Scientific Program

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    ISS 08 - Optimising the Continuum of Care for Patients with Oncogenic-Driven NSCLC - Pfizer Oncology

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      ISS 08.01 - Welcome and Introduction

      07:00 - 07:10  |  Presenting Author(s): Yasushi Goto

      • Abstract

      Abstract not provided

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      ISS 08.02 - Building on Experience and Driving Precision Medicine in ALK+ & ROS1+ NSCLC

      07:10 - 07:35  |  Presenting Author(s): Nicolas Girard

      • Abstract

      Abstract not provided

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      ISS 08.03 - Resistance to ALK and ROS1 Inhibitors: Addressing the Clinical Impact

      07:35 - 07:50  |  Presenting Author(s): Justin F Gainor

      • Abstract

      Abstract not provided

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      ISS 08.04 - Panel discussion

      07:50 - 08:00  |  Presenting Author(s): Yasushi Goto, Justin F Gainor, Nicolas Girard

      • Abstract

      Abstract not provided

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      ISS 08.05 - Meeting Close

      08:00 - 08:00

      • Abstract

      Abstract not provided

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    ISS 09 - The Evolution of Targetable Oncogenic Drivers in NSCLC: Novel Treatment Paradigms - Novartis

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      ISS 09.01 - Welcome and Introduction

      07:00 - 07:05  |  Presenting Author(s): Solange Peters

      • Abstract

      Abstract not provided

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      ISS 09.02 - NSCLC as a Model for Precision Oncology

      07:05 - 07:20  |  Presenting Author(s): Ben J Solomon

      • Abstract

      Abstract not provided

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      ISS 09.03 - Management of ALK+ NSCLC: A Rapidly-changing Landscape

      07:20 - 07:35  |  Presenting Author(s): Solange Peters

      • Abstract

      Abstract not provided

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      ISS 09.04 - Progress in the Treatment of BRAF-Mutated NSCLC: Where Are We Now?

      07:35 - 07:50  |  Presenting Author(s): David Planchard

      • Abstract

      Abstract not provided

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      ISS 09.05 - Expert Panel Q&A (Including Brief Summary and Close)

      07:50 - 08:00  |  Presenting Author(s): Solange Peters, Ben J Solomon, David Planchard

      • Abstract

      Abstract not provided

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    MTE 11 - How to Write a Scientific Paper (Sign Up Required)

    • Type: Meet the Expert
    • Track: Education/Publication/Career Development
    • Moderators:
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      MTE 11.01 - How to Write a Scientific Paper that will be Accepted

      07:00 - 08:00  |  Presenting Author(s): Alex Adjei

      • Abstract

      Abstract not provided

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    MTE 12 - Oncology Nursing (Sign Up Required)

    • 07:00 - 08:00
    • 10/17/2017
    • Location: Room 316
    • Type: Meet the Expert
    • Track: Nursing/Palliative Care/Ethics
    • Moderators:
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      MTE 12.01 - Peripheral Neuropathy in Lung Cancer Patients

