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R, Yokota A, Kamitsuji Y, Takeuchi M, Kuroda J, Tanaka F, Yoshikawa T, Maekawa T: Administration of PLK-1 small interfering RNA with atelocollagen prevents the growth of liver metastases of lung cancer. Mol Cancer Ther 2008, 7: 2904–12.CrossRefPubMed 18. Bu Y, Yang Z, Li Q, Song F: Silencing of polo-like kinase (Plk) 1 via siRNA causes inhibition of growth and induction of apoptosis in human esophageal cancer cells. Oncology 2008, 74: 198–206.CrossRefPubMed 19. Fletcher L, Muschel RJ: The centrosome and the DNA damage induced checkpoint. Cancer Lett 2006, 243: 1–8.CrossRefPubMed 20. Pectasides D, Kamposioras K, Papaxoinis G, Pectasides E: Chemotherapy for recurrent cervical cancer. Cancer Treat Rev 2008, 34: 603–13.CrossRefPubMed Dasatinib in vitro 21. Tao X, Hu W, Ramirez PT, Kavanagh JJ: Chemotherapy for recurrent and metastatic cervical cancer.

Gynecol Oncol 2008, 110: S67–71.CrossRefPubMed Authors’ contributions YZ and YL performed the entire experiment. YY and HZ participated in partial experiment (flow cytometric analysis). JX performed the statistic analysis. HL and CY designed the study and prepared the manuscript. All authors read and Metalloexopeptidase approved the final manuscript.”
“Background Chemotherapy-induced nausea and vomiting is a significant side effect of cancer therapy for many years[1]. CR for acute period and delayed period in the patients receiving highly and moderately emetogenic chemotherapy with the use of 5-HT3 receptor antagonists plus dexamethasone is respectively 68%-90% and 47%-56%. Despite the use of 5-HT3 receptor antagonists plus dexamethasone

has significantly improved the control of the acute CINV, the complete response for the delayed nausea and vomiting has not significantly improved comparing with the sole use of dexamethasone[2]. Recent studies have demonstrated additional improvement in the control of acute and delayed CINV with the use of two new agents, aprepitant, the first agent available in the new drug class of neruokinin-1 receptor antagonists, and palonosetron, a second-generation 5-HT3 receptor antagonist [3–5]. Because without of the application of the two new drugs in China, we still have many chance for improvement with the addition or substitution of new agents in current antiemetic regimens.

Ten

of these segregants were analysed and shown to carry null mutations in the rpoS ORF. It is also demonstrated that the IS1 insertion in rssB is the main factor that upregulates rpoS in MC4100. Results and Discussion Segregation of rpoS mutants in LB stabs LB stabs of MC4100TF have been sent from Ferenci’s laboratory in Australia to Spira’s laboratory in Brazil by air mail on three different occasions. Upon arrival bacteria were streaked on LB agar and isolated colonies were checked for their RpoS status by iodine staining (glycogen accumulation is enhanced by RpoS [23]). MC4100TF stains darkly with iodine, but many colonies from these shipments displayed heterogeneity in iodine staining; this generally means variations in RpoS levels [17, 18]. The third shipment consisted of two LB stabs, one containing MC4100TF and the other one strain BW2952 (MC4100TF carrying a mal::lacZ fusion, but otherwise identical to MC4100TF). Bacteria were Alisertib ic50 removed from each stab, suspended in 0.9% NaCl, diluted and plated on LB agar and stained with iodine. The proportion of low-staining Ulixertinib in vitro colonies in these stabs was between 29% and 61%. This prompted us to ask whether the shipping conditions to which the bacteria were exposed during the transcontinental flights selected mutations that caused the loss of the high-staining phenotype. To mimic the conditions during transport, a single fresh

