Christophe Borg

University of Franche-Comté, Becoinson, Franche-Comté, France

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Publications (85)449.77 Total impact

  • Marine Jary, Dewi Vernerey, Thierry Lecomte, Erion Dobi, Francois Ghiringhelli, Franck Monnien, Yann Godet, Stefano Kim, Olivier Bouche, Serge Fratte, Anthony Goncalves, Julie Leger, Lise Queiroz, Olivier Adotevi, Franck Bonnetain, Christophe Borg
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    ABSTRACT: Background: Baseline prognostic biomarkers stratifying treatment strategies in first-line metastatic colorectal cancer (mCRC) are lacking. Angiopoietin-2 (Ang-2) is proposed as a potential biomarker in several cancers. We therefore decided to establish the additional prognostic value of Ang-2 for overall survival (OS) in first-line mCRC patients. Methods: We enrolled 177 patients treated with a bevacizumab containing chemotherapy in two prospective phase II clinical trials. Patient plasma samples were collected at baseline. Enzyme-linked immunosorbent assays were used to measure Ang-2. Results: The multivariable Cox model identified increased LDH (HR=1.60, 95%CI: 1.04-2.45, p=0.03) and Ang-2 log-transformation level (HR=1.59, 95%CI: 1.14-2.21, p=0.0065) as two significant independent OS prognostic factors. It exhibited good calibration (p=0.8) and discrimination (C-index: 0.64; 95%CI: 0.58-0.68). Ang-2 parameter inclusion in the GERCOR reference model significantly and strongly improved its discriminative ability since the C-statistic increased significantly from 0.61 to 0.63 (bootstrap mean difference=0.07, 95%CI: 0.069-0.077). Interestingly, the addition of Ang-2 binary information with a 5 ng/mL cut-off value to the GERCOR model allowed the reclassification of intermediate-risk profile patients (41%) into two subsets of low and high-risks. Conclusions: Our study provides robust evidence in favor of baseline Ang-2 prognostic value for OS adding to the conventional factors. Its assessment appears to be useful for the improvement in risk stratification for patients with intermediate-risk profile. Impact: Ang-2 ability to predict OS at diagnosis could be of interest in the selection of patients eligible to intermittent or sequential therapeutic strategies dedicated to the optimization of patient's quality of life and chemotherapy cost-effectiveness. Copyright © 2015, American Association for Cancer Research.
    01/2015;
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    ABSTRACT: Alveolar echinococcosis (AE) is a severe chronic helminthic disease that mimics slow-growing liver cancer. Previous studies using murine models suggest that Echinococcus multilocularis (Em) metacestodes have developed mechanisms which impair the natural inflammatory host response. The aim of this study was to investigate in vitro the impact of Em vesicular fluid (VF) on monocytes, monocytes derived dendritic cells and lymphocytes from healthy blood donors. First, assays were performed to investigate whether or not Em-VF influences monocyte-derived dendritic cell (MoDC) differentiation and maturation. Monocytes during differentiation and immature MoDCs were exposed to Em-VF. The effect of Em-VF was assessed using flow cytometry (CD86, CD83, CD80) and immune assays (IL-10 and TGFβ). Second, assays were performed to investigate the interaction between Em-VF, peripheral blood monocyte cells (PBMC) and Toll-like Receptor (TLR) agonists (LPS, PolyIC, R848 and CpG). PBMC were stimulated by each of the TLR agonists with and without Em-VF. The subsequent TGFβ production was assessed. Exposure to Em-VF had bearing on both differentiation and maturation of MoDC, but only partially. A decrease in the expression of co-stimulatory molecules was observed; however, levels of immune-regulatory cytokines were stable. PBMC exposed simultaneously to Em-VF and LPS induced a significant increase of TGFβ (p<0.05, Wilcoxon signed-rank test). Further experiments showed that TGFβ production was lymphocyte-dependent. The assays performed confirmed that Em-VF influences the host immune response. However, only minor changes were observed when investigating the Em-VF impact on cells from healthy blood donors. Assays with TLR agonists suggested that co-stimulation with LPS reinforces the response of healthy blood donors exposed to Em-VF. Copyright © 2014. Published by Elsevier B.V.