      07:00 - 07:30  |  Presenting Author(s): Alex Molassiotis

      • Abstract

      Abstract:
      Introduction Chemotherapy-induced peripheral neuropathy (CIPN) is a common dose-limiting toxicity. Its prevalence and impact on quality-of-life (QOL) has variable documentation in the literature, due to differing assessment modalities utilized. Objectives To discuss the natural history and characteristics of chemotherapy-induced peripheral neuropathy (CIPN) in patients receiving taxane- and platinum-based chemotherapy. Methods for the study Prospective longitudinal study including patients commencing on taxane or platinum-based therapy, with assessment time-points at baseline, end of each chemotherapy cycle, and 6, 9 and 12-months. Assessments of neuropathy included: sensory assessment using 10gr monofilament and cotton wool, clinician neuropathy grading systems: WHO scale(1-item) and NCI-CTCAE(2-items), and FACT&GOG-Ntx scale. Results In total, 348 patients were recruited to undergo up to 10 assessments over 12 months from three centres in Hong Kong (n=215), Singapore (n=95) and UK (n=38). Participants received taxanes (n=157,46%), platinum (n=111,32%) or a combination of both (n=78,22%). CIPN demonstrated cumulative increase through the chemotherapy cycles and reached a peak at 6 months. Each assessment method showed different CIPN incidence The sample included 343 patients providing 2,399 observations. There was wide variation in CIPN prevalence rates (14.2-53.4%) using different assessments. Patient self-reported scales tended to double or triple the CIPN estimates compared to clinician-based or objective measures. Peak prevalence was around cycle six and the 6-month assessment (Figure 1). Prevalence was highest in taxane-based chemotherapy, followed by taxane-platinum combination. Platinum-based chemotherapy showed the lowest CIPN rate. Motor symptoms were more predominant than sensory ones. Time since chemotherapy was the only predictive factor of CIPN (ORs=9.6-66 depending on the scale used). Cumulative dose had no impact in the development of CIPN. There were relatively moderately to low correlations between the scales, suggesting validity issues. Quality of Life was significantly affected (p=0.48 to <0.001 for different domains at 6-months, 9-months,12-months assessment). Conclusions CIPN is common with taxane/platinum chemotherapy although less prevalent in this largely Asian population compared to past studies involving predominantly Caucasians. Current assessment methods are suboptimal and often limited only to sensory problems, while motor disturbances receive less attention. The variability in CIPN prevalence seen in past work may be the result of the type of assessment used. CIPN prevalence may be lower than that reported in the literature. It seems that from the moment CIPN appears it will run its course over time, irrespective of the chemotherapy cumulative dose, raising issues around the current practice of dose reduction/discontinuation. Assessment in practice needs to also consider motor neuropathic problems. Current scales may not be all appropriate to measure CIPN in a valid way, and a combination of scales is needed in practice. Key References: Cavaletti G., Frigeni B., Lanzani F., Mattavelli L., Susani E., Alberti P., CortinovisD., Bidoli P. (2010). Chemotherapy-Induced Peripheral Neurotoxicity assessment: A critical revision of the currently available tools. European Journal of Cancer, 46(3):479-494. Haryani H, Fetzer SJ, Wu CL, Hsu YY. Chemotherapy-Induced Peripheral Neuropathy Assessment Tools: A Systematic Review. Oncol Nurs Forum. 2017; 44(3):E111-E123. Le-Rademacher J2, Kanwar R, Seisler D, Pachman DR, Qin R, Abyzov A, Ruddy KJ, Banck MS, Lavoie Smith EM, Dorsey SG, Aaronson NK, Sloan J, Loprinzi CL, Beutler AS. Patient-reported (EORTC QLQ-CIPN20) versus physician-reported (CTCAE) quantification of oxaliplatin- and paclitaxel/carboplatin-induced peripheral neuropathy in NCCTG/Alliance clinical trials. Support Care Cancer. 2017 Jun 20. doi: 10.1007/s00520-017-3780-y. [Epub ahead of print] McCrary JM, Goldstein D, Boyle F, Cox K, Grimison P, Kiernan MC, Krishnan AV, Lewis CR, Webber K, Baron-Hay S, Horvath L, Park SB; IN FOCUS Delphi working party. Optimal clinical assessment strategies for chemotherapy-induced peripheral neuropathy (CIPN): a systematic review and Delphi survey. Support Care Cancer. 2017 Jun 7. doi: 10.1007/s00520-017-3772-y. [Epub ahead of print] Mols F, Beijers T, Vreugdenhil G, van de Poll-Franse L. Chemotherapy-induced peripheral neuropathy and its association with quality of life: a systematic review. Support Care Cancer. 2014; 22(8):2261-9 Seretny M, Currie GL, Sena ES, Ramnarine S, Grant R, MacLeod MR, Colvin LA, Fallon M. Incidence, prevalence, and predictors of chemotherapy-induced peripheral neuropathy: A systematic review and meta-analysis. Pain. 2014; 155(12):2461-70. Miaskowski C, Mastick J, Paul SM, Topp K, Smoot B, Abrams G, Chen LM, Kober KM, Conley YP, Chesney M, Bolla K, Mausisa G, Mazor M, Wong M, Schumacher M, Levine JD. Chemotherapy-Induced Neuropathy in Cancer Survivors. J Pain Symptom Manage. 2017 Jan 4. pii: S0885-3924(16)31243-X. doi: 10.1016/j.jpainsymman.2016.12.342. [Epub ahead of print] Alberti P, Rossi E, Cornblath DR, Merkies IS, Postma TJ, Frigeni B, Bruna J, Velasco R, Argyriou AA, Kalofonos HP, Psimaras D, Ricard D, Pace A, Galiè E, Briani C, Dalla Torre C, Faber CG, Lalisang RI, Boogerd W, Brandsma D, Koeppen S, Hense J, Storey D, Kerrigan S, Schenone A, Fabbri S, Valsecchi MG, Cavaletti G; CI-PeriNomS Group. Physician-assessed and patient-reported outcome measures in chemotherapy-induced sensory peripheral neurotoxicity: two sides of the same coin. Ann Oncol. 2014; 25(1):257-64. Acknowledgements Cheng H, School of Nursing, The Hong Kong Polytechnic University, Hong Kong SAR; Au JSK, Leung KT, Wong KH, Li YC, Department of Oncology, Queen Elisabeth Hospital, Hong Kong SAR; Lopez V, Chan A, Ng TRD, Sundar R. National University of Singapore, Singapore; Yorke J, The University of Manchester, UK

