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Sanjay Popat
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ESMO-IASLC Best Abstracts (ID 62)
- Event: ELCC 2019
- Type: Proffered Paper session
- Track:
- Presentations: 1
- Moderators:
- Coordinates: 4/11/2019, 14:45 - 16:15, Room B
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Invited Discussant 102O and 103O_PR (ID 675)
14:45 - 16:15 | Presenting Author(s): Sanjay Popat
- Abstract
- Presentation
Abstract not provided
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Lunch & Poster Display session (ID 58)
- Event: ELCC 2019
- Type: Poster Display session
- Track:
- Presentations: 1
- Moderators:
- Coordinates: 4/11/2019, 12:30 - 13:00, Hall 1
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140P - Brigatinib experience on the ALK project (ID 576)
12:30 - 13:00 | Author(s): Sanjay Popat
- Abstract
Background
The ALK Project established a network across the UK with the aim to analyse treatment patterns/outcomes and promote collaborations and research. The treatment pathway for ALK+ patients has been revolutionised in recent years.
a9ded1e5ce5d75814730bb4caaf49419 Methods
A multicentre retrospective analysis across 32 NHS hospitals/trusts identified 196 ALK+ non-small cell lung cancer (NSCLC) patients who were offered treatment by Dec-2018. Patients who received brigatinib during their treatment pathway were selected. The primary aims were 2-years overall survival (OS) and median OS from start of brigatinib. The secondary aims were objective response rate (ORR), incidence of grade 3-4 toxicity and 5-years/median OS from diagnosis of advanced NSCLC.
20c51b5f4e9aeb5334c90ff072e6f928 Results
A total of 50 patients were included with 48% being males, 70% never smoked tobacco and the median age at diagnosis was 50 years. 66% of patients developed brain metastasis at some point during their care and 52% had brain metastasis at the start of brigatinib. Brigatinib was used as the first, second or subsequent ALK inhibitor in 18%, 50% and 32% of cases, respectively. 82% of patients were exposed to other ALK inhibitors during their treatment pathway and 46% received chemotherapy prior to the start of any ALK inhibitor. On a median follow-up (since start of brigatinib) of 10 months, patients stayed on brigatinib for a median of 9 months (95% CI, 3.1-14.9), reaching 14 months (95%CI 11.0-19.9) if no brain metastasis (p = 0.15). The overall ORR was 64% and the incidence of grade 3-4 toxicity was 16%. Median OS from start of brigatinib was not reached and the 2-years OS according to brain metastasis was 61% or 83%, in favour of those without brain metastasis (p = 0.037). The median OS from diagnosis of advanced NSCLC was not reached and the 5-years OS was 55%.
fd69c5cf902969e6fb71d043085ddee6 Conclusions
Brigatinib is well tolerated and an effective treatment even in heavily pre-treated patients or in those with brain metastasis. A nationwide collaboration is possible and revealed the remarkable survival improvements for ALK+ patients with the development of newer generations of ALK inhibitors.
b651e8a99c4375feb982b7c2cad376e9 Legal entity responsible for the study
The Christie NHS Foundation Trust.
213f68309caaa4ccc14d5f99789640ad Funding
Has not received any funding.
682889d0a1d3b50267a69346a750433d Disclosure
All authors have declared no conflicts of interest.
cffcb1a185b2d7d5c44e9dc785b6bb25
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Mini Oral session II (ID 63)
- Event: ELCC 2019
- Type: Mini Oral session
- Track:
- Presentations: 1
- Moderators:
- Coordinates: 4/11/2019, 16:40 - 17:40, Room C
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1O - Impact of MET variants on PD-L1 expression in pleomorphic lung carcinoma (ID 495)
16:40 - 17:40 | Author(s): Sanjay Popat
- Abstract
- Presentation
Background
Pleomorphic Lung Carcinoma (PC) is a rare subtype of NSCLCs poorly responsive to systemic therapy. It is a heterogenous tumour with both epithelial and sarcomatoid components. MET variants are targetable aberrations and have recently been reported to be more frequent in PCs. The relationship between MET and PD-L1 expression is not well understood. We determined PD-L1 expression in PCs and its relationship with MET variants.
a9ded1e5ce5d75814730bb4caaf49419 Methods
80 cases of pleomorphic carcinoma were identified from the biobank and diagnostic archives of Royal Brompton Hospital and Imperial College Healthcare NHS trust. DNA was isolated for determination of a. MET copy number by digital droplet PCR (ddPCR) and b. Genomic MET aberrations by NGS. IHC of PD-L1 (28-8) with % positive cells were scored by two pathologists independently and >49% tumour staining was defined as high.