    Journal of Immunological Methods 12/2014; · 2.01 Impact Factor
  • American Society of Hematology, 56th Annual meeting, 2014, San Fransisco; 12/2014
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    ABSTRACT: Here, we report and investigate the genomic alterations of two novel cases of Non-Hodgkin Lymphoma (NHL) in children with Williams-Beuren syndrome (WBS), a multisystem disorder caused by 7q11.23 hemizygous deletion. Additionally, we report the case of a child with NHL and a somatic 7q11.23 deletion. Although the WBS critical region has not yet been identified as a susceptibility locus in NHL, it harbors a number of genes involved in DNA repair. The high proportion of pediatric NHL reported in WBS is intriguing. Therefore, the role of haploinsufficiency of genes located at 7q11.23 in lymphomagenesis deserves to be investigated.
    Journal of Hematology & Oncology 11/2014; 7:82. · 4.93 Impact Factor
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    ABSTRACT: Cancer-specific splice variants gain significant interest as they generate neo-antigens that could be targeted by immune cells. CD20, a membrane antigen broadly expressed in mature B cells and in B cell lymphomas, is subject to an alternative splicing named D393-CD20 leading to loss of membrane expression of the spliced isoform. D393-CD20 expression is detectable in transformed B cells and upregulated in various lymphoma B cells. In this study, we show that D393-CD20 is translated in malignant B cells and that D393-CD20 specific CD4 T cells producing IFN-γ are present in B-cell lymphoma patients. Then we have investigated whether the 20mer D393-CD20 peptide spanning the splicing site might be targeted by the immune system and we have shown that D393-CD20-specific CD4 Th1 clones could directly recognize malignant B cell lines and kill autologous lymphoma B cells indicating that D393-CD20-derived epitopes are naturally processed and presented on tumor cells. Finally, D393-CD20 peptide-based vaccination induced specific CD8 and CD4 T cell responses in HLA-humanized transgenic mice suggesting the presentation of D393-CD20 derived peptides on both HLA class-I and -II. These findings support further investigations on the potential use of D393-CD20 directed specific immunotherapy in B cell malignancies. This article is protected by copyright. All rights reserved.
    International Journal of Cancer 11/2014; · 6.20 Impact Factor
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    ABSTRACT: Here, we report and investigate the genomic alterations of two novel cases of Non-Hodgkin¿s Lymphoma (NHL) in children with Williams-Beuren syndrome (WBS), a multisystem disorder caused by 7q11.23 hemizygous deletion. Additionally, we report the case of a child with NHL and a somatic 7q11.23 deletion. Although the WBS critical region has not yet been identified as a susceptibility locus in NHL, it harbors a number of genes involved in DNA repair. The high proportion of pediatric NHL reported in WBS is intriguing. Therefore, the role of haploinsufficiency of genes located at 7q11.23 in lymphomagenesis deserves to be investigated.
    American Society of Human Genetics, 2014, Annual Meeting, San Diego; 10/2014
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    ABSTRACT: There are several reports demonstrating the role of CD8 T cells against Leishmania species. Therefore peptide vaccine might represent an effective approach to control the infection. We developed a rational polytope-DNA construct encoding immunogenic HLA-A2 restricted peptides and validated the processing and presentation of encoded epitopes in a preclinical mouse model humanized for the MHC-class-I and II.