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      MTE 12.02 - Advance Care Planning: The Pros and Cons

      07:30 - 08:00  |  Presenting Author(s): Patsy Yates

      • Abstract

      Abstract:
      Patients and their family and friends consistently report that communication with health care providers has a major impact on their experience of lung cancer. In particular, being informed of treatment choices and being involved in care decisions are highly valued elements of health care by patients. Effective communication has become an increasingly important element of person centred care as treatment advances mean that patients with lung cancer are faced with more complex decisions and treatment choices. In this context, the process of advance care planning has grown in popularity as an important strategy to achieve optimal end of life care. Advance care planning is a process where a person discusses their values and healthcare preferences with their family, friends and healthcare team.[1] Advance care planning is a process that can be undertaken at any time and documented to inform health care decisions if the person can no longer communicate them. Various approaches to advance care planning have been described and a range of health care professionals can be involved in the process. Key elements of advance care planning include discussions of personal values and preferences for healthcare at end of life, establishing clear recommendation regarding future treatment, including discussions about palliative care, documenting patient values and preferences in an accessible site in the medical record, and encouraging the patient to discuss wishes with family/proxy.[2] The process also involves discussions about substitute decision makers who will act on the person’s behalf should the patient not be able to do so.[1] Studies report advance care planning improves ongoing and end-of-life care and personal and family satisfaction, and that families of people who have an advance care plan have less anxiety, depression, and stress.[3] However, studies across a number of countries suggest limited uptake by community members and by health care professionals, as well as poor knowledge and skills of health team members in advance care planning.[4] This is due to a range of factors, including health care professionals’ lack of confidence and skills in conducting sensitive and challenging conversations about end of life issues. Health care professionals are encouraged to have advance care planning conversations early, however there is no clear consensus about what early means in this context and how readiness for such conversations is interpreted from patient to patient. Advance care planning can also oversimplify the decision making process, as such decisions are inherently personal, will change of time, and are influenced by a range of sociocultural and health literacy factors. Negotiating the different perspectives of health professionals, family members, and patients is also very complex. In addition, legal issues give rise to confusion about the process in practice and current pressures to contain costs in health care means that some patients could feel pressured to make choices that do not reflect their true preferences. To address these concerns, advance care planning documentation is often extremely complex, creating even more barriers to the process. A further critical limitation of advance care plans is that even when they are documented, they are not accessible in practice, and where they are available, health care professionals and family members do not always follow the documented preferences. Significant advances are being made across many countries to address the limitations of advance care planning and optimise its use in practice. These advances are in areas including health care professional education and skills building, development of tools to guide practice, greater clarity about the inclusion of advance care planning in care pathways, and leveraging off developments in electronic medical records. Important work in terms of community awareness and understanding of advance care planning is also underway. References 1. What is advance care planning? Available at www.advancecareplanning.org.au, accessed 5[th] July 2017 2. NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) for Palliative Care V.1.2016. © 2016 National Comprehensive Cancer Network, Inc. 3. Detering, KM, Hancock, AD, Reade, MC, Silvester, W, 2010, ‘The impact of advance care planning on end of life care in elderly patients: randomised controlled trial’, British Medical Journal, 340: c1345.doi:10.1136 4. Lovell, A, Yates, P. 2014, Advance care planning in palliative care: A systematic literature review of the contextual factors influencing its uptake 2008-2012. 28(8), 1026-35.

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    MTE 13 - Malignant Pleural Mesothelioma: State of the Art (Sign Up Required)

    • 07:00 - 08:00
    • 10/17/2017
    • Location: Room 501
    • Type: Meet the Expert
    • Track: Mesothelioma
    • Moderators:
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      MTE 13.01 - Surgery for Malignant Pleural Mesothelioma

