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Kwun M Fong

Moderator of

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    ES 08 - Molecular Diagnostics and Targeted Therapy (ID 517)

    • Event: WCLC 2017
    • Type: Educational Session
    • Track: Chemotherapy/Targeted Therapy
    • Presentations: 5
    • Now Available
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      ES 08.01 - Overview of Diagnostics and Pathology (Now Available) (ID 7614)

      11:00 - 11:15  |  Presenting Author(s): Tetsuya Mitsudomi

      • Abstract
      • Presentation
      • Slides

      Abstract:
      Recent advances in molecular biology have revealed that lung cancer is not a single disease and that there are subsets of non-small cell lung cancer (NSCLC) with specific genetic alterations that are critical to the growth and survival of cancer cells. Alterations of the EGFR, ALK and ROS1 gene, which are present in a mutually exclusionary fashion, are representative driver oncogene mutations. Targeted drugs against each driver oncogene usually result in dramatic tumor shrinkage and prolongation of progression free survival (PFS) compared with conventional platinum doublet chemotherapy. However, there is only a weak association between WHO pathologic classification 2015 and type of driver oncogenes. Therefore, it is of utmost importance to identify who are likely to benefit from targeted drugs by performing molecular tests for each lung cancer patient who is a candidate for drug therapy. A list of driver oncogenes is further expanding; BRAF, RET, MET, HER2, NTRK1 are being recognized as new drivers that can be exploited in the clinic. It is getting more practical to screen these molecular alterations by use of next generation sequencing technology, rather than to detect each gene alterations one by one using different platforms. We have also known that not all the tumors with mutations of the same gene behave similarly. For example, while deletional mutation in exon 19 and L858R in exon 21 are two representative mutations that sensitize cancer cells to EGFR-tyrosine kinase inhibitors (TKI), G719X in exon 18 has an intermediate sensitivity and insertional mutation in exon 20 or de novo T790M are known to be resistant. It has been shown that there is a heterogeneity in efficacy of EGF-TKIs depending on the class of mutation. For example, afatinib is active among other EGFR-TKIs for exon 18 mutations. Furthermore, a certain molecular context is known to be associated with primary resistance even within lung cancers with the same EGFR mutations. For example, it is reported that mutations in the PI3K/AKT/mTOR pathway (AKT1, PIK3CA, STK11, PTEN) or TP53 mutations are more frequent in non-responders and are associated with shorter PFS. This context dependence may present in other driver oncogenes, too. Acquired resistance is almost inevitable in the treatment of lung cancer with targeted drug. Mechanisms of this resistance has been extensively studied and now we know there are at least 3 types of mechanisms; i.e., 1) target modification by the secondary mutation that alters the affinity between the drug and the target relative to the affinity between ATP and the target (e.g., T790M in EGFR, L1196M in ALK), 2) accessory pathway activation that bypass the inhibitory effect of the drug(e.g., Met amplification in EGFR), and histologic transformation, such as small cell lung cancer transformation and epithelial-mesenchymal transition. We are now able to use the newer generation of TKIs to treat some of the resistance due to the secondary mutation of the target gene. Osimertinib has recently been shown to prolong PFS of patients who acquired resistance to EGFR-TKI through T790M mutation compared with platinum-pemetrexed in the AURA 3 trial. Therefore, detection of this mutation which accounts for about 50~60 % of the acquired resistance against EGFR-TKI is important. However, re-biopsy is sometimes more challenging compared with that in the first-line setting, and therefore detection of T790M in cell-free DNA in plasma has been rapidly developed and is now approved in regulatory authorities in several countries. There is another issue which should be taken into consideration when treating patients with acquired resistance. When there are multiple metastatic lesions, resistance mechanisms may vary from one tumor to another. Hence, it can happen that while one tumor shrinks but others increase in size. It may be reasonable and thus beneficial for patients when treatment is planned according to most prevalent mechanism of resistance in the plasma as a sum of total resistant mechanism. In this talk, I would like to overview recent advances of molecular diagnosis in targeted therapy of lung cancer and also like to discuss future perspectives in this field.