    PLoS ONE 10/2014; 9(10):e108848. · 3.53 Impact Factor
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    ABSTRACT: Numerous chemotherapies have been developed to treat cancers. Now, it is becoming clear that cytotoxic agents not only have a direct effect on cancer cell death, but can also elicit tumour-specific immune responses. We recently showed that 8 patients treated with DCF for squamous cell carcinoma of the anal canal (SCCA) presented an overall survival rate of 62.5 % at 12 months. Half of the patients, with HPV16 positive SCCA, achieved a complete remission. To attempt to understand why such a good clinical response was obtained, we aimed to determine whether DCF regimen could increase antigenicity and immunogenicity in in vitro and in vivo models of HPV16 cancers. C57BL/6 mice were grafted subcutaneously with 3×105 TC1 cells (primary lung epithelial cells of C57BL/6 immortalized with E6 and E7 of HPV16 and transformed with c-Ha-ras). When the tumour size reached 100 mm2, mice were treated either with DCF or CF. The tumours were measured for 15 days and the number of Treg (CD4+ CD25+ FoxP3+) and Myeloid-Derived Suppressor Cells (MDSC, Gr1+, CD11b+) were assessed in the spleen after the sacrifice of the mice. Tumour specific immune responses against E7 and mTERT were analyzed by IFNg ELISPOT. In parallel in vitro studies were conducted with TC1 cells treated by DCF, CF or D. The analysis of calreticulin expression by flow cytometry, and the release of ATP and HMGB1 in the supernatant of treated cells were conducted to highlight the induction of an immunogenic cell death (ICD). The DCF regimen showed the best antitumor effect in TC1 grafted mice compared with CF. Furthermore a lower level of Treg and MDSC was observed in the spleen of mice treated with DCF compared to CF. Reduction of tumour size was linked to the induction of specific anti-E7 and anti-mTERT immune responses. As for the in vitro assessment of ICD, DCF increased the membrane expression of calreticulin and the release of HMGB1. As a whole our preliminary data indicate that the clinical response observed with DCF may be due to efficient modulation of tumour-specific immune responses by (i) inducing in mice a less immunosuppressive environment compared to CF, (ii) promoting the optimal release and presentation of tumour antigens through the induction of immunogenic cell death.
    Revue Francophone des Laboratoires 09/2014; 2014(465):14–15.
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    ABSTRACT: Gemcitabine/Cisplatin (Gem/CDDP) combination has demonstrated a clear survival advantage over gemcitabine alone and has become a new standard in advanced Biliary Tract Carcinoma (aBTC). However, Gemcitabine/Oxaliplatin (GEMOX) combination and Gemcitabine/Carboplatin (Gem/Carb) combination regimens have shown efficacy in phase II trials and there is no comparative study between different platinum salts.We assessed the efficacy and safety of different platinum-based chemotherapies at first line in aBTC patients. We also analysed the second-line chemotherapy.
    BMC Gastroenterology 08/2014; 14(1):143. · 2.11 Impact Factor
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    ABSTRACT: In T3 rectal cancer (RC), preoperative chemoradiotherapy (5-FU-RT) reduces local recurrences, but does not impact overall survival. New therapeutic options are still necessary to improve clinical outcomes.
    Annals of Oncology 08/2014; · 6.58 Impact Factor
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    ABSTRACT: Cisplatin/gemcitabine association has been a standard of care for first-line regimen in advanced biliary tract cancer nevertheless oxaliplatin/gemcitabine regimen is frequently preferred. Because comparative effectiveness in clinical outcomes of cisplatin- versus oxaliplatin-containing chemotherapy is not available, a systematic review of studies assessing cisplatin/gemcitabine or oxaliplatin/gemcitabine chemotherapies in advanced biliary tract cancer was performed. Published studies evaluating cisplatin/gemcitabine or oxaliplatin/gemcitabine in advanced biliary tract cancer were included. Each study was weighted according to the number of patients included. The primary objective was to assess weighted median of medians overall survival (mOS) reported for both regimens. Secondary goals were to assess weighted median of medians progression-free survival (mPFS) and toxic effects were pooled and compared within each arm. Thirty-three studies involving 1470 patients were analyzed. In total, 771 and 699 patients were treated by cisplatin/gemcitabine and oxaliplatin/gemcitabine, respectively. Weighted median of mOS was 9.7 months in cisplatin group and 9.5 months in oxaliplatin group. Cisplatin-based chemotherapy was significantly associated with more grade 3 and 4 asthenia, diarrhea, liver toxicity, and hematological toxicity. Sensitivity analysis including only the studies with the standard regimen of cisplatin (25–35 mg/m2 administered on days 1 and 8) showed that the weighted median of mOS increased from 9.7 to 11.7 months but Gem/CDDP regimen remained more toxic than Gemox regimen. These results suggest that the Gem/CDDP regimen with cisplatin (25–35 mg/m2) administered on days 1 and 8 is associated with survival advantage than Gemox regimen but with addition of toxicity.