      07:00 - 07:30  |  Presenting Author(s): Scott Swanson

      • Abstract

      Abstract:
      Surgical treatment for malignant pleural mesothelioma (MPM) has an interesting history and currently remains the foundation of the best treatment for select cases of MPM. At its outset a radical pleural pneumonectomy was fraught with very high surgical mortality which overshadowed any possible benefit. As surgical technique, anesthesia and post-operative care improved the mortality plummeted to low single digits thus allowing the benefit of surgery to emerge. Currently the median survival for patients with MPM is 21, 19, 14 and 10 months for stage I, II, III and IV disease per IASLC data (1) Certain well selected subgroups of patients treated surgically in a multimodal fashion have a median survival up to 4 years or more (2). The optimal surgical procedure and multimodal protocol is currently in flux but the principles that are important include a complete macroscopic resection either by extended pleurectomy and decortication that generally includes resection of the diaphragm and pericardium or by an extrapleural pneumonectomy that includes the entire pleural envelope, lung and en-bloc pericardium and diaphragm. A complete node dissection is vital as nodal involvement is a negative prognostic factor in most series. Reconstruction of the diaphragm and pericardium is an important feature of the operation and when done well will limit the post-operative morbidity significantly. Intra-operative adjuncts such as photodynamic therapy, heated intrapleural chemotherapy or heated povodone-iodine have been shown in select series to likely improve local control and perhaps survival. Systemic chemotherapy and radiation therapy also are important to the outcome but the exact type and sequence is controversial. (3-5). The correct surgical technique and sequence is critical to a good outcome. Similarly, choosing the best patient for surgery is complex and of vital importance. Generally patients should have reasonable cardiopulmonary reserve and limited co-morbidities. Age is not a sole determinant and probably less important than the functional status of the patient but patients over age 80 should be approached with caution. An extensive cardiopulmonary workup and staging evaluation is mandatory. Assessment of pulmonary function including split function with a quantitative ventilation and perfusion scan, cardiac reserve with an echocardiogram (look at pulmonary artery pressures) and stress test and general assessment of functional status are basic points of information that are needed to move forward with surgery. Evaluation of tumor burden with a magnetic resonance chest scan, PET scan and mediastinal node evaluation with either endobronchial ultrasound or cervical mediastinoscopy are important to avoid operating on patients with disease outside the chest or disease involving N2 nodes. Induction therapy on a protocol is reasonable particularly if patients have mediastinal nodal disease or non-epithelial histology. Also assessment of either tumor thickness or tumor volume helps prognosticate and determine likelihood of nodal involvement. Other factors such as severe pain or a high platelet count portend a poor outcome. Right sided resections particularly pneumonectomy have a higher risk and if at all possible a pleurectomy/decortication procedure is preferred . However if the lung is contracted or so involved by tumor that the only way for complete resection is to remove the lung then it should be done particularly if the functional contribution is 20% or less. A generous posterolateral thoracotomy through the bed of the resected 6[th] rib is carried out. The extrapleural plane is entered and fully mobilized so that it is clear the tumor is resectable. Posteriorly, the aorta and esophagus must be free, apically the tumor should come off the subclavian artery, anteriorly the tumor should be able to be freed from the pericardium. The pericardium is often resected en-bloc with the tumor. It should be opened early to be sure there is no invasion of the heart. Inferiorly the diaphragm is resected bluntly at its origin from the chest wall and care is taken to be sure the pleural recesses are respected such that all of the pleura is taken with the specimen. The peritoneum is left intact from the overlying diaphragm. Care is taken to avoid injury to the inferior vena cava near its entrance into the right atrium. At this point the pleural envelope should be opened and the lung assessed. If the tumor can be completely resected by taking the visceral pleura then this is preferred and the lung is spared. If the lung is so involved that gross tumor will be left behind if significant lung is not removed then a pneumonectomy is carried out. A full mediastinal node dissection is performed and hemostasis is obtained. If an intra-operative adjunct is to be used it is given at this point. Following that, the stump is covered with local tissue, likely a strip of pericardium and in some cases omentum. The pericardium and diaphragm are reconstructed, each with a goretex patch, which has been described in referenced publications. For the left side the operation is very similar other than the inferior vena cava is not an issue and if a pneumonectomy is required is generally well tolerated (6). Newer molecular techniques are proving very useful in aiding the surgeon in making decisions about how aggressive a strategy to use (7). References 1. Rusch VW, Chansky K, Kindler HL et al. The IASLC mesothelioma staging project: proposals for the M descriptors and for revisions of the TNM stage groupings. J. Thorac Oncol. 2016;11:2112-9. 2. Sugarbaker DJ, Gill RR, Yeap BY et al. Hyperthermic intraoperative pleural cisplatin chemotherapy extends interval to recurrence and survival among low-risk patients with malignant pleural mesothelioma undergoing surgical macroscopic complete resection. J Thorac Cardiovasc Surg. 2013;145:955-63. 3. Friedberg JS, Simone CB 2[nd], Culligan MJ, et al. Extended pleurectomy-decortication-based treatment for advanced stage epithelial mesothelioma yielding a of nearly 3 years. Ann Thorac Surg. 2017;103:912-919 4. Lang-Lazdunski L, Bille A, Papa S, et al. Pleurectomy/decortication, hyperthermic pleural lavage with povidone-iodine, prophylactic radiotherapy and systemic chemotherapy in patients with malignant pleural mesothelioma: a 10-year experience. J. Thorac Cardiovasc. Surg. 2015;149:558-65. 5. Sugarbaker DJ, Richards WG, Bueno R. Extrapleural pneumonectomy in the treatment of epithlioid malignant pleural mesothelioma: novel prognostic implications of combined N1 and N2 nodal involvement based on experience in 529 patients. Ann Surg. 2014;260:577-80. 6. Sugarbaker DJ, Norberto JJ, Swanson SJ. Extrapleural pneumonectomy in the setting of multimodal therapy for diffuse malignant pleural mesothelioma. Semin Thorac Cardiovasc Surg. 1997 Oct;9(4):373-382 7. De Rienzo A, Cook RW, Wilkinson J et al. Validation of a gene expression test for mesothelioma prognosis in formalin-fixed paraffin-embedded tissues. J. Mol. Diagn. 2017,19:65-71.