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      ES 08.02 - Update of the Management of EGFR-Positive NSCLC (Now Available) (ID 7615)

      11:15 - 11:30  |  Presenting Author(s): James Chih-Hsin Yang

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      ES 08.03 - Update of the Management of ALK-Positive NSCLC (Now Available) (ID 7616)

      11:30 - 11:45  |  Presenting Author(s): D. Ross Camidge

      • Abstract
      • Presentation
      • Slides

      Abstract:
      ALK positive NSCLC represents 2-7% of advanced NSCLC. Three ALK TKIs have shown positive first line trials against either platinum-doublet chemotherapy (ceritinib and crizotinib) or against crizotinib (alectinib). At least three other first line trials against crizotinib are ongoing (brigatinib, ensartinib and lorlatinib). Activity of different ALK TKIs post crizotinib are characterized by comparable response rates but differing toxicity profiles, durations of benefit and extent of CNS activity. With changes in the first line standard, data post non-crizotinib ALK TKIs continues to emerge with attendant caution re the applicability of both biological and clinical data currently available for clinical decision making. Advances in our understanding of CNS trial endpoints has also helped facilitate cross trial comparisons of CNS activity of these different agents. Chemotherapeutic, radiotherapeutic and immunotherapeutic options other than ALK TKIs have all generated different clinical datasets - defining both some reasonable clinical options and some clearly in need of additional research.

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      ES 08.04 - Emerging Target Therapy in NSCLC (Now Available) (ID 7617)

