Henri Roché

Institut Universitaire de France, Lutetia Parisorum, Île-de-France, France

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Publications (94)667.21 Total impact

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    ABSTRACT: Iniparib is an investigational agent with antitumor activity of controversial mechanism of action. Two previous trials in advanced triple-negative breast cancer (TNBC) in combination with gemcitabine and carboplatin showed some evidence of efficacy that was not confirmed. This phase II randomized neoadjuvant study was designed to explore its activity and tolerability with weekly paclitaxel (PTX) as neoadjuvant treatment in TNBC patients. 141 patients with Stage II-IIIA TNBC were randomly assigned to receive PTX (80 mg/m(2), d1; n = 47) alone or in combination with iniparib, either once-weekly (PWI) (11.2 mg/kg, d1; n = 46) or twice-weekly (PTI) (5.6 mg/kg, d1, 4; n = 48) for 12 weeks. Primary endpoint was pathologic complete response (pCR) in the breast. pCR rate was similar among the three arms (21, 22, and 19 % for PTX, PWI, and PTI, respectively). Secondary efficacy endpoints were comparable: pCR in breast and axilla (21, 17, and 19 %); best overall response in the breast (60, 61, and 63 %); and breast conservation rate (53, 54, and 50 %). Slightly more patients in the PTI arm presented grade 3/4 neutropenia (4, 0, and 10 %). Grade 1/2 (28, 22, and 29 %), but no grade 3/4 neuropathy, was observed. There were no differences in serious adverse events and treatment-emergent adverse events leading to treatment discontinuation among the three arms. Addition of iniparib to weekly PTX did not add relevant antitumor activity or toxicity. These results do not support further evaluation of the combination of iniparib at these doses plus paclitaxel in early TNBC.
    Breast Cancer Research and Treatment 11/2015; 154(2). DOI:10.1007/s10549-015-3616-8 · 3.94 Impact Factor
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    ABSTRACT: Background: Inherited or acquired reticulate hyperpigmentation represents a heterogeneous group of infrequent dermatological conditions. The development of reticulate hyperpigmentation has so far been rarely reported to be associated with chemotherapeutic agents, including fluorouracil, bleomycin or a combination of cytarabine and idarubicin. Case reports: We describe 5 cases of chemotherapy-related reticulate hyperpigmentation in patients treated with different chemotherapeutic regimens, in particular paclitaxel or cytarabine. The lesions were similar in all cases, with reticulate and/or linear hyperpigmented streaks, which were mainly located to the back and buttocks. Histology showed increased melanogenesis, which suggests a direct toxic effect of chemotherapy on melanocytes. Reflectance confocal microscopy was performed in 2 patients showing a similar pattern, with an increased amount of melanin in basal keratinocytes. These features have been compared with the available data through a literature review. Conclusion: Reticulate hyperpigmentation is an underestimated but characteristic complication of chemotherapy. Neither specific management nor discontinuation of the chemotherapeutic regimen is required.
    Dermatology 09/2015; DOI:10.1159/000439047 · 1.57 Impact Factor
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    ABSTRACT: Microarray studies identified a subgroup of molecular apocrine tumors (estrogen receptor [ER] negative/androgen receptor [AR] positive) that express luminal genes including FOXA1. FOXA1 may direct AR to sites normally occupied by ER in luminal tumors, inducing an estrogen-like gene program that stimulated proliferation. Expression of AR and FOXA1 was evaluated by immunohistochemistry in 592 patients with nonmetastatic triple-negative breast cancer (TNBC). Coexpression of AR and FOXA1 was found in 15.2% of patients. These tumors were more frequently lobular, found in older patients and exhibited a lower nuclear grade and a greater degree of node involvement. They less often exhibited lymphocytic infiltrate, pushing margins, syncytial architecture, central fibrosis or necrosis. TNBC with coexpression of AR and FOXA1 seems to behave like luminal tumors with a morphological profile distinct from other TNBC. These biomarkers could be useful to identify a subgroup of TNBC and could have future therapeutic implications.
    Future Oncology 08/2015; 11(16):2283-97. DOI:10.2217/fon.15.102 · 2.48 Impact Factor
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    ABSTRACT: Inflammatory breast cancer (IBC) is a rare and aggressive disease requiring a multimodal treatment. We evaluated the benefit of adding docetaxel-5 fluorouracil (D-5FU) regimen after pre-operative dose-intense epirubicin-cyclophosphamide (EC) and loco-regional treatment in IBC patients PATIENTS AND METHODS: PEGASE 07 was a national randomized phase 3 open-label study involving 14 hospitals in France. Women with non-metastatic IBC were eligible and randomly assigned to receive either 4 cycles of dose-intense EC (E150 mg/m² and C 4000 mg/m² every 3 weeks with repeated hematopoietic stem cell support), then mastectomy with axillary lymph node dissection, and radiotherapy (Arm A) or the same treatment followed by 4 cycles of D-5FU (D 85 mg/m², day 1 and 5FU 750 mg/m²/day continuous infusion, days 1-5 every 3 weeks) administered post-radiotherapy (Arm B). Patients with hormone receptor positive tumors received hormonal therapy. Disease-free survival (DFS) was the primary endpoint. Secondary endpoints included tolerance, pathological complete response (pCR) rate, and overall survival (OS). Between January 2001 and May 2005, 174 patients were enrolled and treated (87 in each arm). Median follow-up was similar in both arms: 59.6 months (95%CI: 58.4-60.3) in arm A and 60·5 months (95%CI: 58.3-61.4) in arm B. The estimated 5-year DFS rates were not different: 55% (95%CI: 43.9-64.7) in arm A and 55·5% (95%CI: 44.3-65.3) in arm B (hazard ratio, HR =0.94 [0.61-1.48]; p=0.81). Identical results were observed for 5-year OS: 70.2% (95%CI: 59.1-78.8) in arm A and 70% (95%CI: 58.8-78.7) in arm B (HR= 0.93 [0.55-1.60]; p=0.814). Following dose-intense EC induction, in-breast and global (breast plus nodes) pCR were 28.9% and 20.1%, respectively. Estrogen receptor and pCR status were independently associated with survival. The addition of D-5FU after pre-operative dose-intense EC and standard local therapy did not improve DFS in IBC. © The Author 2015. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved. For permissions, please email: journals.permissions@oup.com.
    Annals of Oncology 05/2015; 26(8). DOI:10.1093/annonc/mdv216 · 7.04 Impact Factor