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      MTE 13.02 - Systemic Treatments for Malignant Pleural Mesothelioma

      07:30 - 08:00  |  Presenting Author(s): Shirish M Gadgeel

      • Abstract

      Abstract not provided

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    MTE 14 - Imaging of Lung Cancer (Sign Up Required)

    • Type: Meet the Expert
    • Track: Radiology/Staging/Screening
    • Moderators:
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      MTE 14.01 - Computed Tomographic Features of Small Pulmonary Nodules: A Follow-Up Study

      07:00 - 07:30  |  Presenting Author(s): Masahiko Kusumoto

      • Abstract

      Abstract:
      A ground-glass nodule (GGN) is a morphologic description of pulmonary nodule category on thin-section chest computed tomography (CT). Pure GGNs are defined as focal nodular areas of increased pulmonary attenuation through which pulmonary parenchymal structures, such as pulmonary vessels or bronchial structures, can be observed. Part solid nodules present with ground-glass and solid components, in which the underlying pulmonary architecture cannot be visualized, whereas solid nodules are without ground-glass components. These nodules differ in pathological condition and natural history by type, and management corresponding to these differences is required. Transient GGNs, which disappear after 3 months in repeated CT, are likely due to inflammation or infection. If many small GGNs are present, these are more likely to represent atypical adenomatous hyperplasia (AAH), and follow-up with annual CT scans is advised. The majority of persistent solitary pure GGNs are pathologically atypical adenomatous hyperplasia, adenocarcinoma in situ (AIS), and minimally invasive adenocarcinoma (MIA); these nodules do not grow, or progress very slowly. Pure GGNs less than 15 mm in diameter are followed up after 3 months, 1 year, and 2 years with CT. In the meantime, when the GGN increases in size, or if solid components appear in the nodule, a definite diagnosis is made, although such cases are extremely rare. Even when a solid component appears inside the GGN, there are options for further follow-up as long as the diameter of the solid component remains less than 5 mm. A solitary pure GGN that is unchanged for 5 years could remain unchanged even after 10 years. Of solitary pure GGNs 5 mm or less in diameter, approximately 10% will grow, with 1% developing into invasive adenocarcinomas or MIAs. Therefore, it is recommended that solitary pure GGNs smaller than 5 mm be rescanned after 3 to 5 years, in order to look for development of a solid component. In cases of part solid nodules, which present with both ground-glass and solid components, the underlying pulmonary structures cannot be observed. These nodules are more suspicious than pure ground-glass nodules and thus require more aggressive management if they persist. Persistent part solid nodules usually represent lepidic predominant adenocarcinomas or MIAs. In particular, if the margin of a part solid nodule is well-defined on thin-section CT, it is often dianogsed as lepidic predominant adenocarcinoma or MIA. Some inflammatory lesions show part solid nodules on CT; if the nodules do not disappear or decrease in size on CT after 3 months, they are highly likely to be adenocarcinomas. Usually, a lung adenocarcinoma showing part solid nodules on CT does not grow rapidly in 3 months. Therefore, a 3-month CT follow-up is effective for diagnosing a partly solid nodule (which is difficult to diagnose). Small solid nodules are most commonly observed, although few are malignant. These nodules are easily detected on CT, but it is difficult to diagnose their malignancy. Nodules over 10 mm in diameter are suspicious for malignancy, and an attempt should be made to obtain a definitive diagnosis. Solid nodules with a maximum diameter of 5 to 10 mm in smokers should be followed up until after 3 months, 6 months, 1 year, and 2 years on CT. In non-smokers, however, intervals of follow-up could be longer. Solitary nodules less than 5 mm in diameter are very rarely malignant and only require annual follow-up if patients have risk factors such as smoking. The reasons why intervals of follow-up differ between smokers and non-smokers are because smokers have a higher risk of lung cancer, and the tumor doubling time is shorter in the case of lung cancer in smokers. If the size of a nodule increases during follow-up, a definitive diagnosis is needed. If the size of a solid nodule is unchanged for 2 years, the possibility of lung cancer is extremely low, and follow-up observation may be completed; however, in smokers, emphysema is often complicated, and the diagnosis is more difficult as the shape and margin of the nodule also vary. In the case of small cell carcinoma, hilar and mediastinal lymph node metastasis may occur 3 months after nodule detection, and the early diagnosis of small cell lung cancer is extremely difficult. In the present lecture, the outcomes of follow-up of these various small pulmonary nodules will be illustrated. Figure 1CT image at detection Figure 210 years later