      11:45 - 12:00  |  Presenting Author(s): Enriqueta Felip

      • Abstract
      • Presentation
      • Slides

      Abstract:
      As a result of recent advances, systematic genomic testing for patients with non-small cell lung cancer (NSCLC) is the new standard of care in clinical decision-making, due to the identification of driver molecular alterations that have triggered the development of new molecules targeting these specific alterations in cancer cells. Several studies have enabled to conclude that both EGFR-mutant and ALK-positive NSCLC constitute two defined subgroups of oncogene-driven tumors with potentially effective targeted therapy. Furthermore, approximately 15-20% of NSCLC diagnosed in Europe and North America bear EGFR mutations or ALK rearrangements, enhancing the significance of the development of drugs capable of interfering with their intracellular effects. Based on these results, the identification of other activating mutations has been pursued in hopes of improving survival in NSCLC by specifically treating these genomic alterations. These potential therapeutic targets include ROS1, BRAF, RET, HER2, MET exon 14 skipping mutations and NTRK, among others. Here, we seek to review the characteristics of emerging targets that enable interaction with molecules that specifically target these receptors in lung adenocarcinomas, as well as the results of preliminary studies that assess the efficacy of these new strategies applied to NSCLC. ROS1 ROS1 rearrangement characterizes a small subset (1%–2%) of NSCLC and is associated with slight/never smoking patients and adenocarcinoma histology. Crizotinib was shown to harbor relevant activity in ROS1-rearranged NSCLC. A number of agents including ceritinib, lorlatinib and entrectinib are now been developed in order to overcome the resistance to crizotinib. At present, ROS1-rearranged patients represents a clearly defined NSCLC molecular subgroup with highly active therapeutic options. BRAF BRAF mutations occur in 2%–4% of patients with NSCLC, with the most common resulting in a glutamate substitution for valine at codon 600 (V600E). Non‐V600E BRAF mutations make up the remaining BRAF mutations and may be either activating (i.e., G469A/V, K601E, L597R) or inactivating (i.e., D594G, G466V). Efforts targeting BRAF‐mutant NSCLC to date have almost exclusively focused on patients with V600E‐mutant disease. Direct inhibition of mutant BRAF and/or the downstream mitogen-activated protein kinase kinase has led to good outcomes survival in patients with BRAF-mutant metastatic NSCLC. Dabrafenib plus trametinib achieved 63·2% response rate (RR) in BRAF(V600E)-mutant NSCLC. RET RET fusions are detected in 1-2% of lung adenocarcinomas and a number of genes, such as KIF5B, CCDC6, NCO4 and TRIMM33, can act as fusion partners. In a global registry of RET positive NSCLC patients, 41 received a RET inhibitor achieving a median progression-free survival of 2.9 months and a median overall survival of 6.8 months. Response rate was 34% for those patients receiving cabozantinib and 27% for those receiving vandetanib. Overall RET inhibitors strategies seem active in a subgroup of patients with RET-rearranged NSCLC. However, RR is lower to that observed in EGFR-mutated/ALK-positive patients. HER2 HER2 mutations are identified in about 2-4% of NSCLC and are critical for lung carcinogenesis. A number of series shows the chemosensitivity of HER2-driven NSCLC, and the potential interest of HER2-targeted agents. In a recent study, NSCLC patients with HER2 mutations were treated with T-DM1 and achieved a 44% RR. MET Approximately 2-3% of NSCLCs harbor activating mutations of the MET proto-oncogene that cause exon 14 skipping (METex14) and accumulation of c-Met lacking a juxtamembrane domain. Recently, the clinical activity of anti-Met-targeted therapy was demonstrated in patients harboring MET exon 14 skipping lung cancer. MET seems a relevant target in NSCLC and a number of clinical trials with MET inhibitors in this population are now ongoing. NTRK TRK rearrangements represent the molecular driver of a subset of solid tumors, including 1-2% of NSCLCs. Preliminary data indicate that molecularly selected NSCLC patients harboring NTRK fusions derive an unprecedented clinical benefit from Trk-directed targeted therapies. There are two different targeted agents, entrectinib and larotrectinib, that are in phase II testing for any patients who have solid tumors with NTRK rearrangement, including NSCLC patients. Both drugs have achieved dramatic responses, regardless of histology in earlier phase I studies. In a study presented at ASCO 2017, larotrectinib has demonstrated consistent and durable antitumor activity in TRK fusion cancers, across a wide range of ages and tumor types. REFERENCES Shaw AT, Ou SH, Bang YJ, et al. Crizotinib in ROS-1 rearranged non-small-cell lung cancer: N Engl J Med. 2014; 371:1963-1971. Planchard D, Besse B, Groen HJ, et al. Dabrafenib plus trametininb in patients with previously treated BRAF (V600E)-mutant metastatic non-small cell lung cancer: an opne-label, multicentre phase 2 trial. Lancet Oncol. 2016;17:984-993. Gautschi O, Milia J, Filleron T, et al. Targeting RET in Patients With RET-Rearranged Lung Cancers: Results From the Global, Multicenter RET Registry. J Clin Oncol. 2017;35:1403-1410. Mazières J, Barlesi F, Filleron T, et al. Lung cancer patients with HER2 mutations treated with chemotherapy and HER2-targeted drugs: results from the European EUHER2 cohort. Ann Oncol. 2016;27:281-286. Lu X, Peled N, Greer J, et al. MET exon 14 mutation encodes an actionable therapeutic target in lung adenocarcinoma. Cancer Res. 2017 May 18. [Epub ahead of print]. Drilon A, Nagasubramanian R, Blake JF, et al. A Next-Generation TRK Kinase Inhibitor Overcomes Acquired Resistance to Prior TRK Kinase Inhibition in Patients with TRK Fusion-Positive Solid Tumors. Cancer Discov. 2017 Jun 3. [Epub ahead of print]. Hyman DM, Laetsch TW, Kummar S, et al. The efficacy of larotrectinib (LOXO-101), a selective tropomyosin receptor kinase (TRK) inhibitor, in adult and pediatric TRK fusion cancers. J Clin Oncol. 2017;35 (suppl; abstr LBA2501). Riely GL. What, When, and How of Biomarker Testing in Non-Small Cell Lung Cancer. J Natl Compr Canc Netw. 2017;15:686-688. Jordan EJ, Kim HR, Arcila ME, et al. Prospective Comprehensive Molecular Characterization of Lung Adenocarcinomas for Efficient Patient Matching to Approved and Emerging Therapies. Cancer Discov. 2017;7:596-609.

