共查询到19条相似文献,搜索用时 0 毫秒
1.
Desar IM Timmer-Bonte JN Burger DM van der Graaf WT van Herpen CM 《British journal of cancer》2010,103(11):1637-1643
Background:
The combination of sorafenib (vascular endothelial growth factor receptor 2 inhibitor) and sirolimus (mammalian target of rapamycin inhibitor) might work synergistically.Methods:
A phase I dose-escalation study with sorafenib twice a day (b.i.d.) and sirolimus once daily (q.d.) was performed to determine the recommended dose of the combination in patients with solid tumours. Secondary objectives were to determine the safety profile and maximum tolerated dose (MTD), and to evaluate the pharmacokinetics (PK) of the combination.Results:
Dose-limiting toxicities were transaminitis and cutaneous toxicity. The most frequently reported adverse events were elevated transaminases, hypophosphatemia, fatigue, anorexia, diarrhoea, nausea, rash and palmar–plantar erythrodysaesthesia. Sirolimus did not change the PK of sorafenib; in contrast, sorafenib reduced the AUC(0−96) and Cmax of sirolimus. No objective responses were observed; eight patients showed stable disease for a median of 16.3 weeks (range 8–24). The MTD of the combination was sorafenib 200 mg b.i.d. with sirolimus 1 mg q.d.Conclusion:
The combination of sorafenib and sirolimus showed enhanced toxicity, which could not be explained by the PK of both drugs. The relative low doses at the MTD, in combination with the PK results, do not warrant further development of this combination. 相似文献2.
Y Loriot P Mordant N Dorvault T De la motte Rouge J Bourhis J-C Soria E Deutsch 《British journal of cancer》2010,103(3):347-353
Background:
Non-small-cell lung cancer (NSCLC) is an aggressive disease in which vascular endothelial growth factor (VEGF) and epidermal growth factor (EGF) are implicated in tumour growth, tumour resistance to radiation and chemotherapy, and disease relapse. We have investigated the anti-tumoural effects of BMS-690514, an inhibitor of both vascular endothelial growth factor receptor (VEGFR) and epidermal growth factor receptor (EGFR) signalling pathways, as a single agent and in combination with ionising radiation (IR) on several NSCLC cell lines.Methods:
Radiosensitisation of several NSCLC cell lines by BMS-690514 was assessed in vitro using clonogenic assay and in vivo using nude mice.Results:
In vitro studies showed that BMS-690514 alone decreases clonogenic survival of NSCLC cells lines but no potential enhancement of IR response was observed in the combination. In tumour-bearing mice, BMS-690514 alone inhibits the growth of NSCLC xenografts, including the T790M mutation-harbouring H1975 tumour. The concomitant combination of BMS-690514 and radiation did not increase mice survival in comparison with treatment with IR alone. In contrast, BMS-690514 markedly enhances the anti-tumour effect of radiation in a sequential manner on H1299 and H1975 xenografts. Immunohistochemistry revealed a qualitative reduction in vessel area after administrations of BMS-690514, compared with vehicle-treated controls, suggesting that revascularisation may explain the schedule dependency of the tumour-growth delay observed.Conclusion:
The results of association with radiation show that BMS-690514 may be a successful adjuvant to clinical radiotherapy. These findings are of translational importance because the clinical benefits of anti-EGFR and anti-VEGFR therapy might be schedule dependent. 相似文献3.
