idiopathic, IV ATB intravenous antibiotics, M male, NR not reported, Selleck MG 132 pt(s) patient(s), RA rheumatoid arthritis, SAE serious adverse

event, + postive Our patient presented with symptoms and signs related to all three cytopenias: fatigue (due to anemia); fever that responded to broad spectrum antibiotics (due to severe neutropenia); and petechiae and gingival bleeding (due to severe thrombocytopenia). The absence of concomitant drugs (she had been receiving methotrexate and hydroxychloroquine for years) as well as the temporal relationship between the appearance of her symptoms and the first injection of etanercept, strongly suggest a causal link. Moreover, BM recovery from toxic injury corresponded to the discontinuation of etanercept, whereas methotrexate was later continued uneventfully for months. In contrast, in some of the other cases cited, drugs other than anti-TNFα could have been responsible.

Other than listing all hitherto-reported cases of TNF blocking agent-associated aplastic anemia and pancytopenia, the literature review reveals the rarity of the association, considering that hundreds of thousands of patients have been treated. The other striking feature is the complexity Selleckchem VX 770 of the pathogenesis. TNFα is a pleiotropic cytokine, part of a complex cytokine network that regulates hematopoiesis and may affect BM stem cells differently under different circumstances [17, 18]. On one hand, TNFα (and interferon γ) are overexpressed in the BM of patients with acquired aplastic anemia and can be involved in BM stem cell

apoptosis and suppression of erythropoiesis [19, 20]. Thus, treatment with TNFα antagonists can be a useful approach to the treatment of refractory aplastic anemia [21–23]. On the other hand, under different conditions, Y-27632 2HCl TNFα interacting with other cytokines directly enhances the clonal growth of BM progenitors and suppresses hematopoietic stem cell apoptosis [17, 24]. Thus, its blockade can also exert a deleterious effect on hematopoiesis [6]. Since autoimmune mechanisms are believed to have a key role in the pathogenesis of idiopathic aplastic anemia [25], the association between TNF-targeted therapies and induction of autoimmune diseases (particularly, vasculitis and lupus predominantly with infliximab and etanercept) is also a tenable mechanism [26]. In conclusion, TNFα antagonists for the treatment of RA show significant benefit and are generally safe in comparison with other disease-modifying anti-rheumatic drugs [27–29]. BM suppression resulting in severe cytopenia, transient pancytopenia, or aplastic anemia is a well established but fortunately rare SAE of anti-TNFα therapy. Since a steadily increasing number of patients are being treated for longer periods, any serious RG-7388 purchase adverse effect, however rare, may be encountered.

The relative expression of the 12 genes in stages SU5402 in vitro that precede fructification helped elucidate the correlation

between nutrient depletion and fructification (Figure 6) since the genes MpRHEB, MpRHO1-GEF, MpADE, MpMBF, and MpRAB putatively involved in signaling are associated with www.selleckchem.com/products/JNJ-26481585.html internal perception of the signals triggered by nutrient depletion and other stresses, which was noticeable before the primordia appeared. The putative gene MpRHEB is associated with growth regulation probably during nitrogen depletion [54]. Its expression in M. perniciosa increased in reddish pink mycelium, immediately before stress and continued at a high level until the beginning of the primordial and basidiomata phases (Figure 6D). The expression of the high-affinity transporter MpGLU [51] peaked in this mycelium before stress (Figure 6E), strongly indicating a nutritional deficit, namely low external glucose concentration. Moreover, expression of MpCPR and MpCYP was low during this period (Figure 6G and 6K), indicating a lower basal metabolism [48]. The expression of MpRAB (Figure 6J) may indicate nutrient remobilization, since it Sotrastaurin research buy is involved in intracellular traffic [55, 56]. During the water stress applied to trigger in vitro fructification expression of some genes peaked. Transcripts

of putative MpMBF (multi-protein-bridging factor), a co-activator related to tolerance to abiotic stresses in plants [57], increased 2.4-fold (Figure 6I). Other genes with increased expression during this stress period were MpRHO1-GEF (Figure 6H), involved in signaling for the regulation of polarized growth [58] and MpRPL18 (Figure 6L) involved in protein synthesis. Involvement of signalization, probably cAMP-mediated, is likely due the expression of adenylate