    Cancer Medicine 07/2014;
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    ABSTRACT: Perioperative chemotherapy improves the overall survival of resectable gastroesophageal adenocarcinoma (GEA) patients. However, more than 40 % of the patients are not healthy enough to complete their post-operative chemotherapy, and the progression-free survival rate is lower than 35 % at 5 years. In order to optimise neoadjuvant chemotherapy regimen, a pilot study of weekly dose-intensified cisplatin, epirubicin, and paclitaxel (PET) was conducted. The primary objective was a complete resection (R0) rate. Then, a R0 rate ≤80 % was considered as uninteresting, with an expected R0 rate of 92 %. Secondary objectives were the feasibility, safety, histological response rate (Becker score), and survival (Trial registration: NCT01830270). Patients with >T1N0M0 GEA were included. Treatment consisted of eight preoperative cycles of weekly PET regimen at 30/50/80 mg/m(2) of cisplatin, epirubicin, and paclitaxel, respectively. Primary prophylaxis by granulocyte colony-stimulating factor was administered. Surgery was performed 4-6 weeks following the last cycle of chemotherapy. Using Fleming two-step design with a unilateral alpha type one error of 5 % and a statistical power of 80 %, it would be required to include 68 patients. At planned interim analysis for futility, it was required to observe at least 25 of 29 patients with R0 resection to pursue inclusion. At the second step, it was required to observe at least 61 of 68 patients with R0 resection to conclude for promising activity of the dose-intensified chemotherapy. Between May 2011 and January 2013, 29 patients were enrolled. Median age was 62 years (range 39-83 years), and seven (24 %) patients presented signet-ring cell histology. Twenty-seven (93 %) patients underwent surgery. Pathological complete responses (Becker score 1a) were observed in four patients, and nearly complete responses (Becker score 1b) for additional three patients. A R0 rate was achieved for 24 of 29 (82.7 %; 95 % CI 64-94 %) patients. No Becker score 1a/1b response was observed among patients with signet-ring cell GEA. Twenty-one (72 %) patients completed all eight cycles, and 86 % received seven or more cycles. Sixteen (56 %) patients experienced grade 3-4 neutropenia, and five patients had febrile neutropenia. Among non-haematological toxicities, mucositis and fatigue were the most frequent ones. The median-delivered relative dose intensity (DI) was 80 % for cisplatin, 75 % for epirubicin, and 79 % for paclitaxel. However, only 45 % of the patients received at least 80 % of the planned median DI for all three drugs. Despite high R0 and pathological response rates, neoadjuvant PET chemotherapy did not meet the primary end-point and failed to show an acceptable relative DI. PET chemotherapy is not recommended in resectable GEA patients.
    Cancer Chemotherapy and Pharmacology 05/2014; · 2.80 Impact Factor
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    ABSTRACT: Endpoints describe clinical and biological measurements in therapeutic development and assessment. They can be classified in two categories: “patient-centered clinical endpoints” including overall survival (OS) and health related quality of life (QoL), and “tumour-centered clinical endpoints” such as progression-free survival. Surrogate endpoints are tumour-centered clinical endpoints, which intend to substitute for patient-centered clinical endpoints specially OS. The choice of the endpoints in oncology trials is a major problem. The publications of the Consolidated Standards of Reporting Trials (CONSORT) statement encouraged the reporting of clearly defined primary and secondary outcome measures. OS is the gold standard but with the increasing number of effective salvage treatments available in many types of cancer, a higher number of patients included and a longer follow-up is necessary which increases the cost of clinical trials. Thus, tumour-centered clinical endpoints which could be assessed earlier and used as surrogates for overall survival are more and more studied but most of them currently lack standardised definitions enabling a cross comparison of results from different clinical trials and they have not been validated as surrogate endpoints. In addition, the variability of their definition can strongly impact the trial's conclusions by affecting both statistical power and estimation. In this context, QoL constitutes an available and a useful alternative endpoint for trials to ensure treatment benefit in a patient or public health point of view. Methodological researches should be pursued to develop standard outcome definitions for use in cancer clinical trials and to define a standardized analysis of longitudinal QoL data.