colony of MC4100TF was inoculated into an

LB stab, and incubated at room temperature for 7 days. Following the incubation period bacteria were streaked on minimal medium plates supplemented with the alkaline phosphatase (AP) substrate X-P (TGP + X-P); AP expression is inversely almost correlated with RpoS level [18]. Several colonies were light blue, but others showed a more intense blue colour, indicating a low-RpoS status (Figure 1A). Ten of these low-RpoS segregants were isolated and further analysed. Figure 1 Heterogeneity and RpoS status of MC4100TF segregants. (A) Growth of MC4100TF colonies isolated from an LB-stab on TGP +X-P (minimal medium plate supplemented with X-P, a chromogenic substrate for alkaline phosphatase). Light-blue colonies are high-RpoS and the others with a more intense blue colour are low-RpoS segregants. Ten of these low-RpoS segregants were isolated and further analysed. Patches of overnight cultures of MC4100TF segregants (1-10), MC4100TF and MC4100BS were grown on (B) LB-agar and stained with iodine for the detection of glycogen accumulation and on (C) TGP+X-P plates. (D) Bacteria grown overnight in LB medium were assayed for RpoS by immunoblotting with monoclonal anti-RpoS antibodies. 1-10, MC4100TF segregants; BS, MC4100BS; TF, MC4100TF. The segregants were tested for RpoS-dependent phenotypes (iodine staining and AP basal activity), for RpoS concentration by immunoblotting and for the presence of the IS1 insertion in rssB (MC4100TF is rssB::IS1).

The TEM images of the RGO-GeNPs showed that the GeNPs with diameters of 200 nm were deposited on the basal planes of RGO with less wrinkles in Figure 1c,d. The reasons that caused wrinkle reduction were that the GeNPs adsorbed on the reduced graphene oxide layers resulted in the stretching Opaganib of its wrinkles, and under the action of reducing agent NaBH4, the hydrophilic group -COOH,-OH, etc. on the surface of GO decreased [26] and the hydrogen bonding lowered, causing a reduction of the wrinkles. When the reduction was carried out in the presence of PSS, the average size of the GeNPs further decreased, and the dispersibility has significantly improved, as shown in Figure 1e,f.

An authentic photograph of the PSS-RGO-GeNP solution was given in the inset of Figure 1e. Stable aqueous dispersibility of RGO-GeNPs was further improved in the presence of PSS. Figure 1 TEM images of GO, RGO-GeNPs and PSS-RGO-GeNPs at different magnifications. (a,b) GO. (c,d) RGO-GeNPs. (e,f) PSS-RGO-GeNPs. Formation mechanism of RGO-GeNPs Figure 2 showed a schematic illustration of the synthesis route for the RGO-GeNPs and PSS-RGO-GeNPs. The formation

process of the nanocomposites could be divided into two stages. In the first stage, the oxygen-containing groups on GO could also provide plentiful sites to anchor GeO3 2- and make them enrich in some places. Consequently, GeO3 2- was homogeneously dispersed in GO by ultrasonic treatment. In the

RAD001 second stage, the GO nanosheets and the Ge ions could be reduced in situ by sodium borohydride, resulting in GeNP loading on graphene nanosheets to fabricate the RGO-GeNPs. Furthermore, stable black aqueous dispersions ADP ribosylation factor of PSS-RGO-GeNPs was obtained by coating an amphiphilic PSS. Figure 2 Schematic illustration of the preparation of the RGO-GeNPs and the PSS-RGO-GeNPs. The stable dispersions of the PSS-RGO-GeNPs were also analyzed by UV–vis spectroscopy. The UV–vis spectrum of the PSS-RGO-GeNPs in water possesses similar features as that of the PSS itself at approximately 262 nm (Figure 3a). A rising absorption edge from 550 nm into the UV gives an evidence of the PSS-RGO-GeNPs. The FTIR spectrum of RGO-GeNPs at 781 cm-1 showed the formation of Ge-N bond, clearly indicating the interaction between RGO and GeNPs. Although the FTIR spectrum of PSS-RGO-GeNPs exhibits weak PSS absorption features, it only confirms the presence of the PSS component (Figure 3b). Figure 3c showed a powder XRD pattern for a representative sample of as-synthesized GeNPs, which was in agreement with the standard value for Ge (JCPDS card no. 89–5011). An elemental composition analysis employing EDS showed the presence of a strong signal from the Ge atoms, together with C atom and O from the graphene molecules, whereas a Cu atom signal was ascribed to the supporting grid (Figure 3d).

3 to 0.5 times higher compared to the intensity of peaks for their sol-gel-developed WO3 counterparts. This finding has confirmed the thickness-dependent properties of ultra-thin Q2D WO3. Following sintering at 550°C, there is a reduction in the spectral

line width consistent with greater crystalline phase formation. Well-defined bands 712 and 802 cm-1 modes exhibit significant changes, with the mode at 712 cm-1 being particularly sensitive to the cation intercalation [45]. Consequently, these results and observations open up a possibility for the future potential use of 2D WO3 as suitable nanomaterial for various sensing platforms [1, 10, 46] and reaffirmed that the sintering temperature of 550°C more suitable for synthesis of 2D WO3 than 650°C aiming their further exfoliation and cation intercalation. FK228 supplier Electrical CSFS-AFM measurements revealed and further proved the thickness-dependent properties of ultra-thin Q2D WO3 . I-V curves for the sol-gel-developed WO3 nanostructures sintered at 550°C and for exfoliated ultra-thin Q2D WO3 nanoflakes sintered at 550°C and 650°C are presented