20c51b5f4e9aeb5334c90ff072e6f928 Results
78 cases were evaluated for PD-L1 status with a median score of 44%. 23/63 (36%) cases had MET CN of > 2.2. METex14 splice variants were identified in 5/73 (7.2%) cases. 2/73 (2.7%) cases had deleterious MET mutations. By MET CN status: low/normal MET CN (<2.3) median PDL1 expression was higher (50%) than in high MET CN ( > =2.3: 37.5%; P = 0.18). This translates into a significantly fewer number of high PD-L1 expressors (>49%) in cases with high MET CN (>2.2; P = 0.06; Table). There was no significant difference in PDL1 expression between MET mutation vs. wild-type (P = 0.9)
fd69c5cf902969e6fb71d043085ddee6 ConclusionsMET copy number and PDL-1 expression
PD-L1 Expression MET CN < 2.3 MET CN > =2.3 Total PD-L1<50% 20 (50%) 17 (74%) 37 PD-L1 >50% 20 (50%) 6 (26%) 26
PCs have high levels of PD-L1 expression. There is an inverse relationship between MET CN and PD-L1 expression. This has implications when using checkpoint inhibitors for cases with MET copy number gain in NSCLC. Further evaluation is needed to better understand response to checkpoint inhibitors of PC cases with MET CN gain.
b651e8a99c4375feb982b7c2cad376e9 Legal entity responsible for the study
The Royal Marsden Foundation NHS Trust.
213f68309caaa4ccc14d5f99789640ad Funding
National Institute for Health Research (NIHR) and British Lung Foundation.
682889d0a1d3b50267a69346a750433d Disclosure
All authors have declared no conflicts of interest.
cffcb1a185b2d7d5c44e9dc785b6bb25Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.
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Proffered Paper session III (ID 64)
- Event: ELCC 2019
- Type: Proffered Paper session
- Track:
- Presentations: 1
- Moderators:
- Coordinates: 4/12/2019, 08:30 - 10:00, Room A
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106O - Brigatinib (BRG) vs crizotinib (CRZ) in the phase III ALTA-1L trial (ID 166)
08:30 - 10:00 | Author(s): Sanjay Popat
- Abstract
- Presentation
Background
We report results of the first interim analysis (IA) from the ALTA-1L study of BRG vs CRZ in anaplastic lymphoma kinase (ALK) inhibitor–naive, ALK-positive non–small cell lung cancer (ALK+ NSCLC; NCT02737501).
a9ded1e5ce5d75814730bb4caaf49419 Methods
This open-label, multicenter study enrolled patients (pts) with advanced ALK+ NSCLC. Eligible pts had ≤1 prior systemic therapy for advanced NSCLC. Asymptomatic central nervous system (CNS) metastases were allowed. Pts were randomized 1:1 to BRG 180 mg QD with 7-day lead-in at 90 mg or CRZ 250 mg BID. Primary endpoint was blinded independent review committee (BIRC)-assessed progression-free survival (PFS; RECIST v1.1); secondary efficacy endpoints included BIRC-assessed objective response rate (ORR), intracranial ORR (iORR), and intracranial PFS (iPFS). IAs were planned at 50% and 75% of 198 expected PFS events.
20c51b5f4e9aeb5334c90ff072e6f928 Results
275 pts were randomized (BRG/CRZ, n = 137/138); median age (years) 58/60. 26%/27% received prior chemotherapy for advanced disease, and 29%/30% had baseline brain metastases. At data cutoff (19 Feb 2018), with a median follow-up of 11.0/9.3 months (BRG/CRZ) and 99 PFS events, BRG met the prespecified threshold for statistical superiority vs CRZ in the primary endpoint of BIRC-assessed PFS (HR 0.49; 95% CI, 0.33–0.74; log-rank P = 0.0007); BRG median PFS was not reached (NR; 95% CI, NR) vs CRZ 9.8 months (95% CI, 9.0–12.9). Investigator-assessed PFS HR 0.45 (95% CI, 0.30–0.68); log-rank P = 0.0001. Table shows additional efficacy data. Most common grade ≥3 treatment-emergent adverse events (AEs): BRG: increased blood creatine phosphokinase (16.2%) and lipase (13.2%), hypertension (9.6%); CRZ: increased alanine aminotransferase (9.5%), aspartate aminotransferase (5.8%), and lipase (5.1%). Any grade interstitial lung disease/pneumonitis: BRG, 3.7%; CRZ, 2.2%. Discontinuations due to AE (BRG/CRZ): 11.8%/8.8%.
fd69c5cf902969e6fb71d043085ddee6 Conclusions
BRG showed a statistically and clinically significant improvement in PFS vs CRZ in ALK inhibitor–naive ALK+ NSCLC.
b651e8a99c4375feb982b7c2cad376e9 Clinical trial identification
NCT02737501.
