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Paul Baas
Moderator of
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MS 08 - Novel Treatment for Mesothelioma (ID 530)
- Event: WCLC 2017
- Type: Mini Symposium
- Track: Mesothelioma
- Presentations: 7
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MS 08.01 - Today's Challenges in MPM Care (ID 7675)
15:45 - 17:30 | Presenting Author(s): Walter Weder
- Abstract
- Presentation
Abstract not provided
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MS 08.02 - Current Role of RT In MPM (ID 7676)
15:45 - 17:30 | Presenting Author(s): Anna Wrona
- Abstract
- Presentation
Abstract:
Local therapy as the primary treatment modality of early malignant pleural mesothelioma (MPM) remains highly controversial due to lack of clear benefit in comparative clinical trials. In specialized experienced centers, the initial approach is usually surgical resection - extrapleural pneumonectomy (EPP) or pleurectomy/decortication (P/D). No consensus exists with regard to the optimal use of radiotherapy (RT) in MPM. At the present time, there is no evidence to support the use of radical RT as a single modality in MPM, because of the inability to deliver a therapeutic high dose of radiation (e.g. 60Gy in 30 fractions) to the entire pleura without overdosing the surrounding organs at risk. However, RT has been used in the management of MPM in three indications: as prophylaxis to reduce the incidence of recurrence and pain at sites of diagnostic or therapeutic instrument insertion, as part of multimodal definitive treatment (following induction chemotherapy and surgical resection) to improve locoregional control in early-stage disease and for palliation of symptoms (mainly chest wall pain) in patients with advanced disease. During thoracoscopy, thoracocentesis or needle biopsy in patients with MPM, the seeding of tumor cells along the needle tract may occur, leading to painful metastases at the intervention sites in 20-50% of cases [1]. Prophylactic radiotherapy to chest wall sites of invasive procedures has previously been recommended. However, recent randomized studies (e.g. SMART trial) have shown that prophylactic RT should not be routinely used to prevent procedure tract metastases (PTMs) in MPM, as it confers no benefits in terms of chest pain control, analgesia use, survival, QoL and the data on the potential effect on PTMs' incidence reduction are discrepant [1]. Instead patients should undergo careful clinical follow-up allowing the immediate detection and treatment of PTMs. Surgical resection alone in early MPM is associated with high local recurrence rates (69% after P/D and 38% after EPP) [2]. Therefore, to reduce local failure rate conventional RT has been used as a component of potentially curative trimodality treatment. Adjuvant RT was first used in patients after EPP and was delivered with anterior posterior photon fields matched with electron boost fields. A similar hemithoracic RT technique was explored after P/D, but additional block for central part of the lungs was required. The population based studies data on the potential role of adjuvant RT in improving overall survival (OS) are conflicting [3]. However, a subsequent analysis utilizing the National Cancer Database (NCDB) revealed the improvement of the 2-year rate of OS from 20% to 34% in patients with MPM receiving conventional RT after surgery [3]. Without significant improvement in local control and overall survival after P/D, conventional RT has been shown to decrease local recurrence after EPP to 13% and result in a median survival of 17 months [3]. The benefit in local control was strongly dose-dependent and obtained with a median dose of ≥54Gy [3]. Subsequently, the IMRT technique was implemented to improve adjuvant RT outcomes after P/D (IMPRINT approach). This novel method offers better coverage of the extensive, irregularly shaped target, safer dose escalation in the target volume and optimal sparing of OARs, but results in more heterogenous dose distribution, with a larger volume of normal tissue receiving low-dose radiation than in conventional techniques. IMRT was shown to be associated with a lower incidence of local recurrence (14% vs 42%), improved overall survival (median 