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      MTE 14.02 - Diagnostic Intervention for Lung Cancer

      07:30 - 08:00  |  Presenting Author(s): David F Yankelevitz

      • Abstract

      Abstract:
      Diagnostic procedures for lung cancer can broadly be defined as those that lead to the initial diagnosis, evaluation of extent of disease, and obtaining tissue for further characterization of molecular and genetic properties of the cancer. In each of these areas there have been tremendous technologic advances which ultimately lead to added complexity in terms of best utilization of tissue. Tissue can be obtained by the radiologist through either the use of fine needles (either single-needle or co-axial) or through the use of cutting needles which obtain cores of tissues) and through a variety of guidance techniques including fluoroscopy, CT guidance (including CT fluoroscopy), sonography, and MR. Most commonly, now for lung procedures is CT guidance. With the increasing use of CT imaging lung nodules are detected at smaller and smaller sizes and the diagnostic approach becomes increasingly challenging. In addition, since there is better chance for cure when treatment is performed earlier the desire to obtain early diagnosis is strong. The question that arises primarily relates to what level of confidence is needed before a definitive surgical procedure is performed. Factors to be balanced are the diagnostic accuracy of competing non-invasive tests such as growth analysis or PET-CT, compared to needle biopsy. All this must also be balanced with the type of surgical procedure that is being considered and the tremendous improvements that often allow patients to be discharged within 1-2 days post surgery. Evaluating extent of disease includes biopsy of either lymph nodes or other structures such as ribs, adrenal glands, liver etc. Within the chest, evaluation of lymph nodes pre-operatively has been greatly enhanced through the use of bronchoscopy with ultrasound. However, there are many nodal stations that remain difficult to reach using this approach that can be reached with CT guided needle biopsy, including all compartments of the mediastinum and hilum. Lesions outside the lung can also be evaluated including the soft tissues and the ribs. These lesions are often detected on PET-CT and are amenable to needle biopsy. Most rib lesions can easily be accessed with simple aspiration type needles. The need for further characterization of cancers through molecular or genetic testing is rapidly gaining in importance. As new therapeutic techniques become available the need for more complete characterization of tumors becomes increasingly important. Here the question relates to how much tissue is needed to perform the desired test. This is a continuously evolving area and depends on which particular tests are being requested, availability of the institution to perform the particular test, and the potential to obtain the appropriate amount of material given the particular characteristics of the lesion. Critical to these considerations is developing a close working relationship with the pathology department so as to make sure all of these considerations are taken into account prior to performing a procedure. Collaboration with the pathology department is critical on many levels and may need to vary depending on available resources. Best would be having rapid on-site evaluation (ROSE), although this is not always possible. For each situation, a plan as to how to best maximize yield needs to be developed. In this talk, I will outline the many considerations for how best to optimize the diagnostic yield of material obtained by interventional radiologist depending on the characteristics of the lesion and present various strategies to integrate these approaches into various scenarios where tissue is required.

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    MTE 15 - Biomarkers for Immune Checkpoint Inhibitors (Sign Up Required)

    • Type: Meet the Expert
    • Track: Immunology and Immunotherapy
    • Moderators:
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      MTE 15.01 - Mechanisms of Resistance in IO

      07:00 - 07:30  |  Presenting Author(s): Roy S. Herbst

      • Abstract

      Abstract not provided

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      MTE 15.02 - Fast and Deeper Responders with IO: How to Select Them?