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      ES 08.05 - Oncogenomics for Clinicians (Now Available) (ID 7618)

      12:00 - 12:15  |  Presenting Author(s): Matthew Meyerson

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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Author of

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    MTE 22 - Management of Elderly Patients with Lung Cancer (Sign Up Required) (ID 571)

    • Event: WCLC 2017
    • Type: Meet the Expert
    • Track: Nursing/Palliative Care/Ethics
    • Presentations: 1
    • Now Available
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      MTE 22.01 - Any Differences in the Management of Elderly Patients with Lung Cancer between East and West? (Now Available) (ID 7863)

      07:00 - 07:30  |  Presenting Author(s): Kwun M Fong

      • Abstract
      • Presentation
      • Slides

      Abstract:
      Any Differences in the Management of Elderly Patients with Lung Cancer between East and West? Lung cancer is one of the commoner cancers in the world, accounting for 1.6 million cases annually. In many western countries, lung cancer rates have declined in contrast to the predicted increase in the incidence of lung cancer in Asia, especially among males. Many patients with lung cancer are older and this applies to all parts of the world. There are relatively few data for the older age group, since many studies have an age restriction, such that there can be uncertainty in the extrapolation of trial findings to the average older person. On the other hand it is clear that there are differences in lung cancer in the East and the West including genetic and biological differences such as smoking habits between genders, genetic aberrations such as the frequency of EGFR gene mutations, in addition to cultural and local preferences. Moreover clinical trials are often performed either in the East or the West, as are studies of lung cancer in the older population, such that extrapolation may be needed. In the work up of suspected lung cancer, the older patient may be less tolerant of diagnostic tests given the ageing process and potential concurrent co-morbid disease, especially smoking related diseases which can differ between East and West. In addition in terms of treatment apart from well-known somatic mutation differences, ethnic differences in efficacy and toxicity from therapies may differ, in addition to non-patient factors such as affordability, cultural sensitivities and preferences. Thus the challenge in interpreting and applying research and clinical trials data is includes the relative paucity of data on the older population as well as uncertainty whether the data that is available on the older population applies equally to those in the East and the West, even allowing for known biological differences. This presentation will examine knowledge gaps and differences that should be considered for the management of the older person with the lung cancer from the East and West, in the setting of cultural and genetic uniqueness.

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    P1.04 - Clinical Design, Statistics and Clinical Trials (ID 690)

    • Event: WCLC 2017
    • Type: Poster Session with Presenters Present
    • Track: Clinical Design, Statistics and Clinical Trials
    • Presentations: 1
    • Now Available
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      P1.04-003 - The International Lung Screen Trial: A Multi-Centre Study to Evaluate LDCT Screening Selection Criteria and Nodule Management (Now Available) (ID 8141)

      09:30 - 09:30  |  Author(s): Kwun M Fong

      • Abstract
      • Slides

      Background:
      There remain important knowledge gaps surrounding the optimal selection criteria of high-risk individuals for low-dose CT (LDCT) screening for lung cancer and the optimal management of screening-detected pulmonary nodules. The International Lung Screen Trial (ILST) is an international, multi-centre prospective cohort study with recruitment sites in Canada and Australia. The rationale and design for the study are presented here. The PLCO~m2012~ risk prediction model[1] may have higher sensitivity and positive predictive value in identifying individuals who develop lung cancer compared to the United States Preventive Services Task Force (USPSTF) criteria. The PanCan model[2] calculates malignancy probability in screen-detected nodules and provides a risk-based approach to managing pulmonary nodules. Both models will be prospectively tested in this study. Primary aims: (a) to define the optimal selection criteria for LDCT screening, (b) to evaluate pulmonary nodule management using the PanCan nodule risk calculator.