in Figure 8. The current is measured by averaging the data values on the current image corresponding to the same voltage. There were neither significant oxidation nor Proteasome activity reduction peaks recorded during scans. Non-linear behaviour for all samples was observed. This behaviour is typical for the semiconductor nature of the WO3 [21]. However, the electrical performance showed significant difference between the sol-gel-developed WO3 nanostructures and exfoliated Q2D WO3 nanoflakes. It is clearly exhibited that the measured current for Q2D WO3 was about from 5 (650°C) to 10 (550°C) times higher than

Amylase the measured current for the sol-gel-developed WO3 nanostructures. This fact confirms that the CFSF-AFM current originates from the local properties of the material at the tip-sample contact. The higher electrical activity and therefore greater currents for the exfoliated Q2D WO3 nanoflakes appeared to be more related to higher heterogeneous electron exchange rate caused by the quantum confinement effects within the few-layers limit [47]. Consequently, Q2D WO3 nanoflakes can offer reduced power dissipation because of smaller short channel effects [48]. Furthermore, the electrical measurements have also proved that the sintering temperature of 550°C is more suitable and superior for the development of Q2D WO3 nanoflakes with enhanced properties. Figure 8 I-V curves derived from CSFS-AFM images for sol- gel-developed WO 3 and exfoliated Q2D WO 3 nanoflakes. These I-V curves have been obtained by averaging the current values recorded independently for different DC sample bias. LSV voltammograms for commercial WO3 (surface area = 3 m2 g-1) [49] and Q2D β-WO3 nanoflakes sintered at 550°C were recorded in a potential region of +0.1 to -0.2 V at a scan rate of 50 mV s-1 in 1.0 M H2SO4 solution.

Prostaglandins, acting through different receptors of the GPCR family, regulate many cellular functions [27]. In epithelial cells, prostaglandins often enhance proliferation and survival, and several lines of evidence implicate them in oncogenesis [28]. In many tumours, cyclooxygenases (COX-1 and COX-2), which catalyze the rate-limiting step in prostaglandin synthesis, are overexpressed, and the levels of prostaglandins, notably prostaglandin E2 (PGE2), are elevated [28–31]. In hepatocytes,

PGE2 and other prostaglandins enhance Opaganib supplier DNA synthesis [15, 32–34], and COX-2 is overexpressed in many hepatocarcinomas [35, 36]. In the study presented here we examined the Morris hepatocarcinoma cell line MH1C1, which was chosen due to its responsiveness to both EGF and the prostaglandins PGE2 and PGF2α, and investigated the interaction between the pathways mediated by prostaglandin receptors and EGFR. We previously observed that while there was no evidence of transactivation of EGFR induced by prostaglandins or other GPCR agonists in hepatocytes, PGE2 induced phosphorylation of the EGFR in the MH1C1 cells [37, 38]. We have now investigated further the signalling mechanisms involved in this effect. Methods Chemicals Dulbecco’s Modified Eagle’s Medium, Dulbecco’s phosphate-buffered saline, William’s Medium E, glutamine, and Pen-Strep (10.000 U/ml) were from Lonza(Verviers,

Belgium). HEPES was from Gibco (Grand Island, NY). Dexamethasone, insulin, bovine serum albumin, collagen (type I, rat tail), prostaglandin F2α (Tris salt) and epidermal growth factor