20 vs 12 months) and lower rates of grade ≥2 esophagitis (23% vs 47%) when compared with conventional techniques [4]. A potential disadvantage of IMRT is the dose delivered to the contralateral lung that is associated with higher risk of pneumonitis (up to 46% of fatal pneumonitis in early series) [5]. Mean contralateral lung dose >8,5Gy and higher percentage (>80%) of the contralateral lung receiving dose >5Gy were significantly associated with higher risk of pulmonary toxicity. Strict dosimetric constraints, particularly on the contralateral lung (MLD<8,5Gy, V20<10%, V5<60%) and optimal algorithms in treatment planning (e.g. accurate measurement of volumes receiving low radiation doses on the basis of Monte-Carlo algorithm), are critical for radiotherapy planning [4]. Another novel approach employs the combination of IMRT and electrons, that offers better sparing of heart, liver and kidneys [6]. The technical aspects of adjuvant IMRT for MPM can further be improved. When compared to step-and-shoot linac-based IMRT, the use of helical tomotherapy significantly improved target coverage, homogeneity index, lowered average V5<40% and MLD<5Gy for the contralateral lung [7]. Intensity-modulated arc therapy also demonstrated superior V20 and better target coverage in addition to shorter treatment delivery time [8]. Proton therapy was also evaluated in the mentioned setting, offering better sparing of OARs and possibility of further dose escalation to improve target coverage [9]. Whether these dosimetric advantages will translate into clinical benefit, should be assessed in future prospective studies. The trimodality treatment of MPM consisting of induction chemotherapy (pemetrexed+cisplatin), surgical resection and adjuvant radiation has resulted in the best survival outcome thus far in non-randomized cohorts. Accelerated hemithoracic radiation (25Gy in 5 daily fractions), followed by EPP, was evaluated as an alternative. This approach is feasible and associated with encouraging overall survival (median of 51 months) and disease-free survival (47 months) in patients with epithelial cT1-3N0M0 MPM [10]. These promising results should support further studies to clarify the role of hypofractionated pre-operative RT in the management of MPM. Radiotherapy can provide palliation of chest pain in the course of MPM in 50-60% of cases, although the duration of response is often disappointing (2-3 months) [11]. An effective palliation was observed after the dose ≥40Gy and a higher local response rate for patients treated with a 4Gy per fraction regimen compared with those receiving fractions lower than 4Gy was reported (50% vs 39%) [11]. Many aspects of RT for patients with MPM are still not standardized and warrant further investigations. Clinical trials designs will require integration of new systemic therapies, immune modulation and novel technology advances in RT, with the guidance of predictive and prognostic biomarkers, as well as genetic profiling. MPM patients with resectable disease should be encouraged to participate in clinical trials. Bibliography: 1. Arnold DT, Clive AO: Prophylactic radiotherapy for procedure tract metastases in mesothelioma: a review. Curr Opin Pulm Med 2017, 23(4):357-364. 2. Pass HI, Kranda K, Temeck BK, Feuerstein I, Steinberg SM: Surgically debulked malignant pleural mesothelioma: results and prognostic factors. Ann Surg Oncol 1997, 4(3):215-222. 3. Rosenzweig KE: Malignant pleural mesothelioma: adjuvant therapy with radiation therapy. Ann Transl Med 2017, 5(11):242. 4. Shaikh F, Zauderer MG, von Reibnitz D, Wu AJ, Yorke ED, Foster A, Shi W, Zhang Z, Adusumilli PS, Rosenzweig KE et al: Improved Outcomes with Modern Lung-Sparing Trimodality Therapy in Patients with Malignant Pleural Mesothelioma. J Thorac Oncol 2017, 12(6):993-1000. 5. Allen AM, Czerminska M, Janne PA, Sugarbaker DJ, Bueno R, Harris JR, Court L, Baldini EH: Fatal pneumonitis associated with intensity-modulated radiation therapy for mesothelioma. Int J Radiat Oncol Biol Phys 2006, 65(3):640-645. 6. Chan MF, Chui CS, Song Y, Burman C, Yorke E, Della-Biancia C, Rosenzweig KE, Schupak K: A novel radiation therapy technique for malignant pleural mesothelioma combining electrons with intensity-modulated photons. Radiother Oncol 2006, 79(2):218-223. 