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Fiona Blackhall
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MA22 - New Therapeutics, Pathology, and Brain Metastases for Small Cell and Neuroendocrine Tumour (ID 925)
- Event: WCLC 2018
- Type: Mini Oral Abstract Session
- Track: Small Cell Lung Cancer/NET
- Presentations: 1
- Moderators:
- Coordinates: 9/25/2018, 15:15 - 16:45, Room 206 BD
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MA22.03 - SCLC Circulating Tumour Cell Derived Explants: The Clinical Characteristics of Patients Whose Samples Generate CDX (ID 12969)
15:25 - 15:30 | Author(s): Fiona Blackhall
- Abstract
- Presentation
Background
Small cell lung cancer (SCLC) prognosis is dismal, with minimal improvement in recent years. Work with SCLC cell lines and targeted therapies have been disappointing when translated into clinical practice. Circulating tumour cells (CTCs) represent a readily accessible liquid biopsy, which can be used to generate CTC derived explants (CDXs) for the study of SCLC biology and the investigation of biomarkers and therapeutics. These clinically relevant models appear to mirror patient response to therapeutics. Our aim was to assess if the patients whose samples generated a CDX represent the SCLC population, and determine if the clinical features of these patients offer insight into CTC biology.
a9ded1e5ce5d75814730bb4caaf49419 Method
This was a single centre, retrospective analysis of 147 SCLC patients who had participated in The CHEMORES Study in which SCLC patients were asked to donate blood samples for the discovery and validation of novel biomarkers. Paired patient blood samples were taken for CTC enumeration using CellSearch Technology and for attempted CDX model generation. We obtained demographic and clinical information on these patients, and analysed the data for differences between patients whose blood samples generated a CDX and those whose did not.
4c3880bb027f159e801041b1021e88e8 Result
231 paired blood samples were taken from 147 patients, with 45 CDXs successfully generated from 34 patients. CTC number was significantly higher in samples which generated a CDX than those which didn’t, p=0.001. Successful progression samples had a significantly lower CTC number than successful baseline samples, p=0.026. There was no significant difference in age, gender, pack year history, performance status, stage, chemosensitivity or the presence of liver or brain metastases between patients whose samples did and did not generate a CDX. Metastatic burden was significantly higher in patients whose samples generated a CDX, p=<0.001. Progression free (PFS) and overall survival were significantly shorter in patients whose samples generated a CDX, p=<0.001
8eea62084ca7e541d918e823422bd82e Conclusion
CTC number correlates with CDX success, although a specific CTC phenotype may be more important. CTCs at progression may have a more aggressive phenotype than those at baseline. CDXs appeared to represent the SCLC population which is important when translating knowledge gained by studying CDXs into clinical practice. CTCs may play a role in the widespread metastatic dissemination of SCLC and thus survival of patients. Shortened PFS in the absence of difference in chemosensitivity may be due to outliers with particularly long PFS in the unsuccessful group. Further genomic and phenotypic analysis of subpopulations of CTCs may provide further insight.
6f8b794f3246b0c1e1780bb4d4d5dc53Only 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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MS32 - SCLC - From Benchside to Bedside - Clinical Science Session (ID 810)
- Event: WCLC 2018
- Type: Mini Symposium
- Track: Small Cell Lung Cancer/NET
- Presentations: 1
- Moderators:
- Coordinates: 9/26/2018, 13:30 - 15:00, Room 107
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MS32.03 - Liquid Biopsies for Drug Development in SCLC (ID 11542)
14:00 - 14:15 | Author(s): Fiona Blackhall
- Abstract
- Presentation
Abstract not provided
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MTE03 - Clinical Trial Design With Novel Lung Cancer Therapy (Ticketed Session) (ID 813)
- Event: WCLC 2018
- Type: Meet the Expert Session
- Track: Targeted Therapy
- Presentations: 1
- Moderators:
- Coordinates: 9/24/2018, 07:00 - 08:00, Room 105
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MTE03.02 - Novel Trial Design for Precision Medicine (ID 11551)
07:30 - 08:00 | Presenting Author(s): Fiona Blackhall
- Abstract
- Presentation
Abstract not provided
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P1.01 - Advanced NSCLC (Not CME Accredited Session) (ID 933)
- Event: WCLC 2018
- Type: Poster Viewing in the Exhibit Hall
- Track:
- Presentations: 1
- Moderators:
- Coordinates: 9/24/2018, 16:45 - 18:00, Exhibit Hall
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P1.01-26 - Single-Centre Experience of Clinical Outcomes for Advanced Lung Cancer Patients in Phase I Clinical Trials. (ID 13932)
16:45 - 18:00 | Author(s): Fiona Blackhall
- Abstract
Background
Response rates for patients enrolled in early phase clinical trials have historically been reported as 5-10%. An unprecedented number of novel therapeutic options and emerging therapies in lung cancer (LC) have resulted in greater emphasis on early phase clinical trials and molecular stratification.