Preclinical trial of a new dual mTOR inhibitor,MLN0128, using renal cell carcinoma tumorgrafts
下载免费PDF全文
![点击此处可从《International journal of cancer. Journal international du cancer》网站下载免费的PDF全文](/ch/ext_images/free.gif)
Alexandre Ingels Hongjuan Zhao Alan E. Thong Matthias Saar Maija P. Valta Rosalie Nolley Jennifer Santos Donna M. Peehl 《International journal of cancer. Journal international du cancer》2014,134(10):2322-2329
mTOR is a rational target in renal cell carcinoma (RCC) because of its role in disease progression. However, the effects of temsirolimus, the only first‐generation mTOR inhibitor approved by the FDA for first‐line treatment of metastatic RCC, on tumor reduction and progression‐free survival are minimal. Second‐generation mTOR inhibitors have not been evaluated on RCC. We compared the effects of temsirolimus and MLN0128, a potent second‐generation mTOR inhibitor, on RCC growth and metastasis using a realistic patient‐derived tissue slice graft (TSG) model. TSGs were derived from three fresh primary RCC specimens by subrenal implantation of precision‐cut tissue slices into immunodeficient mice that were randomized and treated with MLN0128, temsirolimus, or placebo. MLN0128 consistently suppressed primary RCC growth, monitored by magnetic resonance imaging (MRI), in three TSG cohorts for up to 2 months. Temsirolimus, in contrast, only transiently inhibited the growth of TSGs in one of two cohorts before resistance developed. In addition, MLN0128 reduced liver metastases, determined by human‐specific quantitative polymerase chain reaction, in two TSG cohorts, whereas temsirolimus failed to have any significant impact. Moreover, MLN0128 decreased levels of key components of the two mTOR subpathways including TORC1 targets 4EBP1, p‐S6K1, HIF1α and MTA1 and the TORC2 target c‐Myc, consistent with dual inhibition. Our results demonstrated that MLN0128 is superior to temsirolimus in inhibiting primary RCC growth as well as metastases, lending strong support for further clinical development of dual mTOR inhibitors for RCC treatment. 相似文献
4.
Christina A von Roemeling Laura A Marlow William P Kennedy Gregory T Kennedy John A Copland Michael E Menefee 《American journal of cancer research》2013,3(4):390-401
Historically, metastatic renal cell carcinoma (mRCC) is more resistant to conventional cytotoxic chemotherapeutic agents than other solid tumors. Although significant progress has been made over the last decade with several novel therapeutics, these agents invariably go on to fail, largely due to either intrinsic or acquired resistance. To help overcome, or at least delay resistance, combinatorial therapies utilizing agents with disparate, and ideally complementary, mechanisms of actions are needed. In this report, we assess the novel combination of the mTOR inhibitor, temsirolimus, with the microtubule stabilizing drug ixabepilone in RCC. Our results demonstrate synergy in multiple cell lines of RCC and further evaluation of this combination is warranted in the clinical setting. Activation of the endoplasmic reticulum (ER) stress response pathway may in part explain the combinatorial synergy. We further propose that ER stress induced proteins may serve as early response biomarkers to combinatorial therapy in a clinical trial. 相似文献
5.
Qiaoling Sun Jinghong Zhou Zheng Zhang Mingchuan Guo Junqing Liang Feng Zhou Jingwen Long Wei Zhang Fang Yin Huaqing Cai Haibin Yang Weihan Zhang Yi Gu Liang Ni Yang Sai Yumin Cui Meifang Zhang Minhua Hong Junen Sun Zheng Yang Weiguo Qing Weiguo Su Yongxin Ren 《Cancer biology & therapy》2014,15(12):1635-1645
VEGF/VEGFR signal axis has been proven to be an important target for development of novel cancer therapies. One challenging aspect in small molecular VEGFR inhibitors is to achieve sustained target inhibition at tolerable doses previously seen only with the long-acting biologics. It would require high potency (low effective drug concentrations) and sufficient drug exposures at tolerated doses so that the drug concentration can be maintained above effective drug concentration for target inhibition within the dosing period. Fruquintinib (HMPL-013) is a small molecule inhibitor with strong potency and high selectivity against VEGFR family currently in Phase II clinical studies. Analysis of Phase I pharmacokinetic data revealed that at the maximum tolerated dose of once daily oral administration fruquintinib achieved complete VEGFR2 suppression (drug concentrations were maintained above that required to produce >85% inhibition of VEGFR2 phosphorylation in mouse) for 24 hours/day. In this article, the preclinical data for fruquintinib will be described, including kinase enzyme activity and selectivity, cellular VEGFR inhibition and VEGFR-driven functional activity, in vivo VEGFR phosphorylation inhibition in the lung tissue in mouse and tumor growth inhibition in a panel of tumor xenograft and patient derive xenograft models in mouse. Pharmacokinetic and target inhibition data are also presented to provide a correlation between target inhibition and tumor growth inhibition. 相似文献
6.