7a6a3ffa2dadc03a6151ee2c4d6fa383 Editorial acknowledgement
Professional medical writing assistance was provided by Lauren Gallagher, PhD, (Peloton Advantage, Parsippany, NJ) and funded by Millennium Pharmaceuticals, Inc.
934ce5ff971f1ab29e840a35e3ca96e9 Legal entity responsible for the study
ARIAD Pharmaceuticals, Inc., a wholly owned subsidiary of Takeda Pharmaceutical Company Limited.
213f68309caaa4ccc14d5f99789640ad Funding
ARIAD Pharmaceuticals, Inc., a wholly owned subsidiary of Takeda Pharmaceutical Company Limited.
682889d0a1d3b50267a69346a750433d Disclosure
R. Califano: Honoraria, consulting/advisory role: AstraZeneca, BMS, Roche, MSD, Boehringer Ingelheim, Takeda, Novartis, Pfizer, Lilly Oncology. C. Gridelli: Speakers bureau, advisory role: Pfizer, Roche. A. Delmonte: Consulting/advisory role: AstraZeneca, Boehringer Ingelheim. M.R. Garcia Campelo: Honoraria: ARIAD, AstraZeneca, Roche, Pfizer, BMS, Boehringer Ingelheim; Speakers bureau, advisory role: ARIAD, AstraZeneca, Roche, Pfizer, BMS, Boehringer Ingelheim. A. Bearz: Speakers bureau, advisory role: AstraZeneca, Pfizer, Eli Lilly, BMS, Novartis, Roche, MSD, Boehringer Ingelheim, Takeda. F. Griesinger: Research funding to institution: AstraZeneca, Boehringer Ingelheim, BMS, Celgene, Lilly, MSD, Novartis, Pfizer, Roche, Takeda, Siemens; Consulting or advisory role: ARIAD, AstraZeneca, Boehringer Ingelheim, BMS, Celgene, Lilly, MSD, Novartis, Pfizer, Roche, Takeda, ARIAD, AbbVie, Siemens. E. Felip: Consulting/advisory role: AbbVie, AstraZeneca, Blue Print Medicines, Boehringer Ingelheim, BMS, Celgene, Eli Lilly, Guardant Health, Janssen, Merck KGaA, MSD, Novartis, Pfizer, Roche, Takeda; Speakers bureau: AbbVie, AstraZeneca, Boehringer Ingelheim, BMS, Eli Lilly, Merck KGaA, MSD, Novartis, Pfizer, Roche, Takeda. S. Popat: Research funding to institution: Boehringer Ingelheim, Epizyme, BMS, Clovis Oncology, Roche, Lilly, Takeda; Honoraria: Boehringer Ingelheim, AstraZeneca, Roche, Takeda, Chugai Pharma; Consulting or advisory role: Boehringer Ingelheim, Roche, Novartis, Pfizer, AstraZeneca, BMS, MSD, Guardant Health, AbbVie; Travel, accommodations, expenses: Boehringer Ingelheim, BMS, Merck Sharp & Dohme. A. Morabito: Honoraria: AstraZeneca, Roche, Boehringer Ingelheim, Pfizer, MSD, BMS. S. Ghosh: Honoraria/speakers bureau: Pfizer. M. Tiseo: Speakers bureau, advisory role: AstraZeneca, BMS, Boehringer Ingelheim, Eli Lilly, MSD, Novartis, Otsuka, Pfizer, Pierre Fabre, Roche. J. Haney, D. Kerstein: Employment, stock and other ownership interests: Arîad. D.R. Camidge: Honoraria: AstraZeneca, Takeda, Arrys/Kyn, Genoptix, G1 Therapeutics (DSMB), Mersana Therapeutics, Roche/Genentech, Ignyta, Daichii Sankyo (ILD adjudication committee), Hansoh SRC, Bio-Thera DSMB, Lycera, Revolution Med, Orion, Clovis, Celgene, Novartis); Research funding (ARIAD/Takeda). All other authors have declared no conflicts of interest.
cffcb1a185b2d7d5c44e9dc785b6bb25Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.
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The future of I-O in advanced NSCLC (ID 16)
- Event: ELCC 2019
- Type: Specialty session
- Track:
- Presentations: 1
- Moderators:
- Coordinates: 4/11/2019, 11:00 - 12:30, Room A
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Sequencing of I-O therapies (ID 38)
11:00 - 12:30 | Presenting Author(s): Sanjay Popat
- Abstract
- Presentation
Abstract not provided
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