    Journal de Chirurgie Viscérale. 02/2014;
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    ABSTRACT: The QSOX1 protein (Quiescin Sulfhydryl oxidase 1) catalyzes the formation of disulfide bonds and is involved in the folding and stability of proteins. More recently, QSOX1 has been associated with tumorigenesis and protection against cellular stress. It has been demonstrated in our laboratory that QSOX1 reduces proliferation, migration and invasion of breast cancer cells in vitro and reduces tumor growth in vivo. In addition, QSOX1 expression has been shown to be induced by oxidative or ER stress and to prevent cell death linked to these stressors. Given the function of QSOX1 in these two processes, which have been previously linked to autophagy, we wondered whether QSOX1 might be regulated by autophagy inducers and play a role in this catabolic process. To answer this question, we used in vitro models of breast cancer cells in which QSOX1 was overexpressed (MCF-7) or extinguished (MDA-MB-231). We first showed that QSOX1 expression is induced following amino acid starvation and maintains cellular homeostasis. Our results also indicated that QSOX1 inhibits autophagy through the inhibition of autophagosome/lysosome fusion. Moreover, we demonstrated that inhibitors of autophagy mimic the effect of QSOX1 on cell invasion, suggesting that its role in this process is linked to the autophagy pathway. Previously published data demonstrated that extinction of QSOX1 promotes tumor growth in NOG mice. In this study, we further demonstrated that QSOX1 null tumors present lower levels of the p62 protein. Altogether, our results demonstrate for the first time a role of QSOX1 in autophagy in breast cancer cells and tumors.
    PLoS ONE 01/2014; 9(1):e86641. · 3.53 Impact Factor
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    ABSTRACT: Bevacizumab plus fluoropyrimidine-based chemotherapy is standard treatment for first-line and second-line metastatic colorectal cancer (mCRC). However, to date, there is no current biomarker predictive for the benefit of bevacizumab use for these patients. Preclinical data suggest that the presence of the primary tumor could be involved in less efficient antitumor activity of antiangiogenic agents, but no clinical data currently support this hypothesis. We performed a retrospective analysis of factors associated with overall survival (OS) in a study cohort of 409 mCRC patients. Univariate and multivariate Cox proportional hazard regression models were used to assess the influence of primary tumor resection and bevacizumab use on OS. We evaluated associations linking bevacizumab use and OS among patients who previously underwent or did not undergo primary tumor resection. Results were externally validated in a second independent cohort of 328 mCRC patients. In the study cohort, bevacizumab use and resection of the primary tumor were associated with improved OS. However, subgroup analyses indicate that bevacizumab did not influence survival of patients bearing a primary colorectal tumor (hazard ratio (HR) 0.98, 95 % confidence interval (CI) 0.60-1.61, log-rank test P = 0.6). By contrast, the survival benefit of bevacizumab was restricted to patients who previously underwent primary tumor resection (HR 0.71, 95 % CI 0.55-0.92, P = 0.009). Similar results were observed in the validation cohort. Addition of bevacizumab to chemotherapy is associated with improvement of OS only in patients with primary tumor resection. These data support the rationale to validate prospectively the influence of primary tumor resection on bevacizumab antitumor effect in synchronous mCRC.
    Annals of Surgical Oncology 01/2014; · 3.94 Impact Factor
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    ABSTRACT: Endpoints are measurable clinical and biological findings that are used for the development and assessment of treatment options. In the treatment of cancer, endpoints can be classified into two categories: "patient-centered clinical endpoints" including overall survival (OS) and health-related quality of life (QoL), and "tumor-centered clinical endpoints" such as progression-free survival. Surrogate endpoints are tumor-centered clinical endpoints that can be used as substitutes for patient-centered clinical endpoints, particularly OS. The choice of endpoints in oncology trials is a major problem. The published Consolidated Standards of Reporting Trials (CONSORT) best-practice guidelines encourage the reporting of clearly defined primary and secondary outcome measures. OS is the gold standard of endpoints but as increasing numbers of effective salvage treatments become available for many types of cancer, much larger numbers of patients are included; this requires a longer follow-up period and increases the cost of clinical trials. Thus, tumor-centered clinical endpoints that can be assessed earlier and used as surrogates for overall survival are increasingly studied, but most of them currently lack standardized definitions to enable cross comparison of results among different clinical trials and they have not been validated as surrogate endpoints. In addition, the variability of their definition can strongly impact the trial's conclusions by affecting both statistical power and estimation. In this context, QoL constitutes an available and useful surrogate endpoint for trials to ensure treatment benefit from both the patient and public health points of view. Methodological research should be pursued to develop standard outcome definitions for use in cancer clinical trials and to define a standardized longitudinal analysis of QoL data.