  • Cancer Research 05/2015; 75(9 Supplement):P6-16-07-P6-16-07. DOI:10.1158/1538-7445.SABCS14-P6-16-07 · 9.33 Impact Factor

  • Cancer Research 05/2015; 75(9 Supplement):OT1-1-12-OT1-1-12. DOI:10.1158/1538-7445.SABCS14-OT1-1-12 · 9.33 Impact Factor

  • Cancer Research 05/2015; 75(9 Supplement):P3-05-12-P3-05-12. DOI:10.1158/1538-7445.SABCS14-P3-05-12 · 9.33 Impact Factor

  • Cancer Research 05/2015; 75(9 Supplement):P4-07-08-P4-07-08. DOI:10.1158/1538-7445.SABCS14-P4-07-08 · 9.33 Impact Factor
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    ABSTRACT: This phase 2 randomized study evaluated trebananib (AMG 386), a peptide-Fc fusion protein that inhibits angiogenesis by neutralizing the interaction of angiopoietin-1 and -2 with Tie2, in combination with paclitaxel with or without bevacizumab in previously untreated patients with HER2-negative locally recurrent/metastatic breast cancer. Patients received paclitaxel 90 mg/m(2) once weekly (3-weeks-on/1-week-off) and were randomly assigned 1:1:1:1 to also receive blinded bevacizumab 10 mg/kg once every 2 weeks plus either trebananib 10 mg/kg once weekly (Arm A) or 3 mg/kg once weekly (Arm B), or placebo (Arm C); or open-label trebananib 10 mg/kg once a week (Arm D). Progression-free survival was the primary endpoint. In total, 228 patients were randomized. Median estimated progression-free survival for Arms A, B, C, and D was 11.3, 9.2, 12.2, and 10 months, respectively. Hazard ratios (95% CI) for Arms A, B, and D versus Arm C were 0.98 (0.61-1.59), 1.12 (0.70-1.80), and 1.28 (0.79-2.09), respectively. The objective response rate was 71% in Arm A, 51% in Arm B, 60% in Arm C, and 46% in Arm D. The incidence of grade 3/4/5 adverse events was 71/9/4%, 61/14/5%, 62/16/3%, and 52/4/7% in Arms A/B/C/D. In Arm D, median progression-free survival was 12.8 and 7.4 months for those with high and low trebananib exposure (AUCss ≥ 8.4 versus < 8.4 mg·h/mL), respectively. There was no apparent prolongation of estimated progression-free survival with the addition of trebananib to paclitaxel and bevacizumab at the doses tested. Toxicity was manageable. Exposure-response analyses support evaluation of combinations incorporating trebananib at doses > 10 mg/kg in this setting. ClinicalTrials.gov, NCT00511459. Copyright © 2015. Published by Elsevier Ltd.
    Breast (Edinburgh, Scotland) 03/2015; 24(3). DOI:10.1016/j.breast.2014.11.003 · 2.38 Impact Factor
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    H Roche · J Blum · W Eiermann · Y-H Im · M Martin · L Mina · H Rugo · F Visco · C Zhang · N Lokker · D Lounsbury · J Litton ·
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    ABSTRACT: Poly-ADP-ribose polymerase (PARP) enzymes are important in DNA repair. PARP inhibition induces lethality in tumor cells with mutations in the genes encoding breast cancer susceptibility gene 1 (BRCA1) and breast cancer susceptibility gene 2 (BRCA2). Talazoparib (BMN 673) is a novel, dual-mechanism PARP inhibitor that both potently inhibits the PARP enzyme and effectively traps PARP on DNA, resulting in cell death in BRCA1/2-mutated cells.[1, 2] Talazoparib has shown promising single-agent antitumor efficacy in several solid tumor types and generally well tolerated in an ongoing Phase 1/2 clinical study[3]. This multi-center, global, Phase 3 trial (EMBRACA) compares the safety and efficacy of talazoparib versus physician's choice treatment (capecitabine, eribulin, gemcitabine or vinorelbine) in locally advanced and/or metastatic breast cancer subjects with germline BRCA mutations. The primary study objective is to evaluate progression-free survival (PFS) in subjects treated with talazoparib as a monotherapy compared with those treated with protocol-specific physician's choice. Secondary objectives include objective response rate (ORR), overall survival (OS), and safety. Patients may be eligible if they are ≥18 years, have histologically/cytologically confirmed breast carcinoma, locally advanced and/or metastatic disease, documentation of a deleterious or pathogenic germline BRCA1 or BRCA2 mutation, ≤2 prior chemotherapy-inclusive regimens for locally advanced and/or metastatic disease, prior treatment with a taxane and/or anthracycline in the adjuvant or metastatic setting, ECOG performance status ≤1, and no prior platinum treatment for metastatic disease. Patients (n = 429) will be randomized 2:1 to receive either talazoparib oral capsules (1.0mg/day, 21-day cycles) or physician's choice treatment. All eligible subjects will receive study drug treatment until disease progression or unacceptable toxicity. This trial is enrolling patients from Europe, Asia/Pacific, Israel, South America, and the United States (NCT01945775). © The Author 2015. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved. For permissions, please email: journals.permissions@oup.com.