cyclase that decreased in the yellow and reddish-pink mycelial phases, to return to the original levels observed on white mycelium just after the stress period (Figure 6F). As adenylate cyclase is subject to post-translational regulation, studies of enzymatic activity would be necessary to confirm this hypothesis. The gene p-rho/gef is, therefore, possibly correlated with cAMP Fenbendazole pathways. Repression of the glucose transporter coincided with the repression of the adenylate cyclase gene, which also indicates cAMP signaling. In S. pombe the glucose levels are regulated by adenylate cyclase [59] and in Sclerotinia sclerotiorus the development of reproductive structures is negatively regulated by cAMP [60] Putative aegerolysins and pleurotolysin B of M. perniciosa are differentially expressed during fructification As described for other fungi, probable hemolysins are highly expressed at the fructification stages [47, 61]. We identified three putative genes involved in fructification, two more closely related to the identified AA-Pri1 or PriAs of Agrocybe aerogerita and P. ostreatus, respectively, and one more closely related to pleurotolysin B, also identified in P. ostreatus.

One reason why we did not observe any correlation between the Selleckchem BV-6 18F-FDG uptake and the TP53 and CCND1 status could be that the tumour cells in vitro have an excess of nutrients, and that they must be placed under stress to reveal a correlation. Therefore, the next experimental step will be to treat the cell lines with cisplatin, perhaps providing more insight into the complex and still enigmatic mechanisms behind the intracellular uptake and accumulation

of 18F-FDG. The six cell lines were also tested regarding cisplatin sensitivity. Cisplatin-induced cell death was measured using crystal violet staining, a method evaluated before [9]. A statistical difference was found between the cell lines, demonstrating the usefulness of the model for studying chemosensitivity. Conclusion The results in this present study support selleck the value of tumour cell cultures as a model for prognostic and predictive studies. We found the successful establishment of an in vitro cell line from a tumour to be an independent negative prognostic marker.

Furthermore, we found it feasible to study metabolic activity with 18F-FDG uptake, and other tumour biologic characteristics, including the chemosensitivity of the cell lines. Despite the relatively small number of tumour lines, we found a statistically significant correlation between a shorter tumour selleckchem doubling time and higher 18F-FDG uptake. However, no significant difference was seen between 18F-FDG uptake and other proliferation parameters, including TP53 and CCND1 status. Although, the complex metabolic interactions between host and tumour, which create the microenvironment in vivo, will not be reproducible in cultured cell lines the growing knowledge of tumour cell characteristics will provide more understanding of the clinical behaviour of HNSCC tumours and of prognosis and therapy results for HNSCC patients. Acknowledgements The authors

want to thank Christina Boll and Margareta Ohlsson for valuable assistance with the experimental work. This study was supported by the Swedish Cancer Society (grant no. CAN 2007/1092), the King Gustaf V Jubilee Fund (grant mafosfamide no. 074242), governmental funding of clinical research within the Swedish health care system, the Foundations of the Lund University Hospital, Gunnar Nilsson’s Cancer Foundation (grant no. W121/07), Fru Berta Kamprad’s Foundation for Utforskning och Bekämpning av Cancersjukdomar, and Laryngfonden (grant no. 13-07). The experiments were performed according to current Swedish legislation, and were approved by the Regional Ethics Board of Southern Sweden (LU376-01, M48-06). References 1. Ferley JAM, Boniol M, Heanue M, Colombet M, Boyle P: Estimates of cancer incidence and mortality in Europe in 2006.

It also hopes to coordinate CPG development to prevent redundancy of effort and stimulate consensus (http://​www.​kdigo.​org/​). CARI (R. Walker) CARI is the only Asia Pacific regional group currently producing English language

CPGs available on the web. The key aspects are an absolute need for a good evidence base to construct CPGs and the recognition that implementation must be inherent in the process [10]. ISN (W. Couser) The ISN Commission on Global Advancement of Nephrology (ISN-COMGAN) pointed out the focus shifting from emphasis on renal replacement therapy to the “new nephrology”—the early check details detection and prevention of kidney disease Palbociclib order and its cardiovascular consequences [4]. Core outreach programmes are encompassed under