D Yoshikawa H Ojima A Kokubu T Ochiya S Kasai S Hirohashi T Shibata 《British journal of cancer》2009,100(8):1257-1266
Cholangiocarcinoma is an intractable cancer, with no effective therapy other than surgical resection. Elevated vascular endothelial growth factor (VEGF) and epidermal growth factor receptor (EGFR) expressions are associated with the progression of cholangiocarcinoma. We therefore examined whether inhibition of VEGFR and EGFR could be a potential therapeutic target for cholangiocarcinoma. Vandetanib (ZD6474, ZACTIMA), a VEGFR-2/EGFR inhibitor, was evaluated. Four human cholangiocarcinoma cell lines were molecularly characterised and investigated for their response to vandetanib. In vitro, two cell lines (OZ and HuCCT1), both of which harboured KRAS mutation, were refractory to vandetanib, one cell line (TGBC24TKB) was somewhat resistant, and another cell line (TKKK) was sensitive. The most sensitive cell line (TKKK) had EGFR amplification. Vandetanib significantly inhibited the growth of TKKK xenografts at doses ⩾12.5 mg kg−1 day−1 (P<0.05), but higher doses (50 mg kg−1 day−1, P<0.05) of vandetanib were required to inhibit the growth of OZ xenografts. Vandetanib (25 mg kg−1 day−1) also significantly (P=0.006) prolonged the time to metastasis in an intravenous model of TKKK metastasis. Inhibiting both VEGFR and EGFR signalling appears a promising therapeutic approach for cholangiocarcinoma. The absence of KRAS mutation and the presence of EGFR amplification may be potential predictive molecular marker of sensitivity to EGFR-targeted therapy in cholangiocarcinoma. 相似文献
7.
Mhd Yaser Al-Marrawi Bikramajit Singh Saroya Matthew C Brennan Zhaohai Yang Thomas M Dykes Wafik S El-Deiry 《Cancer biology & therapy》2013,14(8):703-710
Sorafenib, the first agent developed to target BRAF mutant melanoma, is a multi-kinase inhibitor that was approved by the FDA for therapy of kidney and subsequently liver cancer, and is currently in clinical trials for thyroid, lung and brain cancer. Colorectal cancer with V600E BRAF mutation has shown relative resistance to standard chemotherapy regimens, as well as lack of efficacy to vemurafenib in clinical trials. New treatments are needed for BRAF-mutant colorectal cancer. We report a case of a patient with BRAF-mutant metastatic colon cancer whose disease had progressed on FOLFOX plus bevacizumab and subsequent FOLFIRI plus cetuximab. Based on preclinical data published in Nature in 2012 suggesting that successful therapeutic targeting of BRAF in colorectal cancer may require concomitant targeting of the EGFR, we offered this patient without other attractive options the combination of sorafenib plus cetuximab, in off-label use with informed consent. Sorafenib and cetuximab therapy led to a mixed radiographic response with some areas showing dramatic improvement and other areas showing stable disease over a 7-month period which is a notably long period of progression-free survival for V600E BRAF mutated colon cancer. The cetuximab plus sorafenib therapy was very well-tolerated by the patient who remained on it long enough until another therapy option, regorafenib, was approved in September 2012. The patient was offered single agent regorafenib at the time of progression. At the time of progression on single agent regorafenib, panitumumab was combined with regorafenib and this was also well-tolerated and appeared to slow disease progression. Further study of these approaches in the clinic as personalized treatment of BRAF-mutant advanced colorectal cancer is warranted. 相似文献
8.
Yan Song Jinwan Wang Xiubao Ren Jie Jin Li Mao Chris Liang Lieming Ding Lin Yang 《中国癌症研究》2021,33(1):103-114
Objective:This study evaluated the safety and preliminary efficacy of vorolanib,a novel tyrosine kinase inhibitor,for treatment of patients with advanced solid tumors.Methods:During dose escalation,patients received increasing doses of oral vorolanib(50-250 mg once daily)in cycles of four weeks for up to one year.During dose expansion,patients received recommended doses(100 and 200 mg)in 4-week cycles.The primary endpoint was to determine the safety and maximum tolerated dose and/or the recommended phase II dose(RP2 D).The severity and type of adverse drug reactions(ADRs)were assessed using the Common Terminology Criteria for Adverse Events version 4.0.The second endpoint was preliminary efficacy in terms of objective response and progression-free survival(PFS).Results:No dose-limiting toxicity occurred during dose escalation(50-250 mg).Five(26.3%)patients in the escalation cohort(n=19)and 12(48.0%)in the expansion cohort(n=25)experienced grade 3 ADRs.The most common ADRs were hair color changes,fatigue,portal hypertension,hypertriglyceridemia,and proteinuria.During dose expansion,the patients treated with 200 mg and 100 mg(once daily)showed an objective response rate of 22.2%and 5.9%,respectively;the disease control rate was 88.9%and 73.3%,respectively;the median PFS was9.9[95%confidence interval(95%CI):7.4-not reached]months and 3.8(95%CI:1.9-not reached)months,respectively.Conclusions:Oral vorolanib at a dose of 200 mg(once daily)exhibited an acceptable safety profile and favorable clinical benefit for patients with advanced solid tumors.The RP2 D for vorolanib was determined to be 200 mg as a daily regimen. 相似文献
9.