We aimed to evaluate outcomes for patients with LC treated since 2015 with novel agents or combination strategies within an expanding early phase clinical trials unit at The Christie Hospital, Manchester, UK.
a9ded1e5ce5d75814730bb4caaf49419 Method
A database of patients consented to phase I clinical trials was interrogated for LC patients recruited over a three-year period. Clinical characteristics including histological sub-type, line of therapy, molecular phenotype, smoking status and ECOG performance status (PS) were collected for each patient. Patient records were reviewed for clinical trial allocation, treatment response, progression-free survival (PFS), and overall survival (OS).
4c3880bb027f159e801041b1021e88e8 Result
Over a three-year period to March 2018, 153 lung cancer patients were consented to Phase I clinical trials of Investigational Medicinal Products, of whom 113 (74%) commenced treatment. The median age of patients treated was 64y (range 28-84) with a male predominance (54%). All patients had a PS of 0-1 and 25% were non-smokers. Histological subtypes included non-small cell lung cancer (NSCLC), small cell lung cancer (SCLC) and mesothelioma. The overall response rate (RR) by RECIST criteria was 27% across all patients, with a disease control rate of 73%. Median PFS was 6 months, and median OS was 11 months in the entire cohort. Compared with patients with NSCLC, patients with SCLC had worse PFS (7mo vs 3mo, p=0.001) and RR (35% vs 0%). The 28 trials recruiting LC patients in the unit during this period involved therapies targeting EGFR and ROS1, PI3K-mTOR-AKT and RAS-RAF-MEK signalling, DNA repair genes, cell-surface protein overexpression and genes implicated in immune signalling. Novel agents included small molecule inhibitors, monoclonal antibodies, and antibody-drug conjugates, in addition to targeted agents combined with chemotherapy or immune checkpoint inhibitor combinations. Patients had between 0-5 prior lines of therapy with no difference in PFS, OS or RR regardless of prior treatment lines.
8eea62084ca7e541d918e823422bd82e Conclusion
Our data demonstrate clear benefit for lung cancer patient participation in early phase clinical trials. Novel therapeutic agents and evolution of early phase clinical trial design have resulted in promising options for patients with NSCLC, with RR>30% within our unit, regardless of prior treatment status. However, outcomes for SCLC patients lag behind and new therapeutic options are urgently needed.
6f8b794f3246b0c1e1780bb4d4d5dc53
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P1.16 - Treatment of Early Stage/Localized Disease (Not CME Accredited Session) (ID 948)
- Event: WCLC 2018
- Type: Poster Viewing in the Exhibit Hall
- Track:
- Presentations: 1
- Moderators:
- Coordinates: 9/24/2018, 16:45 - 18:00, Exhibit Hall
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P1.16-02 - Support and Information Needs for Patients with NSCLC Receiving Concurrent Chemo-Radiotherapy: Findings from the INSIGHT Study. (ID 12610)
16:45 - 18:00 | Author(s): Fiona Blackhall
- Abstract
Background
The curative intent pathway for patients with non-small cell lung cancer (NSCLC) is complex and burdensome. Concurrent chemotherapy and radiotherapy (chemo-radiotherapy) is used as first line treatment for inoperable stage 3 cancer,and requires the patient to attend multiple investigational procedures, separate appointments for chemotherapy and radiotherapy, intensive monitoring during treatment and multiple follow-up visits post treatment for up to 5 years to monitor late-toxicities and disease recurrence.The aims of this study are to identify the information needs of patients and their carers at key points along the treatment pathway and the preferred methods for information provision. A grant was awarded by the NLCFN to fund this patient experience, qualatative research study.