7. Sterzing F, Sroka-Perez G, Schubert K, Munter MW, Thieke C, Huber P, Debus J, Herfarth KK: Evaluating target coverage and normal tissue sparing in the adjuvant radiotherapy of malignant pleural mesothelioma: helical tomotherapy compared with step-and-shoot IMRT. Radiother Oncol 2008, 86(2):251-257. 8. Scorsetti M, Bignardi M, Clivio A, Cozzi L, Fogliata A, Lattuada P, Mancosu P, Navarria P, Nicolini G, Urso G et al: Volumetric modulation arc radiotherapy compared with static gantry intensity-modulated radiotherapy for malignant pleural mesothelioma tumor: a feasibility study. Int J Radiat Oncol Biol Phys 2010, 77(3):942-949. 9. Krayenbuehl J, Hartmann M, Lomax AJ, Kloeck S, Hug EB, Ciernik IF: Proton therapy for malignant pleural mesothelioma after extrapleural pleuropneumonectomy. Int J Radiat Oncol Biol Phys 2010, 78(2):628-634. 10. de Perrot M, Feld R, Leighl NB, Hope A, Waddell TK, Keshavjee S, Cho BC: Accelerated hemithoracic radiation followed by extrapleural pneumonectomy for malignant pleural mesothelioma. J Thorac Cardiovasc Surg 2016, 151(2):468-473. 11. Davis SR, Tan L, Ball DL: Radiotherapy in the treatment of malignant mesothelioma of the pleura, with special reference to its use in palliation. Australas Radiol 1994, 38(3):212-214.
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MS 08.03 - Basic Science and Surgical Advances in MPM (ID 7677)
15:45 - 17:30 | Presenting Author(s): Raphael Bueno
- Abstract
- Presentation
Abstract not provided
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MS 08.04 - Immunotherapy in MPM (ID 7678)
15:45 - 17:30 | Presenting Author(s): Anna Nowak
- Abstract
- Presentation
Abstract:
The recent success of checkpoint blockade in other malignancies has led a resurgence of interest in this modality for mesothelioma. Historically, occasional responses were seen with cytokine therapy, immunomodulatory gene therapy, and vaccination incorporating suicide genes or immunological adjuvants. However, the availability of checkpoint blockade and identification of mesothelioma tumour antigens has opened the field to a plethora of multicentre clinical trials and to interest in developing immunotherapy for this indication. The cytotoxic T-lymphocyte Antigen 4 (CTLA-4) blocking antibody tremelimumab was the first checkpoint blockade treatment trialled in mesothelioma, with two single arm phase II clinical trials reporting modest objective responses and encouraging stable disease(1, 2). Unfortunately, the subsequent randomised phase IIb study of tremelimumab versus placebo as second-line treatment for pleural mesothelioma, the DETERMINE trial, did not reach its primary endpoint (Kindler et al. in press). The next reported trials examined the efficacy of PD pathway blockade. Results from the phase I KEYNOTE 028 study mesothelioma cohort of 25 pre-treated patients were recently published. Using single agent pembrolizumab, the partial response (PR) rate of 20% was lower than originally reported, although a 72% disease control rate (DCR) was observed(3). All patients were selected for >1% tumour PD-L1 expression. The median duration of response was 12.0 months, with no new safety concerns. Three other trials of single-agent PD-pathway inhibition have been reported subsequently. Preliminary results have been reported from a second study of pembrolizumab as second line therapy, with PR of 21%, DCR of 80%, and median progression free survival (PFS) of 6.2 months(4). The NivoMes study of second-line single agent nivolumab reported a PR rate of 15%, with stable disease rates of 35% and a median PFS of 3.6 months(5). Neither of these studies selected for PD-L1 expression. Finally, the JAVELIN study of Avelumab, a PD-L1 inhibitor, in patients with prior therapy reported a PR rate of 9.4% and DCR of 57%(6). There is no clarity on the importance of PD-L1 expression as a predictor of response. As with other cancers, pseudoprogression and subsequent response can be seen in some patients with the use of checkpoint blockade in mesothelioma. Whilst the results of single-agent therapies have been hailed as promising, only a minority of patients derive durable benefit, and as yet there is no clear predictive biomarker. The current generation of clinical trials are focusing on a. evaluating single agent checkpoint blockade in randomised trials; b. combining immunotherapies; and c. combining checkpoint blockade with existing therapies. The MAPS-2 study recently reported on combination ipilimumab and nivolumab as second or third line treatment(7). 