    Annals of Oncology 03/2015; 26(suppl 2):ii16. DOI:10.1093/annonc/mdv090.1 · 7.04 Impact Factor
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    ABSTRACT: Metastatic breast cancer (MBC) is an incurable disease and represents a complex therapeutic challenge for oncologists. Despite the possibility of prescribing new agents such as tailored therapy, cytotoxic chemotherapy and hormone therapy remain the major treatments for MBC. Several lines of chemotherapy can be proposed for these patients, but beyond the second-line, evidence of effectiveness is lacking and such treatment has important associated toxicity affecting quality of life (QoL). Prospective data on third-line chemotherapy is very poor. There is no recent retrospective data and it mainly includes single-centre experiences. Moreover, prognostic parameters considered in these retrospective studies are limited to clinico-pathological factors. Previous reports don't evaluate prognostic impact of circulating tumour cells (CTC) and baseline QoL. METAL3 METAstatic Line 3 is a prospective, multicentric trial designed to prospectively construct a prognostic score (including selected clinico-pathological factors, CTC and baseline QoL) to identify patients who benefit from third-line chemotherapy for MBC in terms of overall survival (training cohort). Score will then be validated with another cohort (validation cohort). The aim of this paper is to review literature data on third-line chemotherapy for MBC and to describe in detail our prospective study. We hope that this prognostic score could be used by physicians to develop new therapeutic strategies when there will be limited benefit of third-line chemotherapy; this score will also help to improve patient information on their outcome.
    Contemporary Clinical Trials 01/2015; 40. DOI:10.1016/j.cct.2014.11.005 · 1.94 Impact Factor
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    ABSTRACT: Purpose: The BEVERLY-2 single-arm phase 2 trial assessed the efficacy and safety of combining neoadjuvant chemotherapy with bevacizumab and trastuzumab for the treatment of HER2-positive inflammatory breast cancer (IBC). Here we report the results of a pre-planned survival analysis at three years of follow-up, along with the association between outcome and circulating biomarkers and pathological complete response (pCR). Experimental design: Patients received fluorouracil, epirubicin, cyclophosphamide and bevacizumab (cycles 1-4) and docetaxel, trastuzumab and bevacizumab (cycles 5-8) prior to surgery, followed by trastuzumab and bevacizumab for 30 weeks post-surgery. Circulating tumor (CTC) and endothelial cell (CEC) counts were assessed at baseline, cycle 5, pre-operative, post-operative and at one year. Results: 52 patients were included. The 3-year disease-free survival (DFS) rate was 68% and overall survival (OS) rate was 90%. pCR (centrally reviewed) was strongly associated with 3-year DFS (80% and 53% in patients with/without pCR, respectively [p=0.03]). CTC detection also independently predicted 3-year DFS (81% vs. 43% for patients with <1 vs. ≥1 CTC/7.5 mL at baseline [p=0.01]). Patients with no CTC detected at baseline and with pCR had a high 3-year DFS (95%). CEC changes during treatment had no prognostic value. Conclusions: Our study suggests that the prognosis of IBC relies on more than the achievement of pCR and highlights the role of early hematogenous tumor dissemination as assessed by CTCs. Combining these two prognostic factors isolates a subgroup of IBC with excellent survival when treated with bevacizumab and trastuzumab-containing regimens. Copyright © 2014, American Association for Cancer Research.
    Clinical Cancer Research 12/2014; 21(6). DOI:10.1158/1078-0432.CCR-14-1705 · 8.72 Impact Factor
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    ABSTRACT: Objective: This study is a longitudinal follow-up of metastatic breast cancer patients treated with ixabepilone as first-line chemotherapy, with the aim to evaluate the association between a mechanism-based neurotoxicity and the efficacy of ixabepilone. Patients and methods: At the 2 main investigational sites of a phase II clinical trial, 50 patients previously treated with anthracycline received ixabepilone. A chart review was performed to evaluate overall survival (OS) and time to progression (TTP) and to describe the subsequent treatments. Results: The severe neurotoxicity induced by ixabepilone (38%) is correlated with a higher