a9ded1e5ce5d75814730bb4caaf49419 Method
Semi-structured interviews were conducted with 15 patients, and their carer dyads where appropriate, recruited from a cancer centre in Manchester, U.K.
4c3880bb027f159e801041b1021e88e8 Result
Data collection is now complete with 15 patients recruited, of whom 6 were interviewed with a carer dyad. Thematic analysis is on-going and has been employed inductively to identify some of the emerging themes and key issues from the data collected. These include; preferred means of receiving information and level of information given, burden of treatment and earlier access to supportive care, information about life after treatment and the after effects of treatment, and preferred methods to access appropriate support.
8eea62084ca7e541d918e823422bd82e Conclusion
Further research is needed into the on-going needs of this patient cohort and data collection so far highlights areas for consideration when providing information to this patient cohort.
Emerging themes highlight that a specific booklet on concurrent chemo/radiotherapy would be preferred, covering all aspects of treatment, including a personalised treatment plan to include, where relevant mask wearing, the impact of side effects of treatment and how assess support. Early indications are that patients prefer a combination of verbal, written and visual information giving.
Collaboration work to link these patients on the concurrent treatment pathway in with early supportive care is optimal.Implementation of this service as part of the Concurrent treatment pathway will commence as a pilot study in July 2018, to assess the impact of earlier intervention to manage disease burden and treatment side effects, with an aim to reduce hospital admissions.
The evidence suggests further work is needed to improve information giving and support to these patients both pre and post treatment. Additional advice is required to support proactive management, to enhance recovery, whilst addressing the fear and anxiety patients and carers experience due to uncertain outcomes.
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P2.09 - Pathology (Not CME Accredited Session) (ID 958)
- Event: WCLC 2018
- Type: Poster Viewing in the Exhibit Hall
- Track:
- Presentations: 2
- Moderators:
- Coordinates: 9/25/2018, 16:45 - 18:00, Exhibit Hall
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P2.09-06 - Expression of PD-L1 on Routine Non-Small Cell Lung Carcinoma Sections: Comparative Assessment of SP263 (Ventana) and 22C3 (DAKO pharmDx) (ID 13019)
16:45 - 18:00 | Author(s): Fiona Blackhall
- Abstract
Background
The SP263 (Ventana Benchmark) antibody as a predictive immunohistochemical marker for pembrolizumab therapy provides an avenue for local testing. Pathologists without access to the Dako Autostainer Link 48 platform (certified for the Dako 22C3 antibody) have been restricted to referrals at external departments, resulting in an increased turnaround time. Here we report the results of our local verification of SP263.
a9ded1e5ce5d75814730bb4caaf49419 Method
Specimens previously assessed for 22C3 PD-L1 expression at either Royal Liverpool Hospital or Queen Elizabeth Hospital Birmingham were selected from the archives of Wythenshawe Hospital. Cases with less than 100 viable residual tumour cells were excluded. The same tumour block was selected for staining with the Roche SP263 clone and specimens were assessed for tumour proportion score (TPS), immune cell proportion and staining intensity. Assays were reported as disagreeing if a differing TPS changed the therapeutic cut-off ranges.