      07:30 - 08:00  |  Presenting Author(s): Hossein Borghaei

      • Abstract

      Abstract not provided

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    MTE 16 - Technical Issues after Neoadjuvant Chemoradiation - Surgeon's Perspective (Sign Up Required)

    • Type: Meet the Expert
    • Track: Surgery
    • Moderators:
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      MTE 16.01 - Difficulties of Surgery After Induction of Chemoradiotherapy

      07:00 - 07:30  |  Presenting Author(s): Eric Vallieres

      • Abstract

      Abstract:
      Difficulties of surgery after induction chemoradiotherapy (CRT) Surgery after induction therapy can be very challenging. From my own observations, this may particularly be an issue when the patient had nodal involvement at presentation and experienced a good response to the induction treatment (induction CRT or even induction C alone) where fibrosis of the responding lymph nodes may make the hilar vascular mobilization more difficult. The following lines will describe some tips on how to minimize the risks of such resections. Preoperatively: One should always take advantage of the induction therapy period (12 weeks or more) to achieve absolute smoking cessation in these patients. After induction therapy, one should obtain a fresh set of PFTs including a DCO measurement as both radiation and some of the induction chemotherapy agents may have caused significant pneumonitis with resulting altered lung function. If there is a possibility that a pneumonectomy will be required, prepare yourself. (QVQ, stress echo). Radiation esophagitis may have brought some nutritional issues, consider an alimentary “boost” when a significant weight loss has occurred during the induction phase of therapy. If there may be a risk that the SVC will be clamped, repaired or replaced, discontinue the port-o-cath preoperatively. Finally, make sure to review all imaging, particularly the pre-induction therapy CT. Surgery Personally, I approach these cases via open thoracotomy, though some have reported successful resections on MIS platforms. All patients get an epidural catheter preop. If one anticipates, issues with the SVC with a R upper lobar resection, get infra diaphragmatic IV access preop. Emphasize w anesthesia, in the preoperative area, the absolute need to keep these patients dry: an irradiated mediastinum cannot handle excess fluid. At entry, I prepare/ harvest the intercostal muscle, without dividing it. (I now keep the omentum for “later”, if needed to manage for a complication, and spare the serratus anterior in all cases). If accessible, I usually clear zone 7 first, with frozen section read. (The frozen section information/ feedback during this type of surgery can be very useful to have when one gets into a tough surgical corner…) If one is attempting a lobectomy and anticipates possible difficulties in the hilum, one should consider obtaining early circumferential control of the main veins and main PA (if possible), and even do so intrapericardially if needed. Similarly, early division of the azygos vein on the right, may help when one anticipates difficulties accessing the main R PA and surrounding structures. One may have to alter their “routine” sequence of dividing the central structures. With both upper lobes, when bulky fibrotic changes are present in the suprahilar areas, proceeding retrograde, from the fissures up is often very helpful. As well, dividing open the upper lobe bronchi from the back can help access and control the often fibrosed and foreshortened proximal lobar PA branches. On the left, I will identify the vagus nerve low down, away from the fibrotic field and follow it up into the AP window to minimize the risks of inadvertently injuring the recurrent nerve. During the case, I constantly remind anesthesia to keep these patients dry. For pneumonectomies, we give a steroid bolus before dividing the main PA , similarly we initiate amiodorone prophylaxis by infusion. In a R pneumonectomy, when we have stapled the bronchial stump, I add an additional non resorbable monofilament stitch to reinforce both ends of the bronchial stapled line. Finally, we cover all of our bronchial stumps with the IC muscle flap. POSTOP Remember to keep the patient dry. We give amidorone prophylaxis for 72 hours after pneumonectomies’ or other patients considered at elevated risk of going into atrial fibrillation post op. Beware of possible left vocal cord palsy after L pneumonectomy and left upper lobectomy: we keep these patients NPO until we are confident that their cords are OK. If there are any concerns, we get an immediate laryngoscopy. If the left cord is found to be paretic, we immediately get VC medialization (not negotiable)

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      MTE 16.02 - Surgery for Stage IIIA NSCLC - Surgeon's Perspective