Francesca Chiarini Annalisa Lonetti Gabriella Teti Ester Orsini Daniela Bressanin Alessandra Cappellini Francesca Ricci Pier Luigi Tazzari Andrea Ognibene Mirella Falconi Pasqualepaolo Pagliaro Ilaria Iacobucci Giovanni Martinelli Sergio Amadori James A. McCubrey Alberto M. Martelli 《Oncotarget》2012,3(12):1615-1628
Signaling through the phosphatidylinositol 3-kinase (PI3K) pathway and its downstream effectors, Akt and mechanistic target of rapamycin (mTOR), is aberrantly activated in acute myeloid leukemia (AML) patients, where it contributes to leukemic cell proliferation, survival, and drug-resistance. Thus, inhibiting mTOR signaling in AML blasts could enhance their sensitivity to cytotoxic agents. Preclinical data also suggest that allosteric mTOR inhibition with rapamycin impaired leukemia initiating cells (LICs) function. In this study, we assessed the therapeutic potential of a combination consisting of temsirolimus [an allosteric mTOR complex 1 (mTORC1) inhibitor] with clofarabine, a nucleoside analogue with potent inhibitory effects on both ribonucleotide reductase and DNA polymerase. The drug combination (CLO-TOR) displayed synergistic cytotoxic effects against a panel of AML cell lines and primary cells from AML patients. Treatment with CLO-TOR induced a G0/G1-phase cell cycle arrest, apoptosis, and autophagy. CLO-TOR was pro-apoptotic in an AML patient blast subset (CD34+/CD38−/CD123+), which is enriched in putative leukemia initiating cells (LICs). In summary, the CLO-TOR combination could represent a novel valuable treatment for AML patients, also in light of its efficacy against LICs. 相似文献
10.
A.C Begg K.K Fu D.C Shrieve T.L Phillips 《International journal of radiation oncology, biology, physics》1979,5(9):1433-1439
The combined effects of Cyclophosphamide (CY) and radiation on the EMT6/SF tumor growing subcutaneously in mice were studied using both the growth delay assay and an in vitro assay. When drug was given between 48 hr before and 48 hr after radiation, cyclic variations in response were seen with the in vitro assay, e.g. the response was always greater when drug was given 1 or 8 hr compared with 4 hr after irradiation, Combined CY and radiation using doses which reduced survival to approx. 10% when each agent was given alone (120 mg/kg CY and 800 rad) produced slight potentiation at some time intervals. With the growth delay assay at these doses apparent potentiation was seen but which was probably due to the slower regrowth rate of tumors after combined treatment. No potentiation was seen with either assay when a lower drug dose (50 mg/kg) was used. Potentiation was seen with the growth delay assay, however, when larger doses were used (150 mg/kg CY, 1500 or 2000 rad X-rays), indicating a marked dose dependence for potentiation. 相似文献
11.
