one species are also favorable for another species. Alternatively, positive co-occurrence may result buy Tipifarnib from synergism. On the other hand, there existed an overall negative co-occurrence between Stagonospora sp. and Ms7Mb4, significantly preferring leaves [17] and roots [15], respectively. This could

have resulted from strongly contrasting niche preferences, severe competition for the same substrates or from the secretion of toxins (antagonism). Our results suggest that it is rather unlikely that antagonism by any of the other three fungi is responsible for the differential colonization of roots by Microdochium spp. Since the fungal community on common reed is larger than addressed here, we cannot rule out that other endophytes may 17-AAG solubility dmso exert such influences. Conclusions This study supports the concept that niche partitioning allows for differential colonization of common reed by the fungal species investigated. Therefore, Megestrol Acetate a purely neutral model is unlikely to explain the assembly of the mycoflora of common reed. Nonetheless, it remains to be shown to what extent stochastic factors could also contribute to variations in the composition, distribution and diversity of this fungal community. Acknowledgements This work was financially supported by the Deutsche Forschungsgemeinschaft through SFB 454 (Bodenseelitoral). We thank Dr. Jan Nechwatal

(Universität Konstanz) for providing the temperature data for Lake Constance and for discussion of the data. We gratefully acknowledge Dr. Willi Nagl (Universität Konstanz) for advice on statistics, Dr. Ulrike Damm (CBS, Utrecht) for advice on taxonomy, and Michael Koch (Universität Konstanz) for technical help. Electronic supplementary material Additional file 1: Details of isolates studied. This file provides a list of 21 Microdochium isolates used in this study, including accession numbers of ITS sequences and information about their origins. (PDF 11 KB) Additional file 2: Specificity of nested-PCR assays targeting Microdochium spp. This file documents the specificity of the assays employed. A) First PCR step using primers ITS1F and ITS4. M = 100 bp size standard, water: no template DNA included, P. australis: genomic DNA of axenically grown reed plants, genomic DNAs from fungal isolates 4/97-9 (Humicola sp.), 6/97-38 (Chaetomium sp.), 6/97-54 (PF-6463922 order Fusarium sp.), A4 (Fusarium sp.), 5/97-16 (Microdochium phragmitis), 5/97-54 (M.

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