(EGF) were obtained from Sigma-Aldrich Selleckchem CH5424802 (St.Louis, MO). GF109203X ([2-[1-(3-dimetylaminopropyl)-1 H-indol-3-yl]-male-imide]) and GM6001/Galardin (N-[(2R)-2 (hydroxamidocarbonylmethyl)-4-methylpentanoyl]-L-tryptophan methylamide) were from Calbiochem (San Diego, CA). Gefitinib was a gift from AstraZeneca (Cheshire, UK). [6-3 H]thymidine (20–30 Ci/mmol) and myo-[2-3 H]inositol (15.0 Ci/mmol) were from PerkinElmer (Boston, MA). AL8810 (9α,15R-dihydroxy-11β-fluoro-15-(2,3-dihydro-1 H-inden-2-yl)-16,17,18,19,20-pentanor-prosta-5Z,13E-dien-1-oic acid),L161982 (N-[[4'-[[3-butyl-1,5-dihydro-5-oxo-1-[2-(trifluoromethyl)phenyl]-4 H-1,2,4-triazol-4-yl]methyl][1,1'-biphenyl]-2-yl]sulfonyl]-3-methyl-2-thiophenecarboxamide), (+)fluprostenol, PJ34 HCl and prostaglandin E2 (PGE2) were from Cayman Chemical (Ann Arbor, MI). SC51322 (8-chloro-2-[3-[(2-furanylmethyl)thio]-1-oxopropyl]hydrazide, dibenz[b,f][1,4]oxazepine-10(11 H)-carboxylic acid) was obtained from BIOMOL Research Laboratories (Plymouth Meeting, PA). The Src inhibitor CGP77675 was a gift from Novartis Pharma AG (Basel, Switzerland). All other chemicals were of analytical quality. Antibodies against phosphorylated AktSer473, total Akt, dually phosphorylated ERKThr202/Tyr204, GAPDH and phospho-ShcTyr239/240 were obtained from Cell Signaling Technology (Boston, MA).

2; ± 0.8 0.65 251 ± 35 −1.0; ± 3.1 0.56 Unclear (1/91/7) PC+G 13:13.3 ± 36.2 0.6; ± 0.9 0.25 248 ± 41 −2.4; ± 4.9 0.38 Likely trivial (0/77/23) (PC V PC+G) – −0.4; ± 0.9 0.49 – 1.4; ± 4.2 0.56 Unclear (14/85/1) Descent 2 37.5 – 46.4 CON 12:54.9 ±

37.3 – - 270 ± 42 – - – PC 12:55.7 ± 32.3 0.1; ± 0.8 0.78 267 ± 35 −0.6; ± 4.1 0.80 Unclear (1/95/4) PC+G 12:52.5 ± 35.3 −0.3; ± 1.1 0.63 273 ± 44 1.8; ± 6.4 0.61 Unclear (13/84/3)     (PC V PC+G) – 0.4; ± 0.7 0.29 – −1.7; ± 4.8 0.53 Likely trivial (0/92/8) Note: CL = confidence limits; OR = odds ratio; P = probability; Outcomes were assessed by using the following criteria: trivial <0.4%, small 0.4 – 1.1%, moderate 1.2-2.0%, large 2.1-3.2%, very large 3.3 – 5.1%, and extremely large >5.2% change in performance time. Rectal

temperature towards the end XL184 order of the stabilization phase (t=−65 min before the TT) was considered to be the baseline value for each trial. At this time point, there were no differences in rectal temperature between trials (P>0.05, Figure 1a). Relative change in rectal temperature at the end of the warm-up and just prior to Dabrafenib ic50 the time trial was significantly lower in the PC+G compared with the CON trial (P<0.05). Relative change in rectal temperature continued to rise during the time trial in all trials, such that there was no difference in relative change in rectal temperature between treatments during this phase (CON, 1.33 ± 0.27°C.h-1; PC, 1.45 ± 0.32°C.h-1; PC+G, 1.39 ± 0.26°C.h-1; P>0.05). Figure 1b shows the changes

in heart rate during each trial. Figure 1 Relative change in rectal temperature (a) and heart rate (b) throughout the experimental trial. Significant time effects from t=−65 min before TT (arrow) are denoted by dark symbols. Significant time effect from t=−180 min to t=−150 min following drink ingestion with and without glycerol ingestion denoted by alpha (α). Significant effects of precooling treatment (1; PC and 2; PC+G) compared with CON are denoted by a star symbol (*1,*2, ADAM7 respectively). Significant interaction between PC and PC+G treatments are denoted by a hash (#) symbol. Collection of ‘first-waking’ urine samples on the morning of each trial, mean changes in body mass, fluid consumed and urine volume produced during the trials are presented in Table 2. The time course of urine production represented in Figure 2a and the corresponding specific gravity of these samples is represented in Figure 2b. Due to the inclusion of slushie ingestion being part of the precooling intervention, the amount of sports drink ingested by subjects inside the heat chamber (t=−120 min to end of the time trial or ~3.5 h) was greater in PC (1,335 ± 211 ml) and PC+G (1,356 ± 206 ml) trials, compared with the CON (299 ± 214 ml, P<0.001) trial, which provided a further ~80 g of carbohydrate.