125 participants were rapidly recruited to this phase IIb clinical trial, and were randomised to receive either nivolumab alone, or nivolumab with ipilimumab. In the intention to treat population, the disease control rate was 51.6% for the combination and 39.7% for nivolumab alone, with PR rates of 24.2% and 17.5% respectively. PFS was 5.6 months in the combination arm vs. 4.0 months in the nivolumab arm, and there was a promising survival signal in the combination arm. Nevertheless, as with this combination in other settings, toxicity was substantial (although manageable) and three treatment-related deaths were reported. Further maturity of these data is awaited. Ongoing clinical trials of single agent checkpoint blockade included the randomised phase III CONFIRM trial, comparing nivolumab with placebo in 336 previously treated patients (NCT03063450), and the randomised phase III PROMISE-Meso study, comparing pembrolizumab with chemotherapy in the second line (plus) setting in 142 patients (NCT02991482). These studies should be sufficient to confirm results of the previous single agent/single arm trials, with further single agent studies of PD1 blockade in the second/third line setting unlikely to move the field forward substantially unless they are focussed on biomarker questions. The successful rapid recruitment of MAPS-2 augurs well for rapid completion of other combination immunotherapy studies. The CA-209-743 (CheckMATE 743) trial is comparing platinum based chemotherapy to combination nivolumab and ipilimumab in 600 patients (NCT02899299). The INITIATE trial (NCT03048474) is testing nivolumab and ipilimumab in just 33 patients, but with a biomarker focus. The completed NIBIT-Meso 1 trial is a phase II study of tremelimumab and durvalumab for which results are likely to be available soon (NCT02588131), with a further phase II trial of the same agents and similar design open in the USA (NCT03075527). Finally, in combinations of checkpoint inhibitors with conventional therapies, the most mature concepts are combinations with chemotherapy in the first line setting. Two single arm phase II clinical trials of identical design are combining cisplatin and pemetrexed first line chemotherapy with durvalumab, one Australian (ACTRN 12616001170415) and one in the USA (NCT02899195). A randomised phase II study in Canada is comparing first line cisplatin/pemetrexed with either pembrolizumab or chemotherapy plus pembrolizumab (NCT02784171). The Australian ‘DREAM’ study has completed recruitment. All trials are incorporating biomarker studies, which may prove particularly challenging in the context of concurrent chemotherapy. No discussion on immunotherapy in mesothelioma would be complete without comment on anti-mesothelin strategies. The anti-mesothelin immunotoxin SS1P has undergone phase I testing, however neutralising antibody development mandated combination with immunosuppressive pre-treatment moving forward. Durable responses have been seen in small numbers of patients(8). The chimeric monoclonal mesothelin antagonist MORAb-009 (Amatuximab) has completed early phase testing and is now in phase III combined with cisplatin and pemetrexed (NCT02357147). Mesothelin is also being used as the target antigen in Chimeric Antigen Receptor (CAR) T cell therapy in pilot testing. Finally, anetumab ravtansine is an antibody drug conjugate linking a human anti-mesothelin monoclonal antibody to the spindle poison DM4(9). Results have recently been released suggesting no benefit over single agent vinorelbine in a second-line phase IIb study (NCT02610140). This abstract is not exhaustive, with other immunotherapies under investigation including dendritic cell therapy, CAR-T cell therapy, and allogeneic tumour cell vaccine therapies amongst others. It remains unclear which immunotherapies, in which combinations, and at which point in the disease trajectory will be permanently integrated into management. Biomarker studies to predict both toxicities and outcomes are likely to be critical to guide patient selection. REFERENCES 1. Calabro L, et al. (2013) Tremelimumab for patients with chemotherapy-resistant advanced malignant mesothelioma: an open-label, single-arm, phase 2 trial. Lancet Oncol 14(11):1104-1111. 