Kazuki Kuroshima Hirofumi Yoshino Shunsuke Okamura Masafumi Tsuruda Yoichi Osako Takashi Sakaguchi Satoshi Sugita Shuichi Tatarano Masayuki Nakagawa Hideki Enokida 《Cancer science》2020,111(5):1607-1618
Sunitinib, a multitargeted receptor tyrosine kinase inhibitor including vascular endothelial growth factor, has been widely used as a first‐line treatment against metastatic renal cell carcinoma (mRCC). However, mRCC often acquires resistance to sunitinib, rendering it difficult to treat with this agent. Recently, Rapalink‐1, a drug that links rapamycin and the mTOR kinase inhibitor MLN0128, has been developed with excellent therapeutic effects against breast cancer cells carrying mTOR resistance mutations. The aim of the present study was to evaluate the in vitro and in vivo therapeutic efficacy of Rapalink‐1 against renal cell carcinoma (RCC) compared to temsirolimus, which is commonly used as a small molecule inhibitor of mTOR and is a derivative of rapamycin. In comparison with temsirolimus, Rapalink‐1 showed significantly greater effects against proliferation, migration, invasion and cFolony formation in sunitinib‐naïve RCC cells. Inhibition was achieved through suppression of the phosphorylation of substrates in the mTOR signal pathway, such as p70S6K, eukaryotic translation initiation factor 4E‐binding protein 1 (4EBP1) and AKT. In addition, Rapalink‐1 had greater tumor suppressive effects than temsirolimus against the sunitinib‐resistant 786‐o cell line (SU‐R 786‐o), which we had previously established, as well as 3 additional SU‐R cell lines established here. RNA sequencing showed that Rapalink‐1 suppressed not only the mTOR signaling pathway but also a part of the MAPK signaling pathway, the ErbB signaling pathway and ABC transporters that were associated with resistance to several drugs. Our study suggests the possibility of a new treatment option for patients with RCC that is either sunitinib‐sensitive or sunitinib‐resistant. 相似文献
12.
Sunami T Nishio K Kanzawa F Fukuoka K Kudoh S Yoshikawa J Saijo N 《Cancer chemotherapy and pharmacology》1999,43(5):394-401
Purpose: TAS-103 [6-((2-(dimethylamino) ethyl)amino)-3-hydroxy-7H-indeno(2,1-c)quinolin-7-one dihydrochloride] is a newly synthesized
dual inhibitor of topoisomerase I and II. Since anticancer drugs are used in combination with other drugs for effective chemotherapy,
we investigated the cytotoxic effect of TAS-103 in combination with other conventional anticancer agents, such as cisplatin,
vindesine, doxorubicin, 5-fluorouracil, and the antitopoisomerase inhibitors SN-38 and etoposide in vitro. Methods: Inhibition of the growth of the human small-cell lung cancer cell line SBC-3 was evaluated using the tetrazolium dye (MTT)
assay. Drug interactions were evaluated by isobologram analysis and the determination of combination indices supplemented
by a three-dimensional model. Results: Simultaneous use of TAS-103 and cisplatin had a supradditive effect, but combinations of TAS-103 with other drugs had an
additive or marginally subadditive effect. Three-dimensional model analysis added more information about the synergistic concentration
ranges of two drugs (cisplatin 200–400 nM and TAS-103 7–10 nM). Sequential use of TAS-103 and cisplatin had only an additive effect. Conclusion: These results suggest that the concomitant use of TAS-103 and cisplatin has a greater cytotoxic effect on cancer cells than
single drug use, and may provide a beneficial effect in the treatment of small-cell lung cancer.
Received: 23 March 1998 / Accepted: 15 September 1998 相似文献
13.
14.
Xiao X Wu J Zhu X Zhao P Zhou J Liu QQ Zheng L Zeng M Liu R Huang W 《International journal of cancer. Journal international du cancer》2007,121(9):2095-2104
ZD6474 is a vascular endothelial growth factor receptor (VEGFR) and epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor. The present study was undertaken to investigate the direct antiproliferative effect of ZD6474 on human nasopharyngeal carcinoma (NPC) in vitro and the antitumor activity on NPC xenografts in vivo. Results indicated that ZD6474 treatment inhibited EGFR phosphorylation and led to a dose- and time-dependent decrease in NPC cell (CNE-1, CNE-2 and C666-1) proliferation. Further investigation demonstrated G0/G1 cell cycle arrest in all 3 cell lines, which was associated with an upregulation of p21 and/or p27, and downregulation of CDK4, CDK6 and CDK2. ZD6474 treatment also induced apoptosis in CNE-1 and CNE-2 cells. The apoptosis mechanisms involved reduction of Bcl-2 and/or Bcl-XL, induction of Bak and/or Bax, and activation of caspases-3, -9 and/or -8. The in vivo antitumor activity was evaluated in CNE-2 and C666-1 xenografted nude mice. Administration of ZD6474 (25-100 mg/kg/day, once-daily, p.o.) produced a dose-dependent inhibition of tumor growth and prolonged survival in both models. This study suggests that ZD6474 exerts direct antiproliferative effects on NPC cell lines in vitro by inducing G0/G1 arrest and apoptosis, and potent antitumor effects on NPC xenografts in vivo. It indicates that ZD6474 may offer a new and effective treatment for human NPC. 相似文献
15.