    Journal of Visceral Surgery 01/2014; · 1.32 Impact Factor
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    ABSTRACT: Everolimus is an inhibitor of mammalian target of rapamycin, approved in patients with metastatic renal cell carcinoma. Besides, mammalian target of rapamycin inhibition has the ability to modulate T-lymphocyte homeostasis. Here, we report the case of a metastatic renal cell carcinoma patient treated with everolimus who presented unexpected prolonged tumor response. The monitoring of immune responses showed strong antitumor T-cell activation at the time of disease control, whereas a profound immunosuppression occurred when tumor progressed. Thus, a change of immune functions is associated with everolimus treatment. Our observation suggests that everolimus could shape immune responses, which in turn could contribute to its efficacy.
    Journal of immunotherapy (Hagerstown, Md.: 1997) 01/2014; 37(1):51-4. · 3.20 Impact Factor
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    ABSTRACT: Optimization of chemotherapy effectiveness in metastatic colorectal cancers (mCRC) is a major endpoint to enhance the possibility of curative intent surgery. FOLFIR3 has shown promising results as second-line chemotherapy for mCRC patients previously exposed to oxaliplatin. The clinical efficacy of FOLFIRI3 was never determined in association with bevacizumab in non-previously treated mCRC patients. We conducted a phase 2 clinical trial to characterize the response rate and toxicity profile of FOLFIRI3-bevacizumab as initial treatment for mCRC. Sixty-one patients enrolled in 3 investigation centers were treated with FOLFIRI3-bevacizumab (median of 10 cycles) followed by a maintenance therapy combining bevacizumab and capecitabine. Levels of plasma angiopoietin-2 (Ang-2) were measured by enzyme-linked immunosorbent assay at baseline. Overall response rate (ORR) was 66.7% (8% of complete and 58% of partial responses). The disease control rate was 91.7%. After a median time of follow-up of 46.7 months, 56 patients (92%) had progressed or died. The median progression free survival (PFS) was 12.7 months (95% CI: 9.7-15.8 months). The median overall survival (OS) was 24.5 months (CI 95%: 10.6-38.3 months). Twenty-one patients underwent curative intent-surgery including 4 patients with disease initially classified as unresectable. Most common grade III-IV toxicities were diarrhea (15%), neutropenia (13%), asthenia (10%), and infections (4%). Hypertension-related medications needed to be increased in 3 patients. In multivariate analysis, surgery of metastases and Ang-2 levels were the only independent prognostic factors for PFS and OS. Indeed, baseline level of Ang-2 above 5 ng/mL was confirmed as an independent prognostic factor for progression free survival (HR = 0.357; 95%CI: 0.168-0.76, p = 0.005) and overall survival (HR = 0.226; 95%CI: 0.098-0.53, p = 0.0002). As front-line therapy, FOLFIRI-3-bevacizumab is associated with an acceptable toxicity and induced promising objective response rates. However, unfavorable clinical outcomes were observed in patients with high levels of angiopoietin 2.
    BMC Cancer 12/2013; 13(1):611. · 3.32 Impact Factor

Publication Stats

2k Citations
449.77 Total Impact Points

Institutions

  • 2007–2014
    • University of Franche-Comté
      • Institut FEMTO-ST
      Becoinson, Franche-Comté, France
  • 2011
    • Centre Hospitalier Régional et Universitaire de Besançon
      Becoinson, Franche-Comté, France
  • 2008–2011
    • Unité Inserm U1077
      Caen, Lower Normandy, France
  • 2004–2011
    • French Institute of Health and Medical Research
      • • Unité d’Immunologie des Tumeurs et Immunothérapie U1015
      • • Unité d’Immunologie, Dermatologie, Oncologie U976
      Lutetia Parisorum, Île-de-France, France
  • 2005
    • Centre Léon Bérard
      Lyons, Rhône-Alpes, France
    • Institut de Cancérologie Gustave Roussy
      • Department of Clinical Biology
      Île-de-France, France