2. Calabro L, et al. (2015) Efficacy and safety of an intensified schedule of tremelimumab for chemotherapy-resistant malignant mesothelioma: an open-label, single-arm, phase 2 study. Lancet Respir Med 3(4):301-309. 3. Alley EW, et al. (2017) Clinical safety and activity of pembrolizumab in patients with malignant pleural mesothelioma (KEYNOTE-028): preliminary results from a non-randomised, open-label, phase 1b trial. Lancet Oncol 18(5):623-630. 4. Kindler H, et al. (2016) OA13.02 Phase II Trial of Pembrolizumab in Patients with Malignant Mesothelioma (MM): Interim Analysis. J Thorac Oncol 12(1):S293-294. 5. Quispel-Janssen J, et al. (2016) OA13.01 - A Phase II Study of Nivolumab in Malignant Pleural Mesothelioma (NivoMes): With Translational Research (TR) Biopies. J Thorac Oncol 12(1):S292-293. 6. Hassan R, et al. (2016) Avelumab (MSB0010718C; anti-PD-L1) in patients with advanced unresectable mesothelioma from the JAVELIN solid tumor phase Ib trial: Safety, clinical activity, and PD-L1 expression. J Clin Oncol 34:abstr 8503. 7. Scherpereel A, et al. (2017) Second- or third-line nivolumab (Nivo) versus nivo plus ipilimumab (Ipi) in malignant pleural mesothelioma (MPM) patients: Results of the IFCT-1501 MAPS2 randomized phase II trial. J Clin Oncol, p LBA8507. 8. Hassan R, et al. (2013) Major cancer regressions in mesothelioma after treatment with an anti-mesothelin immunotoxin and immune suppression. Sci Transl Med 5(208):208ra147. 9. Golfier S, et al. (2014) Anetumab ravtansine: a novel mesothelin-targeting antibody-drug conjugate cures tumors with heterogeneous target expression favored by bystander effect. Mol Cancer Ther 13(6):1537-1548.
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MS 08.05 - New Biological Insights (ID 7679)
15:45 - 17:30 | Presenting Author(s): Yoshitaka Sekido
- Abstract
- Presentation
Abstract:
Malignant mesothelioma (MM) is a mesodermally derived, primarily pleural or peritoneal tumor with aggressive behavior. The incidence of this once-rare tumor is increasing rapidly because of the widespread use of asbestos. In Japan, the annual number of MM-related deaths in 2015 was approximately 1,400, which is 3-fold higher than that observed 20 years ago. The median survival of patients with malignant pleural mesothelioma is 9 to 18 months after diagnosis, which necessitates urgent development of more effective new therapeutic modalities against this aggressive disease. Neurofibromatosis type 2 (NF2) is a tumor suppressor gene that is deleted or mutated in approximately 40% of MM tumors. The gene product of NF2, Merlin, suppresses MM cell proliferation, at least in part, by regulating the Hippo signaling pathway. Hippo signaling is a tumor-suppressive pathway, and alterations in the components of this pathway, including LATS2, SAV1, and AJUBA, have been detected in MM cells. Inactivation of the Hippo signaling pathway leads to the constitutive activation of YAP and TAZ, downstream transcription coactivators that are regulated by this pathway. We previously reported that inhibition of YAP in Merlin-deficient MM cells reduces cell proliferation and inhibits anchorage-independent growth, whereas expression of an active YAP mutant in immortalized mesothelial cells induces oncogenic transformation. While the oncogenic roles of YAP has been extensively studied in MM cells, the possible pro-oncogenic functions of TAZ, a homolog of YAP, is not well understood. Using a panel of MM cell lines, we observed that approximately 65% of these cell lines show activation (underphosphorylation) of TAZ. We knocked down TAZ with shRNA-TAZ in MM cells with high TAZ activation and detected strong inhibition of cell proliferation, anchorage independent growth, cell motility, and invasion in vitro. Meanwhile, immortalized mesothelial cells transduced with a constitutive activated form of TAZ (TAZ S89A mutant) showed enhancement of these in vitro phenotypes and tumorigenicity in nude mice. Using microarray analyses, we