overall response rate to ixabepilone (79 vs. 48%; p = 0.042), a longer TTP (11.4 vs. 6.8 months; p = 0.023) and a longer OS (36.6 vs. 19.9 months; p = 0.05). After ixabepilone discontinuation, patients received a median of 4 subsequent chemotherapy lines (range 1-12). Among the 31 patients who received taxanes, neither the neurotoxicity incidence under treatment with taxanes nor the response was affected by a previous occurrence under ixabepilone treatment. Conclusion: These findings suggest that neurotoxicity development under ixabepilone treatment is a predictor of treatment outcomes as well as a favorable prognostic factor. It highlights the risk-to-benefit ratio issue of ixabepilone. We noticed the possibility to treat patients with taxanes after ixabepilone without systematic recurrent neurotoxicity.
    Oncology 11/2014; 88(3):180-188. DOI:10.1159/000367808 · 2.42 Impact Factor
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    ABSTRACT: IntroductionTriple Negative Breast Cancers (TNBC) represent about 12% to 20% of all breast cancers (BC) and have a worse outcome compared to other BC subtypes. TNBC often show a deficiency in DNA double-strand break repair mechanisms. This is generally related to the inactivation of a repair enzymatic complex involving BRCA1 caused either by genetic mutations, epigenetic modifications or by post-transcriptional regulations.The identification of new molecular biomarkers that would allow the rapid identification of BC presenting a BRCA1 deficiency could be useful to select patients who could benefit from PARP inhibitors, alkylating agents or platinum-based chemotherapy.Methods Genomic DNA from 131 formalin-fixed paraffin-embedded (FFPE) tumors (luminal A and B, HER2+ and triple negative BC) with known BRCA1 mutation status or unscreened for BRCA1 mutation were analysed by array Comparative Genomic Hybridization (array CGH). One highly significant and recurrent gain in the 17q25.3 genomic region was analysed by fluorescent in situ hybridization (FISH). Expression of the genes of the 17q25.3 amplicon was studied using customized Taqman low density arrays and single Taqman assays (Applied Biosystems).ResultsWe identified by array CGH and confirmed by FISH a gain in the 17q25.3 genomic region in 90% of the BRCA1 mutated tumors. This chromosomal gain was present in only 28.6% of the BRCA1 non-mutated TNBC, 26.7% of the unscreened TNBC, 13.6% of the luminal B, 19.0% of the HER2+ and 0% of the luminal A breast cancers. The 17q25.3 gain was also detected in 50% of the TNBC with BRCA1 promoter methylation. Interestingly, BRCA1 promoter methylation was never detected in BRCA1 mutated BC. Gene expression analyses of the 17q25.3 sub-region showed a significant over-expression of 17 genes in BRCA1 mutated TNBC (n¿=¿15) as compared to the BRCA1 non mutated TNBC (n¿=¿13).Conclusions In this study, we have identified by array CGH and confirmed by FISH a recurrent gain in 17q25.3 significantly associated to BRCA1 mutated TNBC. Up-regulated genes in the 17q25.3 amplicon might represent potential therapeutic targets and warrant further investigation.
    Breast cancer research: BCR 11/2014; 16(6):466. DOI:10.1186/s13058-014-0466-y · 5.49 Impact Factor
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    ABSTRACT: A selective and accurate analytical method is needed to quantify tamoxifen and its phase I metabolites in a prospective clinical protocol, for evaluation of pharmacokinetic parameters of tamoxifen and its metabolites in adjuvant treatment of breast cancer. The selectivity of the analytical method is a fundamental criteria to allow the quantification of the main active metabolites (Z)-isomers from (Z)'-isomers. An UPLC-MS/MS method was developed and validated for the quantification of (Z)-tamoxifen, (Z)-endoxifen, (E)-endoxifen, Z'-endoxifen, (Z)'-endoxifen, (Z)-4-hydroxytamoxifen, (Z)-4'-hydroxytamoxifen, N-desmethyl tamoxifen, and tamoxifen-N-oxide. The validation range was set between 0.5ng/mL and 125ng/mL for 4-hydroxytamoxifen and endoxifen isomers, and between 12.5ng/mL and 300ng/mL for tamoxifen, tamoxifen N-desmethyl and tamoxifen-N-oxide. The application to patient plasma samples was performed.
    Journal of Pharmaceutical and Biomedical Analysis 08/2014; 100C:254-261. DOI:10.1016/j.jpba.2014.07.033 · 2.98 Impact Factor