COMGAN [11]. The ISN Fellowship programme now emphasises training in clinical epidemiology and outcomes research. The ISN Continuing Nephrology Education (CNE) programme supports over 50 educational events each year, reaching over 10,000 health-care workers, with an emphasis on early detection and treatment of CKD. The restructured ISN Sister Centre programme supports 40 centre relationships worldwide aimed at progressing the developing centre through to becoming a regional, independent focus for promotion of all aspects of renal health care. The ISN Research and Prevention Committee has developed the programme for detection and Entospletinib mouse management of CKD, hypertension, diabetes and cardiovascular diseases. Diversity

and specificity of CKD in Asia Speakers dealt with CKD in the COMGAN regions, first from the two most populous countries, China and India, then a mix of developing and developed countries of differing sizes and economies. Highlighted was the urgent need to develop strategies to combat CKD, given the huge population of Asia, the high prevalence of CKD and the poor economic state of much of the region. China (W. Chen) A randomly selected population-based screening Baricitinib study in southern China (both rural and urban) showed 10.6% had proteinuria, haematuria or reduced estimated GFR. Independent risk factors were age, hypertension and diabetes. India (V. Jha) CKD, diabetes and hypertension have been identified as increasing in prevalence in several small surveys. Diabetes is the commonest cause of end-stage renal diseases (ESRD); 73% of ESRD patients present less than 3 months before diagnosis [12]. Korea (H. J. Chin) A nationwide survey from health checks in 39 hospitals indicated a prevalence of CKD stages 1, 2, 3 or more of 1.39, 3.64 and 2.67%, respectively, with very similar risk factors to Western countries, and a particularly high prevalence in the elderly. Nepal (S. K. Sharma) In this country, where renal replacement therapy (RRT) cannot be afforded, a door-to-door screening and intervention programme was conducted. Of 3,218 people over 20, CKD was detected in 10.6%.

RT explored potential oligomerization of FliI. JM coordinated

the work and edited the manuscript. All authors read and approved of the final manuscript.”
“Background Enterococci are part of the normal flora in human intestines and are also a leading cause of nosocomial infections [1, 2]. These organisms are somehow able to migrate from the gastrointestinal tract into the bloodstream and cause systemic infections such as bacteremia and even endocarditis [2–4]. Although many strains of enterococci seem to be harmless commensals, particular subgroups of Enterococcus faecalis and Enterococcus faecium predominate among Erastin chemical structure isolates from nosocomial enterococcal infections. In E. faecalis, numerous factors important for virulence have been characterized. For example, the Fsr system, a homologue of the staphylococcal Agr system, has been shown to be selleck products important for virulence due, at least in part, to its control of gelatinase and a serine protease expression via a quorum-sensing mechanism buy VX-689 [5–7]. Microarray studies also indicated that the Fsr system regulates other genes important for virulence [8], one of which is the locus encoding Ebp pili [8], whose subunits are encoded by the ebp

operon [9]. A non-piliated ebp mutant, producing much less biofilm than the parent strain, was shown to be attenuated in a rat model of endocarditis [9] and in a murine urinary tract infection model [10]. We previously described EbpR as an important activator of the ebpABC operon encoding the pili in E. faecalis OG1RF [11]. Although ebpR is not essential for ebpABC expression, we detected 100-fold less ebpABC mRNA in a ΔebpR mutant compared to the OG1RF parent strain. In addition, even in the presence of an intact ebpR gene, only 5-20% of the cells, grown aerobically in BHI or in TSBG, were found to produce pili (detected by electron microscopy or immunofluorescence) [9, 11]. These results imply that other regulatory

and/or environmental factors may affect pilus production. Bicarbonate is a major element of the mammalian body for reaching and maintaining homeostasis. In equilibrium with CO2, Ribonucleotide reductase H2CO2 and CO3 2-, depending on pH, temperature, and CO2 pressure, bicarbonate does not diffuse freely across the membrane and needs specific transporters [12]. In the stomach, HCO3 – is secreted by the surface mucus cells, where it gets trapped in the mucus and forms part of the mucus-HCO3 – barrier, thereby maintaining a pH gradient of pH 2 in the lumen to pH 7 at the mucosal epithelium interface. Interestingly, some microbial pathogens have been shown to respond in vivo to CO2 (from 5 to 20%) and/or HCO3 – (10-100 mM) by enhancing production of factors important for virulence (Staphyloccocus aureus [13], Vibrio cholerae [14], group A streptococcus [15], Bacillus anthracis [16, 17], Cryptococcus neoformans [18] and Citrobacter rodentium [19]). Regulatory proteins have been described which mediate the CO2/HCO3 – response at the transcriptional level in B.