identified that while most upregulated genes were common between the TAZ and YAP activated cells, TAZ induced transcription of genes encoding cytokines and their receptors more than YAP. Among the upregulated cytokines, we observed that TAZ binds to the promoter region of the gene encoding IL1-beta along with TEAD transcription factors, which increased IL1-beta transcription and subsequently cell proliferation of immortalized mesothelial cells. In contrast, IL1-beta knockdown or an IL1 receptor antagonist inhibited cell proliferation of MM cells, suggesting that IL-beta signaling suppression may have stronger inhibitory effects on MM cells with TAZ activation. The mevalonate pathway has recently been reported to play a pivotal role in regulating the downstream events of the Hippo pathway. We identified antitumor effects of statin on MM cells with Hippo signaling pathway inactivation. Statin attenuated proliferation and migration of MM cells harboring a NF2 mutation by accelerating YAP phosphorylation/inactivation. Interestingly, not all MM cells with NF2-Hippo pathway inactivation exhibited statin sensitivity. All the statin high-sensitive MM cell lines had increased p-YAP/YAP ratios (inactivation) after statin exposure, whereas in statin low-sensitive cells, the p-YAP/YAP ratio was generally low or unchanged. Genetically, the statin high-sensitive MM cells harbored NF2 and/or LATS2 mutations without BAP1 mutation, whereas BAP1 mutations were frequently identified in statin low-sensitive cells. Indeed, the Y-MESO-25 cell line, carrying both NF2 and BAP1 mutations, regained moderate statin-sensitivity after transfection with a wild-type BAP1 plasmid, indicating that BAP1 mutations interfered with the anti-proliferative effects of statins on MM cells with Hippo pathway inactivation. However, the interactions between BAP1 and the Hippo pathway remain to be elucidated. In conclusion, YAP and TAZ activation via NF2-Hippo pathway inactivation is essential for MM cells to acquire more malignant phenotypes, and therefore, detailed understanding of the biology of this pathway is required to develop new therapeutic modalities against MM based on dysregulation of this pathway.
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MS 08.06 - Molecularly Stratified Therapy (ID 7680)
15:45 - 17:30 | Presenting Author(s): Hedy Lee Kindler
- Abstract
- Presentation
Abstract not provided
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MS 08.07 - Achieving Equitable Access to Novel Treatments for all Patients (ID 7681)
15:45 - 17:30 | Presenting Author(s): Liz Darlison
- Abstract
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Abstract:
The UK has the highest incidence of Mesothelioma in the world with over 2700 cases diagnosed in 2014 (Cancer Research UK 2017). Data for 80% of these patients was submitted and analysed as part of the UK’s National Lung Cancer Audit Mesothelioma Report (NLCAMR) 2016 (Royal College of Physicians [RCP] 2016). The report confirmed that an increasing number of patients are receiving chemotherapy in the UK particularly patients with a good performance status; 53% compared to 41% in the audit’s 2014 report. The current audit does not identify the proportion of patients who receive their treatment as part of a clinical trial however the report recommends “All patients should be offered access to relevant clinical trials even if this requires referral outside of their network” (RCP 2016). With an increasing number of mesothelioma clinical trials now available in the UK, and more in development, facilitating seamless movement of patients from one specialist clinical team to another is essential. Mesothelioma UK, a national charity dedicated to improving outcomes for those affected by Mesothelioma, is establishing a comprehensive package of services and resources specifically to support this. The charity’s vision, for ensuring equitable access to treatment and trials is outlined in the charity’s 2016-2021 Strategy, The Next Five Years (Mesothelioma UK 2016). This presentation provides insight into readily transferable measures Mesothelioma UK has developed to support equitable access to treatment and care across the UK. References Cancer Research UK 2017 (Last viewed August 4th 2017).