      Method:
      We aim to recruit 4,000 high-risk individuals with 5 years follow up. Eligible participants are current or former smokers, aged 55-80 years, with a PLCO~m2012~ lung cancer risk of ≥1.51% over 6 years or USPSTF criteria (age as above, plus ≥30 pack year history of smoking and smoking cessation <15 years ago). Exclusion criteria include: symptoms suspicious of lung cancer, severe co-morbidity, previous lung cancer and chest CT within the last 2 years. Baseline assessment includes interview, smoking status assessment and pulmonary function testing. Eligible individuals are offered a baseline screening LDCT and subsequent interval surveillance LDCTs dependent on the PanCan risk score. Participants with no nodules or nodule risk score of <1.5% will have biennial LDCT screening. Participants with nodule malignancy risk score ≥10%, or significant growth in subsequent scan will be considered suspicious for lung cancer and undergo clinical review for further investigation. The primary outcome is the proportion of lung cancers detected by either selection criteria. Secondary outcomes include: number needed to screen, cancer detection rate, lung cancer mortality, cancer stage distribution, resection rate, number of interval cancers, recall rate, invasive procedure rate, benign biopsy/surgery rate, screening-related adverse events and comprehensive healthcare economic evaluation.

      Result:
      This study is currently in its recruitment phase. Results will be reported in future conferences and peer-reviewed publications.

      Conclusion:
      The ILST trial will provide a clearer understanding on the optimum selection criteria for LDCT screening for lung cancer and prospective validation of the PanCan model. ClinicalTrials.gov number: NCT02871856 References: Tammemägi MC et al (2013). NEJM; 368:728-736. McWilliams A et al (2013). NEJM; 369:910-919.

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    P2.02 - Biology/Pathology (ID 616)

    • Event: WCLC 2017
    • Type: Poster Session with Presenters Present
    • Track: Biology/Pathology
    • Presentations: 1
    • Now Available
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      P2.02-002 - Digital Multiplexed Detection of Single Nucleotide Variants (SNV) in Non-Small Cell Lung Cancer Using NanoString Technology (Now Available) (ID 7881)

      09:30 - 09:30  |  Author(s): Kwun M Fong

      • Abstract
      • Slides

      Background:
      Non-small cell lung cancer (NSCLC) is a heterogeneous disease characterised by somatic mutations in many genes, some of which are actionable drivers. Modern management of NSCLC requires the identification such driver variants to predict sensitivity to targeted drug therapies. Current methods for mutation detection exhibit varying diagnostic accuracies and limitations. In this study, we determined the utility of a novel high-throughput assay by NanoString for mutation testing in comparison to an alternate platform. This is the first presentation of this combination of NanoString technologies in NSCLC.

      Method:
      Mutational status was evaluated using the nCounter SPRINT Profiler and the Vantage 3D DNA SNV Solid Tumour Panel in a cohort of 174 fresh-frozen NSCLC tumours, utilising digital counting of unique barcoded probes to detect 104 SNV, multi-nucleotide variants (MNVs) and InDels from 25 genes of clinical significance. 5ng of tumour-derived gDNA was subjected to multiplexed pre-amplification and hybridisation of variant-specific probes to unique fluorescent barcodes. Positive variant calls required raw digital count levels above 200, with a raw-count fold-change above the reference DNA sample greater than 2.0 and a statistical significance of p<0.01. SNV calls by the nCounter assay were made by comparison to a previous study using MALDI-TOF mass spectrometry. An agreement analysis was performed for variants common to both platforms to determine positive, negative and overall percentage agreement (PPA, NPA and OPA). A subset of discordant cases were validated using ddPCR.

      Result:
      The nCounter SNV assay detected at least one variant in 102/174 (58.6%) cases. Seven (4.0%) cases harboured two SNVs. KRAS variants were detected in 79 (45.4%) cases, EGFR in 6 (3.5%), PIK3CA in 3 (1.7%), TP53 in 3 (1.7%). Overall agreement analysis revealed PPA, NPA and OPA of 96.0%, 93.2% and 94.8% respectively. 5/9 discordant samples were available for validation using ddPCR. 4/5 validated cases favoured the nCounter assay, with one case harbouring a KRAS G12V variant confirmed at a fractional abundance of 1.15%.

      Conclusion:
      This study found the performance of the nCounter SNV assay and a contemporary platform to be highly concordant. The advantages of this technology include low DNA input, digital data output, reduced turn-around-time (<24hr) and customisability for inclusion of novel variants. The nCounter SNV assay is a robust and sensitive method for translational cancer research.