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    ABSTRACT: Background Despite high initial sensitivity to chemotherapy, triple-negative breast cancer (TNBC) is associated with a poor prognosis, highlighting the need for novel therapeutic strategies. The aim of this multicenter, randomized, open-label phase II trial was to assess the efficacy of ixabepilone as monotherapy, and the combination of ixabepilone plus cetuximab, as first-line treatment in patients with TN locally advanced non-resectable and/or metastatic breast cancer. Patients and Methods Women were randomly assigned to receive either ixabepilone (40 mg/m2) every 21 days (n = 40), or ixabepilone (40 mg/m2) every 21 days plus cetuximab (400 mg/m2 loading dose, followed by 250 mg/m2) once weekly (n = 39). The primary endpoint of the trial was to estimate the response rates of ixabepilone monotherapy and ixabepilone plus cetuximab combination therapy. Results Of 79 randomized patients, 77 were treated. Based on an intent-to-treat analysis, an objective response rate of 30% (95% confidence interval [CI], 16.6, 46.5) was observed in the monotherapy arm, and 35.9% (95% CI, 21.2, 52.8) in the combination arm. Median progression-free survival was 4.1 months in both treatment groups. Safety findings were consistent with the known individual toxicity profiles of ixabepilone and cetuximab. Skin and subcutaneous tissue disorders were more common with combination therapy, as were discontinuations due to adverse events. Conclusion Ixabepilone monotherapy and the ixabepilone and cetuximab combination demonstrated similar levels of clinical activity in first-line treatment of advanced TNBC, with a predictable safety profile. Further investigation of novel therapies for TNBC is required in order to improve patient outcomes.
    Clinical Breast Cancer 08/2014; 15(1). DOI:10.1016/j.clbc.2014.07.007 · 2.11 Impact Factor
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    ABSTRACT: Treatment of HER2-positive metastatic breast cancer with ado-trastuzumab emtansine (T-DM1), a novel antibody-drug conjugate, has resulted in both improved progression-free and overall survival. Recognition and treatment of diverse adverse events related to T-DM1 is critical for safety and tolerability. The most frequent adverse events with T-DM1 include fatigue, diarrhea, anemia, elevated transaminases, and mild-to-moderate hemorrhagic events, which are thought to be related to induced thrombocytopenia. Here, we present five case series of cutaneous and mucosal telangiectasias, definitely related to T-DM1. The development of telangiectasias represents a newly recognized adverse effect of T-DM1. We provide description and timing of the telangiectasias and review the mechanisms that may explain the formation of these vascular lesions in association with T-DM1. Further, we describe associated bleeding events and propose that induced telangiectasias could represent an additional cause of T-DM1-associated hemorrhage.
    Breast Cancer Research and Treatment 06/2014; 146(2). DOI:10.1007/s10549-014-3001-z · 3.94 Impact Factor
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    ABSTRACT: To examine the association between baseline body mass index (BMI), and disease-free survival (DFS) and overall survival (OS) in a large French early-stage breast cancer population included in the UNICANCER Programme d'Action Concerté Sein-01 (PACS01) and PACS04 phase III randomised trials. After a median follow-up of 5.9years, this report analyses 4996 patients with node-positive breast cancer, and randomly assigned to adjuvant anthracycline-based chemotherapy combined or not with taxanes. Univariate analyses were used to study the effects of well known prognostic factors and BMI on DFS and OS. BMI was obtained at baseline, before chemotherapy initiation, and obesity was defined as a BMI⩾30kg/m(2). Cox proportional hazards regression models were secondly used to assess the influence of BMI after adjusting for other factors. Exhaustive analysis of the dose intensity delivered was also studied for comparison between obese and non-obese patients. Obese patients initially present with more advanced disease at diagnosis compared to non-obese patients. By univariate analysis, obesity was moderately associated with poorer DFS (hazard ratio (HR)=1.18 [1.01-1.39] P=0.04), but mostly with poorer OS (HR=1.38 [1.13-1.69] P=0.002). Delivered dose intensity of anthracyclines and taxanes was not significantly different between obese and non-obese patients. After adjustment for disease characteristics, BMI had no influence either on DFS or OS. This report suggests that in a French population, obesity has no impact on breast cancer prognosis when modern adjuvant chemotherapy, at the appropriate dose intensity, is delivered.
    European journal of cancer (Oxford, England: 1990) 12/2013; 50(3). DOI:10.1016/j.ejca.2013.11.013 · 5.42 Impact Factor
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    Fabien Despas · Henri Roche · Guy Laurent ·