*polymorphism MSH6 gene (c.116G > A) associated with slight increased risk of XL184 research buy CRC in males. **VUS: variant of uncertain clinical significance. ***confirmed after repeating the test. ****NE: not evaluable. In group B, IHC showed MMR deficiency in 24 out of 40 patients (60%) and MSI –H in 21 (52.5%). Germline mutation analysis was performed in all

24 patients and a deleterious mutation in the corresponding IHC lacking protein was detected in 15 (62.5%), 8 in MLH1 gene and 7 MSH2, all these patients were MSI-H. IHC detected an altered expression of MSH2 in another MSI-H patient, whereas the deleterious mutation was found in MLH1. In the remaining 5 out of 21 MSI –H patients the germline mutation analysis revealed: A deleterious mutation in the MSH2 gene in three patients with normal or not assessable MMR expression at IHC. A missense variant of uncertain clinical significance of MLH1 gene: c.376 T > A. (p.Tyr126Asn) in one case with MLH1 altered expression at IHC. The available data on the clinical impact of this variant are so far not unequivocal [38]. No deleterious mutation in the four MMR genes analyzed was found in one case with lack of expression selleck chemicals llc of MSH2 at IHC. In Group C, IHC revealed normal expression of

MMR protein and MSS in all patients (Table 2). Diagnostic accuracy of molecular screening tests and of clinical variables In our series, we observed the following diagnostic accuracy Branched chain aminotransferase of molecular screening tests in predicting germline mutations of MMR genes: MSI analysis had a sensitivity of 100%, a specificity of 94.8% (CI 86.2-100) a diagnostic accuracy of 95.7% (CI 92.1-99.4), a PPV of 80% (CI 72.0-88.0), a NPV of 100% and an AUC of 0.97 (standard error, SE = 0.01); IHC had a sensitivity of

75% (IC 66.0-84.0), a specificity of 85,6% (CI 72.8-98.4) a diagnostic accuracy of 83.8% (CI 77.1-90.4), a PPV of 51.7% (CI 41.8-61.7), a NPV of 94.3% (CI 84.2-100) and an AUC of 0.80 (SE = 0.05) (Figure 1). Figure 1 ROC curve analysis of molecular screening tests. The two ROC curves represent the diagnostic accuracy of Microsatellite Instability analysis (MSI) and Immunoistochemistry (IHC) to identify and select MMR deficient early onset colorectal cancer patients for mutational analysis. Accuracy is measured by the Area Under the Curve (AUC) and is significantly higher in MSI than IHC (AUC 0.97 vs 0.80, p = 0.001). Considering the clinical variables gender, stage, cancer site and multiplicity, the presence of extracolonic cancers and Amsterdam II criteria, a logistic regression model was performed to evaluate the independent variables predictive of MSI-H phenotype in early onset CRC. The unique factors associated with MSI-H were Amsterdam II Criteria (P < 0.0001) and right-sided CRC (P < 0.0001). In fact, in the Amsterdam group we observed that 80.9% of right-sided vs 26.

These variables were included in the final RDA (Fig. 2a). Logged forest and grass cover were more strongly associated with axis 1 which largely comprises a gradient of occurrence of Tropical-climate Specialists and Subordinate Camponotini, both being found more commonly in logged forest with high grass cover (Fig. 2a). The remaining significant environmental variables (old growth forest, humus depth, leaf litter depth, forest quality, slope, small saplings cover, and bare ground cover) were associated with axis 2 (Fig. 2a; Table 5a). In the latter case, all variables were positively associated, except for bare

ground cover which was negatively associated. Ant functional groups were variable in their associations with this disturbance gradient (Fig. 2a) PD-0332991 research buy with some functional groups positively correlated with axis 2 and therefore low disturbance sites (Generalised Myrmicinae; Specialist Predators; and to a lesser extent, Hot-climate Specialists), and some negatively correlated with axis 2 and therefore

associated with high selleck disturbance sites (Opportunists; Cryptic species; and to a lesser extent Dominant Dolichoderinae). Fig. 2 Ordination tri-plots showing redundancy analysis (RDA) of ant functional group occurrence (a) and termite feeding group occurrence (b) and marginally significant environmental variables in quadrats across all habitat types. For ants (a) axis 1 explained 17.6 % of assemblage variation and axis 2 explained an additional 11.1 % of the variation. For termites b axis 1 explained 36.3 % of the variation and axis 2 accounted for an additional 2.5 % of variation. Abbreviations for functional and feeding groups are as for Fig. 1, with Grp I–Grp IV representing termite Groups I–IV Table 5 Intraset correlation coefficients of Amrubicin marginally significant environmental variables for the first two axes of the RDA for functional and feeding