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    P2.13 - Radiology/Staging/Screening (ID 714)

    • Event: WCLC 2017
    • Type: Poster Session with Presenters Present
    • Track: Radiology/Staging/Screening
    • Presentations: 1
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      P2.13-011 - Optimal Selection Criteria for LDCT Lung Cancer Screening (ID 9628)

      09:30 - 09:30  |  Author(s): Kwun M Fong

      • Abstract

      Background:
      Lung cancer screening programs with low dose computed tomography (LDCT) could be economically viable if they targeted high-risk people. The optimal selection criteria have not been defined in prospective clinical trials. The goal of this prospective study is to test the hypothesis that lung cancer screening based on a highly predictive risk model: The Prostate, Lung, Colon, Ovarian (PLCO~m2012~) is superior to applying National Lung Screening Trial (NLST)-like criteria.

      Method:
      Participants were enrolled through three screening studies, two in Canada (Vancouver and Alberta) and one in London, UK. Eligibility included a PLCOm2012 6-year lung cancer risk ≥1.5% or NLST-like criteria (≥30 pack-years smoking history and quit ≤15 years with some variation in age limits – 55 to 80 years in BC, 55 to 74 in Alberta and 60 to 75 in UCL). The proportion of participants who have been found to have lung cancer or high risk lung nodules, requiring repeat imaging studies or biopsy prior to the next scheduled annual screening were compared between the two selection methods.

      Result:
      The demographics of participants are shown in Table 1. To date, 1,533 received a LDCT, of these, 341 met the PLCOm2012 criteria alone, 169 met NLST-like criteria and 1023 met both criteria. Twenty-seven participants have been found to have lung cancers. All 27 met the PLCOm2012 selection criteria alone while 62% met NLST- like criteria. No lung cancer was found in participants who met NLST-like criteria alone. There are 129 participants with suspicious lung nodules under close surveillance or scheduled for biopsy. Among these, 97% met the PLCOm2012 criteria and 74% met NLST-like criteria.

      Table 1. Clinical and Demographic Features of Study Cohorts
      Study Site British Columbia Alberta London Total
      No. Contacted 802 1661 1990 4453
      No. Eligible 364 741 812 1917
      No. Screened 241 688 604 1533
      Age (yrs) 65+/- 6.3 63.5 +/- 4.2 66+/-4.2 64.8+/- 5.7
      Sex (female/Male) 91F:150M 342F:346M 273F:331M 706M;827M
      Current:Former Smoker 103CS:138Ex 341CS:347Ex 443CS:161Ex 887CS:646Ex
      Pack Years (Mean +/-SD) 47.3+/-22 42.4+/-15.8 47.7+/-22.3 45.3+/-19.8
      Median Follow-up(months) 7.5 9.7 9.7
      No. of lung Cancers 3 7 17 27
      Participants with suspicios nodules 21 41 67 129


      Conclusion:
      Our preliminary results show that fewer people are eligible for screening using NLST-like criteria compare to a highly predictive risk model such as PLCOm2012. Thirty-seven percent more participants with lung cancer are identified by PLCOm2012.

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    P3.06 - Epidemiology/Primary Prevention/Tobacco Control and Cessation (ID 722)

    • Event: WCLC 2017
    • Type: Poster Session with Presenters Present
    • Track: Epidemiology/Primary Prevention/Tobacco Control and Cessation
    • Presentations: 1
    • Now Available
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      P3.06-008 - Lung Cancer Pathways: A Five-Year Program to Reduce Impact Through Epidemiological Modelling and Investment in Prioritized Interventions (Now Available) (ID 9858)

      09:30 - 09:30  |  Author(s): Kwun M Fong

      • Abstract
      • Slides

      Background:
      Pathways is a five-year program of targeted research to identify and implement those interventions that will have the greatest impact in reducing lung cancer incidence and mortality, and improving quality of life. It includes a sharply-focused research program to identify relevant interventions and health actions, a consultative phase with national and international experts to prioritise ‘best value’ interventions, whilst considering the broader political and economic issues around implementation and policy change. A final decision and investment stage will direct funding and research activities to implement the ‘best value’ interventions in lung cancer prevention, screening, early intervention, treatment and supportive care.