4c3880bb027f159e801041b1021e88e8 Result
Expression levels of 22C3 and SP263 were compared across 100 cases (43 resections, 26 biopsies, 26 lymph node aspirates, 5 node excisions); 59 adenocarcinomas, 33 squamous carcinomas, 8 not otherwise specified (70 primary, 30 metastatic). The TPS ranges (<1%, 1 - 49%, > 50%) were in agreement for 78 samples. Of the 22 cases with differing ranges, 15 reflected a TPS of <10% and 7 had greater differences e.g. 10% versus 60%. Reasons for discrepancies included faint membranous staining on a few of the 22C3 sections (not apparent on SP263), scoring of carcinoma in situ, possible scoring of cells at a deeper block level, and variation in interpretation by the scoring pathologists. The overall Pearson correlation coefficient (r) was 0.9025, p < 0.00001.
Table 1 Comparison of PD-L1 Ventana SP263 and Dako 22C3 tumour proportion scores SAMPLE DIAGNOSIS SP263 >/= 1% >/= 50% Liverpool
22C3
Birmingham
22C3
Discrepancy Pleural biopsy
Adenocarcinoma
1
No
No
1
N/A
No
Pleural biopsy
Adenocarcinoma
10
No
No
60
N/A
Yes
EBUS node
Metastatic adenocarcinoma
0
No
No
0
N/A
No
EBUS node
Metastatic adenocarcinoma
0
No
No
1
N/A
Yes
Resection
Adenocarcinoma
40
Yes
No
10
N/A
No
EBUS node
Metastatic squamous carcinoma
2
No
No
10
N/A
No
Resection
Adenocarcinoma
5
Yes
No
<1
N/A
Yes
EBUS node
Metastatic adenocarcinoma
0
No
No
0
N/A
No
Bronchial biopsy
Squamous carcinoma
10
Yes
No
70
N/A
Yes
Bronchial biopsy
Squamous carcinoma
0
No
No
0
N/A
No
EBUS node
Metastatic squamous carcinoma
<1
No
No
<1
N/A
No
EBUS node
Metastatic adenocarcinoma
<1
No
No
0
N/A
No
Bronchial biopsy
Squamous carcinoma
40
Yes
No
40
N/A
No
Resection
Squamous carcinoma
5
Yes
No
10
N/A
No
Lung biopsy
Adenocarcinoma
0
No
No
0
N/A
No
Lymph node biopsy
Metastatic adenocarcinoma
100
Yes
Yes
100
N/A
No
Resection
Adenocarcinoma
<1
No
No
N/A
<1
No
Lung biopsy
Adenocarcinoma
0
No
No
N/A
0
No
Resection
Adenocarcinoma
0
No
No
0
N/A
No
Resection
Adenocarcinoma
10
Yes
No
N/A
5 to 10
No
Resection
Adenocarcinoma
20
Yes
Yes
N/A
20-30
No
Resection
Squamous carcinoma
2 to 4
Yes
No
N/A
3 to 5
No
Bronchial biopsy
Squamous carcinoma
<1
No
No
N/A
<1
No
Bronchial biopsy
Squamous carcinoma
2 to 4
Yes
No
1
N/A
No
Lymph node biopsy
Metastatic adenocarcinoma
100
Yes
Yes
100
N/A
No
Bronchial biopsy
NOS
<1
No
No
N/A
<1
No
Bronchial biopsy
Adenocarcinoma
0
No
No
1
N/A
Yes
Resection
Adenocarcinoma
2 to 4
Yes
No
10
N/A
No
Lymph node biopsy
Metastatic squamous carcinoma
80
Yes
Yes
70
N/A
No
EBUS node
Metastatic adenocarcinoma
80
Yes
Yes
80
N/A
No
Bronchial biopsy
Squamous carcinoma
0
No
No
N/A
<1
No
EBUS node
Metastatic adenocarcinoma
90
Yes
Yes
80
N/A
No
Pleural biopsy
Adenocarcinoma
0
No
No
10
N/A
Yes
Bronchial biopsy
Squamous carcinoma
0
No
No
0
N/A
No
Bronchial biopsy
Squamous carcinoma
5
Yes
No
N/A
0
Yes
EBUS node
Metastatic squamous carcinoma
50
Yes
Yes
50