By comparing three SEM images of Figure 3, one can see that the concentration of PVP has less influence on the yield of silver nanowires when PVPMW=1,300,000 was used. However, it is found that the concentration of PVP contributes to the control of diameter

of the synthesized nanowire. In Figure 3a, there are short nanorods, long nanowires, and some nanoparticles selleckchem (<10%). Figure 3b shows the yield of silver nanowires with uniform diameter and length increased to about 95% which is similar to the result shown in Figure 3c. From the above comparison study, it should be noted that varying the MWs of PVP is more efficient on the shape control of silver nanocrystals than varying the concentrations of PVP. Figure 3 SEM images of silver nanocrystals obtained by varying the concentration of PVP MW=1,300,000 . (a) 0.143 M, (b) 0.286 M, and (c) 0.572 M. Optical property

characterization UV-visible NIR spectrophotometer can also be used to confirm the morphologies of silver nanocrystals. The resonance bands of the plasmonic nanocrystals are mainly dependent on the distribution of the electromagnetic field on the surface of the metal nanocrystals. In other words, metal nanoparticles with check details selleck chemical different shapes and sizes should have different optical signatures. Figure 4a exhibits the extinction spectra of the silver solution with different PVPs at 0.286 M. As shown in Figure 4a, the rodlike shape prepared with PVPMW=8,000 has a broad scattering selleck chemicals llc band from the visible to the near-infrared wavelengths leading to the white color shown in the inset in Figure 1a. Because the structure joined together can trap light effectively [30], such rodlike nanostructure can be used as a hot spot. The extinction

spectra of the silver nanostructure solution using PVPMW=29,000 have a main resonance peak at 430 nm and a shoulder peak at 360 nm corresponding to the nanosphere [17]. In comparison, that of PVPMW=40,000 exhibits a redshift and broader absorption range ascribed to the irregular shapes of the products. In the extinction spectrum of the solution with PVPMW=1,300,000, there are two resonance peaks at 390 and 350 nm belonging to the optical signature of silver nanowire [19]. Figure 4 The optical characteristics of the silver solution. (a) The extinction spectra of the silver nanostructure solution obtained with different PVPs of 0.286 M. (b) The extinction spectra of the silver nanostructure solution obtained at different concentrations of PVPMW=29,000, (c) The extinction spectra of the silver nanostructure solution obtained at different concentrations of PVPMW=40,000. (d) The extinction spectra of the silver nanostructure solution obtained at different concentrations of PVPMW=1,300,000. Figure 4b,c,d shows the extinction spectra of the silver nanostructure solution obtained at different concentrations of PVPMW=29,000, PVPMW=40,000, and PVPMW=1,300,000, respectively.

The properties of graphene, including a high intrinsic mobility [1, 2], a large theoretical specific surface area, and a high chemical stability, are potentially useful in

applications ranging from chemical sensors to transistors [3–8]. Toward exploiting Temsirolimus order these unique properties of graphene, several research groups have attempted to fabricate large-scaled graphene oxide sheets [9–12]. Graphene oxide (GO) is a layered material consisting of hydrophilic oxygenated graphene oxide sheets bearing oxygen functional groups on their basal planes and edges [13]. It is a useful platform for fabricating functionalized graphene that can potentially confer improved mechanical, thermal, or electronic properties. The numerous chemical functionalities on a GO surface are expected to JNJ-26481585 purchase readily lend themselves to further chemical see more functionalization. Graphene-based materials, therefore, show promise in a variety of technological applications. The use of GO surfaces as catalysts of synthetic transformations is a relatively new research area

with outstanding potential. Current efforts are directed toward harnessing the oxygen carriers present on GO surfaces as heterogeneous catalysts [14–16]. In this study, we systematically compared and investigated the oxidation of aniline to form azobenzene on monolayer graphene (EG) or graphene-oxide-like (GOx) surfaces fabricated with benzoic acid. Moreover, we focus on examining the difference between EG and GOx surfaces in one substrate, simultaneously.