      Method:
      A microsimulation model (‘Policy1’) has been designed using a powerful, flexible platform that can be programmed with information about multiple aspects of lung cancer to formulate an evidence base for determining the ‘best value’ interventions by comparing the impact and costs of interventions. These aspects include the ‘natural history’ of the disease, prevention actions (including tobacco control and lifestyle interventions), individual risk factors and screening behaviours, and cancer treatment type and uptake in various population subgroups. Policy1 is informed by work programs in statistical projections of lung cancer mortality (based on available mortality data and Australian smoking survey data), systematic reviews, big data and epidemiological analysis, and implementation science, to address health behaviour change and contextual factors. A Scientific Advisory Committee (SAC) of key stakeholders provides content expertise and strategic advice about pursuing detailed analyses selected interventions.

      Result:
      The statistical projections program indicates that lung cancer mortality rates for males will continue to decline and plateau after 2035, while for females, the mortality rate is expected to decrease steadily after 2014. Data from over sixty years of Australian tobacco smoking surveys has been used to estimate smoking prevalence, tobacco consumption, quit rates and duration of smoking. Seven scoping reviews have been completed in the areas of preventative strategies, early diagnosis, treatment regimens and clinical practice guidelines, health services interventions, psychosocial and palliative care. Key questions have been formulated and presented to the SAC to guide selection of ‘best value’ interventions for detailed exploration.

      Conclusion:
      Pathways presents an innovative approach to addressing those interventions that are likely have the greatest impact on improving lung cancer outcomes. The program will make a significant contribution to reducing the burden of illness in the Australian population by engaging with key stakeholders, guiding future research priorities, and translating research evidence into action.

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    WS 01 - IASLC Supporting the Implementation of Quality Assured Global CT Screening Workshop (By Invitation Only) (ID 632)

    • Event: WCLC 2017
    • Type: Workshop
    • Track: Radiology/Staging/Screening
    • Presentations: 3
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      WS 01.16 - Session 3: Added Value to Lung Cancer CT Screening Programs (ID 10654)

      11:30 - 11:30  |  Presenting Author(s): Kwun M Fong

      • Abstract
      • Slides

      Abstract not provided

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      WS 01.32 - Canada & Australia (ID 10677)

      15:00 - 15:20  |  Presenting Author(s): Kwun M Fong

      • Abstract
      • Slides

      Abstract:
      The Prince Charles Hospital (TPCH) and UQ Thoracic Research Centre is partnering several sites in Australia to undertake an international lung cancer CT screening trial with the British Columbia Cancer Centre in Canada. The Australian sites include The Prince Charles Hospital, St Vincents Hospital in Sydney, Royal Melbourne Hospital and the Epworth Hospital Box Hill in Victoria, Sir Charles Gardiner Hospital and the Fiona Stanley Hospital in Western Australia. Around the world, lung cancer causes over one million deaths each year – more than any other cancer. In Australia alone, some 12,000 new cases of lung cancer will be diagnosed each year, while about 8,880 Australians will succumb to this terrible disease. It is the biggest cause of cancer deaths and only 15% survive beyond 5 years after diagnosis currently. Lung cancer is typically diagnosed at an advanced stage, when treatments are effective. So this international trial aims to identify how we can best detect lung cancer earlier, using modern low dose CT scanners and computerised detection. This trial will prospectively compare the effectiveness of the USPTSF and the PLCOm2012 risk stratification models for improving the effectiveness and cost effectiveness of CT screening for lung cancer. Substudies planned include QoL, smoking cessation, CAD and comorbid diseases.

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      WS 01.43 - 5. How Can IASLC Lead Global Lung Cancer Progress Over the Next 10 Years? (ID 10688)

      18:00 - 18:00  |  Presenting Author(s): Kwun M Fong

      • Abstract
      • Slides

      Abstract not provided

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