N/A
No
Bronchial biopsy
Squamous carcinoma
2 to 4
Yes
No
10
N/A
No
EBUS node
Metastatic adenocarcinoma
70
Yes
Yes
N/A
70
No
EBUS node
Metastatic adenocarcinoma
100
Yes
Yes
100
N/A
No
Bronchial biopsy
Squamous carcinoma
1
Yes
No
20
N/A
No
Resection
Adenocarcinoma
5
Yes
No
0
N/A
Yes
Resection
Adenocarcinoma
0
No
No
0
N/A
No
EBUS node
Adenocarcinoma
<1
No
No
0
N/A
No
Resection
Adenocarcinoma
5
Yes
No
10
N/A
No
EBUS node
Sarcomatoid carcinoma
0
No
No
0
N/A
No
Resection
Adenocarcinoma
0
No
No
N/A
<1
No
Lymph node biopsy
Metastatic squamous carcinoma
0
No
No
N/A
<1
No
Resection
Adenocarcinoma
60
Yes
Yes
N/A
60-70
No
Bronchial biopsy
Squamous carcinoma
0
No
No
0
N/A
No
Pleural biopsy
Adenocarcinoma
2 to 4
Yes
No
10
N/A
No
Lung biopsy
Squamous carcinoma
0
No
No
5
N/A
Yes
EBUS node
Metastatic adenocarcinoma
5
Yes
No
30
N/A
No
Resection
Pleomorphic carcinoma
70
Yes
Yes
80
N/A
No
Resection
Squamous carcinoma
0
No
No
1
N/A
Yes
Bronchial biopsy
Squamous carcinoma
10
Yes
No
20
N/A
No
Resection
Adenocarcinoma
50
Yes
Yes
N/A
10 to 20
Yes
Resection
Adenocarcinoma
0
No
No
N/A
<1
No
Resection
Pleomorphic carcinoma
1
Yes
No
20
N/A
No
Resection
Adenocarcinoma
0
No
No
0
N/A
No
Resection
Adenocarcinoma
10
Yes
No
N/A
2 to 3
No
EBUS node
Metastatic adenocarcinoma
100
Yes
Yes
100
N/A
No
Resection
Adenocarcinoma
5
Yes
No
N/A
<1
Yes
EBUS node
Metastatic adenocarcinoma
100
Yes
Yes
100
N/A
No
EBUS node
Metastatic squamous carcinoma
50
Yes
Yes
N/A
80
No
Resection
Adenocarcinoma
90
Yes
Yes
95
N/A
No
Resection
Adenocarcinoma
<1
No
No
N/A
<1
No
Resection
Adenocarcinoma
0
No
No
1
0
Yes
Resection
Adenocarcinoma
<1
No
No
5
N/A
Yes
Resection
Adenocarcinoma
20
Yes
No
20
N/A
No
Bronchial biopsy
NOS
50
Yes
Yes
60
N/A
No
Resection
Adenocarcinoma
2 to 4
Yes
No
N/A
5 to 10
No
Resection
Adenocarcinoma
0
No
No
10
N/A
Yes
Soft tissue
NOS
1
Yes
No
20
N/A
No
Bronchial biopsy
Sarcomatoid carcinoma
<1
No
No
N/A
<1
No
EBUS node
Metastatic adenocarcinoma
70
Yes
Yes
N/A
60 to 70
No
Pleural biopsy
Adenocarcinoma
80
Yes
Yes
N/A
70
No
Resection
Squamous carcinoma
<1
No
No
1
0
Yes
Resection
Adenocarcinoma
50
Yes
Yes
N/A
5 to 10
Yes
Resection
Adenocarcinoma
10
Yes
No
50
N/A
Yes
Resection
Adenocarcinoma
0
No
No
0
N/A
No
Resection
Squamous carcinoma
1
Yes
No
N/A
<1
Yes
Resection
Squamous carcinoma
100
Yes
Yes
100
N/A
No
Resection
Squamous carcinoma
5
Yes
No
10
No
Resection
Squamous carcinoma
70
Yes
Yes
N/A
70 to 80
No
Resection
Squamous carcinoma
90
Yes
Yes
N/A
10 to 20
Yes
EBUS node
Squamous carcinoma
<1
No
No
N/A
<1
No
EBUS node
Adenocarcinoma
0
No
No
N/A
0
No
EBUS node
Metastatic adenocarcinoma
70
Yes
Yes
N/A
80
No
EBUS node
Metastatic squamous carcinoma
50
Yes
No
N/A
70
No
Resection
Adenocarcinoma
<1
No
No
N/A
<1
No
EBUS node
Metastatic adenocarcinoma
40
Yes
No
30
N/A
No
Resection
Squamous carcinoma
90
Yes
Yes
N/A
100
No
Resection
Adenocarcinoma
40
Yes
No
40
N/A