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Author of
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OA 02 - Mesothelioma: Challenges For New Treatment (ID 653)
- Event: WCLC 2017
- Type: Oral
- Track: Mesothelioma
- Presentations: 1
- Moderators:S. Hasegawa, Anna Nowak
- Coordinates: 10/16/2017, 11:00 - 12:30, F205 + F206 (Annex Hall)
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OA 02.02 - Ipilimumab and Nivolumab in the Treatment of Recurrent Malignant Pleural Mesothelioma: A Phase II Study (ID 9389)
11:00 - 12:30 | Presenting Author(s): Paul Baas
- Abstract
- Presentation
Background:
There is an increasing interest in the use of IO therapy in Mesothelioma (MPM). We previously reported on the effect of nivolumab (s.a) in patients with recurrent MPM with a disease control rate of 50% at 12 weeks. We therefore decided to test the effect of the combination of nivolumab and ipilimumab in recurrent MPM.
Method:
Patients with previously treated MPM and a PS of 0-1 are consented in this single arm prospective study. Pleural lesions must be available for biopsy before and after 6 weeks of treatment.Nivolumab is administered at a fixed dose of 240 mg (q2w) until progression and combined with ipilimumab (1mg/kg) on week 1, 7, 13 and 19. CT scans are performed every 6 weeks for analysis and duration of response. The primary endpoint is disease controle rate at 12 weeks. Translational research is performed on paired biopsies. A Simon’s minimax two-stage design is used to identify a DCR of >50%. Therefore 33 patients will be included.
Result:
From October 2016 until August 2017 38 patients gave informed consent. Three patients did not start due to progression or impossibility to biopsy. Two stopped after 1 cycle (due to progression or withdrawn consent). At time of analysis (August 29) 25 patients could be evaluated for response. At 12 weeks a DCR of 72% (18/25) and ORR of 28% (7/25) is observed. Two patients continued treatment after progression at 6 weeks; 1 achieved a PR after 4 months , and the other one is stable. Of the first 11 patients that have been in study for 6 months, 5 have PR, 1 SD and 4 PD. Toxicity is mild. SAE’s reported in the 38 patients occurred in 11 patients with grade 3 or 4 toxicity. No grade 5 toxicity was observed.
Conclusion:
In this interim analysis nivolumab plus ipilimumab meets the primary endpoint for patients with recurrent malignant mesothelioma. Toxicity is mild. The full data set will be presented at the WCLC.
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SH 04 - WCLC 2017 Highlights of the Previous Day (ID 754)
- Event: WCLC 2017
- Type: Scientific Highlights
- Track: Biology/Pathology
- Presentations: 1
- Moderators:
- Coordinates: 10/18/2017, 07:00 - 08:00, F203 + F204 (Annex Hall)
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SH 04.01 - Chemotherapy/Targeted Therapy, Nursing/Palliative Care/Ethics and SCLC/Neuroendocrine Tumors (ID 10932)
07:00 - 08:00 | Presenting Author(s): Paul Baas
- Abstract
- Presentation
Abstract not provided
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