Raman spectroscopy and high-resolution photoemission spectroscopy (HRPES) were used to characterize the surface-bound products. The carboxyl groups introduced onto the graphene surface upon oxidation Calpain by benzoic acid to GOx allowed aniline to react with the oxygen carriers. The oxidation of aniline proceed via a reaction between the aniline amine groups and the oxygen groups on the GOx surface under ultra-high vacuum (UHV) conditions maintaining a 365-nm UV light exposure. Generally, it is hard to distinguish the difference between EG and GOx surfaces in one substrate due to the large size of the HRPES beam. Hence, no previous systematic experimental studies have examined the oxidation of aniline on a GOx surface. However, this study is meaningful with regards to indicating this distinctive difference using the feature of micro Raman spectroscopy. Methods A Si-terminated 6H-SiC(0001) substrate (Cree Research, Durham, NC, USA) was used to fabricate EG. The substrate was degassed, annealed at 1,200 K under a Si flux (1 Å/min), and graphitized at temperatures up to 1,500 K (for 2 min) to produce a monolayer of graphene (EG). The annealing temperature was monitored using an infrared pyrometer (with an emissivity of 0.9). A GOx surface was fabricated by exposing the EG surface to benzoic acid (Sigma Aldrich, purity, 97%, St. Louis, MO, USA).

Cell morphology was evaluated using a BX60 fluorescence microscope equipped with a DP50 digital camera (Olympus, Japan). Mitochondrial membrane potential (ΔΨm) assay Mitochondrial membrane selleck kinase inhibitor potential was assessed by flow cytometry using JC-1 (5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethylbenzimidazolocarbocyanine iodide; Sigma). JC-1 undergoes potential-dependent accumulation in mitochondria. In healthy cells, the dye accumulates in mitochondria, forming aggregates with red fluorescence (FL-2 channel), whereas in apoptotic cells the dye remains in the cytoplasm in a monomeric form and emits green fluorescence (FL-1 channel). Cells were harvested by centrifugation 48 h post-treatment, suspended in 1 ml

of complete culture medium at approximately 1 × 106 cells/ml and incubated with 2.5 μl JC-1 solution in DMSO (1 mg/ml) for 15 min at 37°C in the dark. Stained

cells were washed with cold PBS, suspended in 400 μl of PBS and then examined with a FACSCalibur flow cytometer equipped with CellQuest software (BD Biosciences, San Jose, CA, USA). PARP cleavage assay Caspase-3 and caspase-7 cleave poly(ADP-ribose) polymerase (PARP). PARP cleavage was detected by flow cytometry using Anti-PARP CSSA FITC Apoptosis Detection Kit (Invitrogen) IWR-1 supplier according to manufacturer’s protocol. The FITC-conjugated anti-PARP antibody employed in the kit specifically recognizes the 85 kDa fragment of cleaved PARP. The cells meant for the assay were harvested 48 h post-treatment and washed twice with PBS just before use. The level of cleaved PARP protein was expressed as fluorescence intensity that was assessed using CellQuest and the free WinMDI software package written by Joseph Trotter of the Scripps Institute Protein tyrosine phosphatase (La Jolla, CA, USA). Cell cycle analysis After exposure to the tested compounds, the cells were washed with cold PBS and fixed at −20°C in 70% ethanol for at least 24 h. Next, the cells were washed free of ethanol and stained with 50 μg/ml PI and 100 μg/ml RNase solution in PBST (PBS supplemented with 0.1% v/v Triton X-100) by 30 min incubation

in the dark at room temperature. Cell DNA content and the distribution of the cells in different phases of the cell cycle were determined by flow cytometry employing MacCycle (Phoenix Flow Systems, San Diego, CA, USA) and CellQuest software packages. Flow cytometry Flow cytometry analyses were run on a FACSCalibur flow cytometer (BD Biosciences, San Jose CA, USA), and analyzed by CellQuest software (BD Biosciences, San Jose, CA, USA) and WinMDI 2.9 software. The DNA histograms Temsirolimus order obtained were analyzed using the MacCycle software. Results Chemistry The N-substituted pentabromobenzylisothioureas were obtained following the direct strategy shown in Fig. 1. The reaction was performed using pentabromobenzyl bromide and the respective thiourea. The products—isothiouronium bromides—crystallized from the reaction mixture after concentrating. The compounds were characterized using 1H-NMR and elemental analyses.

At diagnosis, 75% are non-invasive bladder cancer. The invasive bladder cancers may spread outside the bladder and affect other organs. Bladder cancer’s staging, treatment and prognosis depend on how deeply it has invaded urinary bladder [3]. Fortunately, about 80% of patients with non-muscle invasive disease can be successfully treated using the surgery.