No
EBUS node
Metastatic adenocarcinoma
80
Yes
Yes
N/A
70 to 80
No
EBUS node
Metastatic squamous carcinoma
1
Yes
No
N/A
<1
Yes
Bronchial biopsy
Squamous carcinoma
1
Yes
No
1
N/A
No
EBUS node
Metastatic adenocarcinoma
5
Yes
No
60
N/A
Yes
Primary EBUS
Pleomorphic carcinoma
100
Yes
Yes
90
N/A
No
Resection
Adenocarcinoma
90
Yes
Yes
90
N/A
No
Lymph node biopsy
Adenocarcinoma
<1
No
No
<1
N/A
No
Tumour expression profiles of PD-L1 are similar for the 22C3 and SP263 antibodies, with a rate of variation similar to previous reports. Cases that are discrepant may reflect differences in pathologist interpretation rather than the assay.
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P2.09-15 - A Next Generation Sequencing (NGS) RNA-Scan Multiplex Panel (QIAseq) to Identify Gene-Rearranged Non-Small Cell Lung Cancer (ID 12777)
16:45 - 18:00 | Author(s): Fiona Blackhall
- Abstract
Background
Oncogenic fusion gene rearrangements are detected in up to 10% of advanced NSCLC with important therapeutic (eg. ALK, ROS1) or translational impact (eg. RET, NTRK1). The ‘QIAseq’ fusion panel is a 31-gene NGS multiplex assay that synchronously detects multiple oncogene fusion transcripts from formalin-fixed paraffin-embedded (FFPE) tissue derived RNA (Figure 1).
a9ded1e5ce5d75814730bb4caaf49419 Method
QIAseq analysis was undertaken in 33 samples (31 NSCLC samples, 2 commercial controls). 12/31 NSCLC samples were positive controls with a known fusion genotype identified by Quantide X NGS or FISH +/- RT-PCR. The remaining 19/31 fusion negative NSCLC controls included 6 samples with EGFR/KRAS/NRAS mutations. Analysis required a minimum 2x 5ųM thick FFPE scrolls with >30% neoplastic cell content. Manual RNA extraction was undertaken in all samples except n=6 (ExScale automation extraction). NGS fusion breakpoints, crossing and spanning reads were calculated in QIAseq fusion-detected samples. An additional validation cohort of 40 NSCLC samples, including 20 with unknown fusion status will optimise QIAseq thresholds for fusion detection.
4c3880bb027f159e801041b1021e88e8 Result
48 QIAseq sequencing experiments was undertaken in 33 samples with ≥2 sequencing runs in 12 samples. QIAseq analysis detected a corresponding NGS fusion breakpoint in 14/14 (100%) positive controls including EML4-ALK (n=8), CLTC-ALK (n=1), CD74-ROS1 (n=3), CCDC6-RET (n=1) and 5-fusion control (n=1). QIAseq analysis was negative in 17/19 (89.4%) negative controls samples including all KRAS (n=4), NRAS (n=1) and EGFR (n=1) mutation samples. QIAseq detected novel fusion gene CD74 Exon 6-CAMK2A Exon 2 in n=1 sample subsequently confirmed on Sanger sequencing. Two separate runs detected TPM3 Exon 8-S100A7A Exon 2 fusion in n=1 sample not identified with Sanger sequencing. Both fusions have uncertain clinical significance. Validation cohort results will be presented.