  • Henri Roché ·
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    ABSTRACT: The natural history of breast diseases has changed overtime and successive therapeutic strategies have been adapted accordingly. Recently, biological findings on geno- and phenotypic characteristics of tumor cells offer new basis for the development of treatments that target homogenous and various subtypes of breast cancer. Unfortunately, traditional clinical research tools are not in phase with rapid changes in both biological knowledge of the disease and new targeted agents. New methodological approaches are urgently needed to validate such changes and improvements in prognosis.
    Bulletin du cancer 09/2013; 100(9). DOI:10.1684/bdc.2013.1805 · 0.60 Impact Factor

Publication Stats

3k Citations
667.21 Total Impact Points


  • 2015
    • Institut Universitaire de France
      Lutetia Parisorum, Île-de-France, France
  • 2012-2015
    • Institut de France
      Lutetia Parisorum, Île-de-France, France
  • 2002-2015
    • Institut Claudius Regaud
      Tolosa de Llenguadoc, Midi-Pyrénées, France
  • 2004-2014
    • Paul Sabatier University - Toulouse III
      Tolosa de Llenguadoc, Midi-Pyrénées, France
  • 2010
    • French Institute of Health and Medical Research
      Lutetia Parisorum, Île-de-France, France
  • 2004-2009
    • Centre Jean Perrin
      Clermont, Auvergne, France
  • 2007
    • Cornell University
      Итак, New York, United States
  • 2005
    • Centre Léon Bérard
      Lyons, Rhône-Alpes, France
  • 2000
    • Institut Paoli Calmettes
      • Cancer Research Center of Marseille (CRCM)
      Marsiglia, Provence-Alpes-Côte d'Azur, France