group structure of ants and termites Ants/termites Environmental variables Axis 1 Axis 2 a. Ants Forest quality −0.114 0.621 Slope −0.422 0.546 Small saplings cover 0.254 0.449 Leaf litter cover 0.587 0.639 Bare ground cover −0.362 −0.428 Grass cover 0.390 −0.367 Humus depth 0.043 0.667 b. Termites Forest quality 0.868 −0.181 Slope 0.593 0.011 Tall poles cover 0.695 0.103 Leaf litter cover 0.370 −0.353 Bare ground cover −0.384 0.692 Old growth forest (OG) and logged forest (LF) were omitted because they were nominal variables For termites, forest quality, slope, cover of tall poles, leaf litter and bare ground were strongly associated with feeding group structure (Table 4) and were the variables included in the final RDA (Fig. 2b). Old growth forest, forest quality, slope, tall poles and leaf litter cover were positively associated with axis 1, while logged forest and bare ground cover had negative axis 1 scores (Fig. 2b; Table 5b).

6750.13147). Electronic supplementary material Additional file 1: Figure S1: Formulation

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Although the results of this study are of value in supporting the use of oxaliplatin in gastric cancer, the main question is how the treatment of this disease might be significantly improved in an era in which chemotherapy-related benefits seem to have reached a plateau. Furthermore,

current practice is increasingly shifting toward to a more individualized treatment approach. In this regard, several molecularly targeted agents have proved effective in combination with chemotherapy in advanced gastric carcinoma [17]. Given the activity and tolerability, as well as the short time to response (median, 6 weeks), observed in this study, EOD may represent an appropriate regimen HDAC inhibitor to be used also in the neoadjuvant setting and in combination with targeted agents. However, to better define the role of this combination comparative trials with other active regimens in gastric cancer (e.g. EOX, FLO) should be carried out. References 1. Kamangar F, Dores GM, Anderson WF: Patterns of cancer incidence, mortality, and prevalence across five continents: defining priorities

to reduce cancer disparities in different geographic regions of the world. J Clin Oncol 2006, 24: 2137–2150.CrossRefPubMed 2. Ferlay J, Autier P, Boniol M, Heanue M, Colombet M, Boyle P: Estimates of the cancer incidence and mortality in Europe in 2006. Ann Oncol 2007, 18: 581–592.CrossRefPubMed 3. Wagner AD, Grothe W, Haerting J, Kleber Selleck FK506 G, Grothey A, Fleig WE: Chemotherapy in advanced gastric cancer: a systemic review and meta-analysis based on aggregate data. J Clin Oncol 2006, 24: 2903–2909.CrossRefPubMed 4. Van Cutsem E, Velde C, Roth A, Lordick F, Köhne CH, Cascinu S, Aapro M: Expert opinion on management of gastric and gastro-oesophageal junction adenocarcinoma on behalf of the European Organisation for Research and Treatment of Cancer (EORTC)-gastrointestinal cancer group. Eur J Cancer 2008, 44: 182–194.CrossRefPubMed 5. Louvet C, André T, Tigaud JM, Gamelin E, Douillard next JY, Brunet R, Francois E, Jacob JH, Levoir D, Taamma A, Rougier P, Cvitkovic E, de Gramont A: Phase II study of oxaliplatin, fluorouracil, and folinic acid in locally

advanced or metastatic gastric cancer patients. J Clin Oncol 2002, 20: 4543–4548.CrossRefPubMed 6. Al-Batran SE, Atmaca A, Hegewisch-Becker S, Jaeger D, Hahnfeld S, Rummel MJ, Seipelt G, Rost A, Orth J, Knuth A, Jaeger E: Phase II trial of biweekly infusional fluorouracil, folinic acid, and oxaliplatin in patients with advanced gastric cancer. J Clin Oncol 2004, 22: 658–663.CrossRefPubMed 7. De Vita F, Orditura M, Matano E, Bianco R, Carlomagno C, Infusino S, Damiano V, Simeone E, Diadema MR, Lieto E, Castellano P, Pepe S, De Placido S, Galizia G, Di Martino N, Ciardiello F, Catalano G, Bianco AR: A phase II study of biweekly oxaliplatin plus infusional 5-fluorouracil and folinic acid (FOLFOX-4) as first-line treatment of advanced gastric cancer patients.