Historically, two-thirds of patients have tumour recurrence within 5 years. High-grade tumours have a significantly worse prognosis. Both high-grade T1 tumours and carcinoma in situ have the potential to progress and even metastasize [4]. Patients with invasive bladder cancer require a radical cystectomy. Controversy exists as to whether neoadjuvant or adjuvant chemotherapy improves survival in patients with invasive bladder cancer, despite a number of randomised controlled trials. So far selleck chemicals Enzalutamide order there are no data to confirm what is the best combination of treatments (neoadjuvant chemotherapy, adjuvant with or without radiotherapy) to treat invasive bladder cancer [5]. The modest results with currently drugs, suggest the urgent need to identify new agents [6]. Sirolimus

is a macrocyclic lactone that was first discovered as a product of the soil bacteria Streptomyces hygroscopicus. It was originally used as an immunosuppressant drug to help prevent rejection in organ transplantation, particularly in kidney transplant operations, but the authors of a number PD184352 (CI-1040) of recent reports have indicated that it may have other potential biological effects as an anti-cancer medicine [7, 8]. Both the immunosuppressive and anti-cancer properties of sirolimus are due to the inhibition of the mammalian target of the sirolimus (mTOR) signalling pathway, which controls mRNA translation

and induces angiogenesis and cell proliferation. Angiogenesis and a high proliferative index correspond to a poor prognosis for urothelial bladder cancer patients [9, 10]. Sirolimus forms a complex with the immunophilin prolyl isomerase FK binding protein complex (FKBP-12) that binds with high affinity to mTOR [11, 12]. This interaction inhibits mTOR kinase activity and subsequently decreases the phosphorylation of 4E binding protein-1 and the inhibition of the 40S ribosomal protein p70 S6 kinase [13–15]. Sirolimus’s antineoplasic effects have been related to its capacity to inhibit the translation learn more machinery involved in the regulation of G1- to S-phase transition in cell cycle [16, 17]. Cell growth and proliferation in numerous cancer types are often regulated by the mammalian target of sirolimus (mTOR) pathway through p7056 kinase, ribosomal S6 protein, and eukaryotic initiation factor 4 E-binding protein 1 [18]. Recently there has been an enormous increase in our understanding of the molecular mechanisms underlying sirolimus’s therapeutic anti-cancer properties. Alterations in the pathway regulating mTOR occur in many solid malignancies including bladder cancer.

More recently, a wave of randomized clinical trials with superiority design was successfully completed, and novel

active drugs such as docetaxel [6], S1 [7] and trastuzumab [8] changed the landscape of the clinical management of gastric cancer. Other agents including CP-868596 molecular weight capecitabine [9], oxaliplatin [10] and this website irinotecan [11] have proven antitumor activity, thus expanding the spectrum of therapeutic options available in the first-line setting. Even though novel active drugs and combinations entered the therapeutic scenario, second-line treatment has been historically considered largely empirical. Furthermore, geographic distributions exist in chemotherapy administration beyond first-line, being prevalently adopted in Asian countries. Indeed, the rates of administration of subsequent

chemotherapy significantly differed among phase III studies conducted in front-line, spanning from 14% in the UK REAL 2 study [9] to 75% in the Japanese SPIRITS trial [7]. The clinical proof-of-concept for second-line chemotherapy stemmed from two recent randomized phase III trials, demonstrating the superiority of second-line monotherapy (docetaxel or irinotecan) over BSC [12, 13]. Nevertheless, it is foreseeable that a widespread adoption of second-line chemotherapy will further be limited by Geneticin concentration multiple factors. Firstly, the non-Asian study was prematurely closed when only one-third of the preplanned 120 patients were enrolled [12]. As a result, evidence supporting second-line chemotherapy in non-Asian patients are

still scattered being mostly extrapolated from the Korean study. Secondly, the different biological background of gastric cancer arising in Asian and Western patients must be taken into account as a potential confounding factor [14]. Finally, single-agent therapy may result suboptimal, at least for patients with good performance status. On this basis, we conducted a retrospective study in order to evaluate the activity and safety of FOLFIRI given as a second-line therapy in a cohort Thalidomide of docetaxel-pretreated metastatic gastric cancer patients. Methods The study population was composed by patients with metastatic gastric or GEJ cancer who experienced disease progression on or after first-line docetaxel-containing chemotherapy. Patients were treated at three Italian cancer centers between 2005 and 2012. The majority of patients was selected from the “Regina Elena” National Cancer Institute, Rome. Medical records were reviewed in order to obtain information on demography, treatment received, safety and outcomes. Patients with histologically confirmed, docetaxel-pretreated metastatic gastric cancer who received FOLFIRI in second line were eligible for the study.