Natural killer,but not natural killer T,cells play a necessary role in the promotion of an innate antitumor response induced by IL-18 总被引:7,自引:0,他引:7
Hashimoto W Tanaka F Robbins PD Taniguchi M Okamura H Lotze MT Tahara H 《International journal of cancer. Journal international du cancer》2003,103(4):508-513
IL-18 administration promotes innate immunity resulting in significant antitumor effects in multiple murine tumor models. Here, we examined the effector population mediating the innate immunity. Most NK cells and some NKT cells express IL-18Rs without prior stimulation (65% positive in NK cells, 18% positive in NKT cells), though few naive T cells do. In vivo depletion of NK cells, but not NKT cells, using AsGM1 antibody significantly reduces IL-18-induced cytotoxicity. However, NK-like activity of hepatic MNCs for the NK target YAC-1 was present in Valpha 14 NKT cell-deficient animals. Furthermore, administration of rIL-18 greatly reduced B16 pulmonary metastases in vivo in NKT cell-deficient animals. When sorted NK and NKT cells were exposed to IL-18 in vitro, NK cells showed more IFN-gamma production and cytolysis against YAC-1 than NKT cells in response to IL-18. These results are consistent with the notion that NK cells, but not NKT cells, are the major effectors in IL-18-induced innate immunity. 相似文献
16.
Long‐term survival of a child with refractory anaplastic large cell lymphoma following therapy with an antisense oligonucleotide,topotecan, and vinblastine
下载免费PDF全文
![点击此处可从《Hematological oncology》网站下载免费的PDF全文](/ch/ext_images/free.gif)
Grazyna Wrobel Radosław Chaber Jolanta Rygier Jolanta Bonar Katarzyna Muszynska‐Roslan Alicja Chybicka 《Hematological oncology》2015,33(1):52-55
Anaplastic large cell lymphoma includes a subset of highly aggressive tumours and has a relapse rate of 30% at 2 years. Relapsed patients often have poor clinical outcome. The use of antisense oligonucleotides to down‐regulate Bcl‐2 protein can reverse chemotherapy resistance. The authors describe an 11‐year‐old boy with recurrent anaplastic large cell lymphoma who had received double high‐dose chemotherapy followed by autologous haematopoietic stem‐cell transplantation, had refractory disease and then had achieved long‐term remission with the use of an antisense oligonucleotides in combination with vinblastine and topotecan. Copyright © 2011 John Wiley & Sons, Ltd. 相似文献
17.
Richard Schwab Istvan Petak Mihaly Kollar Ferenc Pinter Edit Varkondi Andrea Kohanka Helga Barti-Juhasz Julia Schönleber Diana Brauswetter Laszlo Kopper Laszlo Urban 《Lung cancer (Amsterdam, Netherlands)》2014
The initial radiotherapy of a 73 years old Caucasian male patient with advanced squamous cell lung carcinoma was terminated due to severe pericarditis. Subsequently, the tumor sample was analyzed for possible targets with comprehensive molecular diagnostics. EGFR, KRAS and PIK3CA genes were wild type, ALK and ROS1 were negative for rearrangement, but c-MET was amplified by fluorescent in situ hybridization. The kinase inhibitor crizotinib is already in clinical use for the treatment of ALK positive non-small cell lung cancers, but it is also known to be a potent c-MET inhibitor. The patient was treated with the standard dose of twice a day 250 mg crizotinib as a monotherapy. Major partial response to therapy was confirmed by chest CT and PET/CT after 8 weeks on therapy. C-MET expression is associated with poor prognosis and resistance to EGFR inhibitors. This case may indicate that c-MET tyrosine kinase inhibitors can be an effective targeted treatment option for squamous cell carcinoma patients, and future clinical trials should be expanded for this patient group as well. 相似文献
18.
Belani CP Wu YL Chen YM Kim JH Yang SH Zhang L Peterson P Orlando M 《Journal of thoracic oncology》2012,7(3):567-573
19.
Morice P Rouanet P Rey A Romestaing P Houvenaeghel G Boulanger JC Leveque J Cowen D Mathevet P Malhaire JP Magnin G Fondrinier E Berille J Haie-Meder C 《The oncologist》2012,17(1):64-71