8eea62084ca7e541d918e823422bd82e Conclusion
QIAseq detects NSCLC oncogenic fusions with high sensitivity and specificity. Future applications include optimising use of small biopsy specimens for synchronous gene rearrangement screening and identification of novel gene fusion targets.
6f8b794f3246b0c1e1780bb4d4d5dc53
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P2.13 - Targeted Therapy (Not CME Accredited Session) (ID 962)
- Event: WCLC 2018
- Type: Poster Viewing in the Exhibit Hall
- Track:
- Presentations: 1
- Moderators:
- Coordinates: 9/25/2018, 16:45 - 18:00, Exhibit Hall
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P2.13-01 - Brigatinib Use in England – Where Next? (ID 14260)
16:45 - 18:00 | Author(s): Fiona Blackhall
- Abstract
Background
ALK positive NSCLC is estimated to account for 1,600 cases per year in England. Brigatinib is a next generation ALK inhibitor with proven efficacy after crizotinib but its role in 1st line is still under investigation. If licensed in Europe it may further extend survival for this rare group of patients.
a9ded1e5ce5d75814730bb4caaf49419 Method
We conducted a multicentre retrospective study across hospitals from the National Health System (NHS) in England on ALK positive patients who were offered treatment with the newer generations of ALK inhibitors. For this analysis, patients who received treatment with brigatinib through Compassionate use program or clinical trials between 2012 and 2018 were selected. The primary aims were time of exposure to brigatinib (as a surrogate of clinical benefit) and the objective response rate (ORR). The secondary aim was the incidence of grade 3-4 toxicity. And an exploratory aim analysed the value of ALK inhibitors treatment sequence.
4c3880bb027f159e801041b1021e88e8 Result
A total of 30 patients with an ALK positive lung adenocarcinoma were included with a median age of 50 years. 53% of patients were female and 77% never smoked. 90% presented at diagnosis with metastatic disease and 63% developed brain metastasis. The median follow-up time since the start of brigatinib was 9.7 months and 53% of patients were on brigatinib at the time of analysis. In 57% of cases brigatinib was only used after a 2nd line of treatment. Only 6 patients were treated in the first line setting. The overall median time of exposure was 12.1 months (95% CI, 4.7 to 19.6) with a maximum exposure of 30 months. The ORR was 50% within the 28 evaluable patients. Median overall survival was not reached. Only 1 patient had grade 3-4 toxicity with increased AST. The use of brigatinib in 1st and 2nd lines (13 patients) did not reach a median exposure time and the ORR was 69%. Brigatinib post-crizotinib (9 patients) had a higher exposure time compared with post-ceritinib (13 patients), respectively, 9.1 (95% CI, 0.5 to 25.7) and 6.6 months (95% CI, 2.6 to 10.6). However the first sequence was more often used in 1st/2nd lines (50% vs 15%).
8eea62084ca7e541d918e823422bd82e Conclusion
Brigatinib is an active and very well tolerated drug. Despite being used mainly in heavily pre-treated patients, our data confirm a meaningful clinical benefit in this population. Its efficacy may be higher in earlier lines and we found no clear signal favouring a specific sequence of treatment.
6f8b794f3246b0c1e1780bb4d4d5dc53
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PL02 - Presidential Symposium - Top 5 Abstracts (ID 850)
- Event: WCLC 2018
- Type: Plenary Session
- Track: Advanced NSCLC
- Presentations: 1
- Moderators:
- Coordinates: 9/25/2018, 08:15 - 09:45, Plenary Hall
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PL02.04 - Discussant - PL02.03 (ID 14737)
08:40 - 08:45 | Presenting Author(s): Fiona Blackhall
- Abstract
- Presentation
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