      07:30 - 08:00  |  Presenting Author(s): Gail Elizabeth Darling

      • Abstract

      Abstract:
      Surgery for Stage IIIA NSCLC - Surgeon's Perspective Gail E Darling MD FRCSC, University Health Network, University of Toronto, Toronto Canada Outline Indications for operating on IIIA Choice of Induction regimen: chemotherapy vs chemoradiation Restaging the mediastinum: why or why not? how (EBUS vs med, redo med?) , Factors in decision making whether or not to proceed with surgery after induction Salvage resection after definitive chemoradiation Indications for Surgery for Stage IIIA NSCLC 1.T3N1M0, T4N0M0, T4N1M0: if primary is resectable with R0 resection 2.T1-3N2M0: single station microscopic N2, resectable with R0 resection, selected multistation N2 if microscopic N2 and nodal disease is resectable with R0 3.Patient is fit for planned resection Contraindications to surgery for Stage IIIA NSCLC 1. Extracapsular N2 2. Fixed bulky nodes 3. Inability to achieve an R0 resection 4. T4N2 5. Patient not fit for planned resection (right pneumonectomy required?) Choice of Induction: Chemotherapy alone vs Chemoradiation 1. Intergroup 0139 trial: concurrent cisplatin + etoposide + 45 Gy improved disease free survival over surgery alone 2. SAKK trial: RCT Chemo vs chemoRT ( sequential) →No difference in survival 3. Concurrent chemoRT higher rates of mediastinal downstaging compared to chemotherapy alone 4. Radiation may be undesirable if sleeve resection of bronchus or artery is planned Restaging after Induction therapy 1. CT scan: to assess response but primarily to confirm resectability and exclude progression 2. PET: to rule out progression; assess response to determine if surgery is required? 3. Mediastinum: a) restage only if surgeon will not operative if persistent N2. Intergoup 0139 trial reported best survival if mediastinum was sterilized by induction but even if persistent disease survival was better with surgery than chemoRT alone. B) Restaging: if first mediastinal staging was performed by mediastinoscopy PET is most accurate; EBUS/EUS not reliable (sampling error); redo mediastinoscopy difficult, not reliable. If first staging was performed by EBUS/EUS then mediastinoscopy is appropriate and reliable for restaging. Factors in Decision Making to Proceed with Surgery after Induction 1. Patient is fit ( recovered fully from induction, good performance status) 2. Cancer has not progressed 3. Lack of radiographic response is not a contraindication to resection 4. R0 resection is possible Salvage Surgery after Definitive Chemoradiation 1. Patient is fit with good performance status 2. Primary site is only site of disease

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    MTE 17 - Neuroendocrine Tumor (Sign Up Required)

    • 07:00 - 08:00
    • 10/17/2017
    • Location: Room 418
    • Type: Meet the Expert
    • Track: SCLC/Neuroendocrine Tumors
    • Moderators:
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      MTE 17.01 - Pathological Features of Neuroendocrine Tumors

      07:00 - 07:30  |  Presenting Author(s): Yuichi Ishikawa

      • Abstract

      Abstract:
      In the WHO 2015 classification, neuroendocrine tumors (NETs) have become one of the 4 major histological types of lung cancer. NET includes typical carcinoid (TC), atypical carcinoid (AC), small cell lung carcinoma (SCLC) and large cell neuroendocrine carcinoma (LCNEC). In this presentation, I’ll talk about problems of diagnosis of SCLC, and challenge “common knowledges” of NETs as follows: 1. SCLC is highly malignant and only very rarely the patients survive after 5 years. What are pathological characteristics of tumors with longer survival? 2. There are no subtypes of SCLC, only combined SCLC is described in the WHO 2015. Isn’t subtyping of pure SCLC needed? Also, is SCLC a hilar-type cancer? 3. Diagnosis of SCLC doesn’t require immunohistochemistry (IHC) although IHC is used to diagnose even adenocarcinoma and squamous cell carcinoma. Isnt’ IHC useful for SCLC? 4. NET includes TC, AC, SCLC and LCNEC. Is this a spectrum of NET, showing progression of NET? In other words, does AC progress to LCNEC? 5. For adenocarcinoma diagnosis, transcription factor TTF-1 is useful even when the tumor doesn’t express glandular phenotypes such as mucin and CEA. In case of NET, we usually pay attention to NE phenotypes such as synaptophysin and NCAM, not to transcription factors. Aren’t transcription factors such as ASCL1 and INSM 1 useful for SCLC diagnosis? 6. Is the Kulchitsky an origin of SCLC? I’d like to answer these questions, mainly based on our own experiences.

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      MTE 17.02 - Surgical Strategy for the Treatment of Neuroendocrine Tumors

      07:30 - 08:00  |  Presenting Author(s): Enrico Ruffini  |  Author(s): Pier Luigi Filosso, P. Lyberis, A. Oliaro

      • Abstract

      Abstract:
      Neuroendocrine tumors (NETs) are a distinct subgroup of neoplasms arising from the neuroendocrine cells. Due to the peculiar morphological, immunohistochemical and molecular characteristics, NETs are usually classified as a separate group of tumors among solid malignancies. Thoracic NETs include the pulmonary and the thymic NET. Pulmonary NETs (PNETs) comprise well-differentiated neuroendocrine tumors (typical carcinoid), moderately-differentiated neuroendocrine tumors (atypical carcinoid), the latter two grouped as Bronchial Carcinoids (BCs); large cell neuroendocrine carcinoma (LCNEC) and small-cell lung carcinoma (SCLC). There are also two preneoplastic conditions, the Diffuse Idiopathic Pulmonary Neuroendocrine Cell Hyperplasia (DIPNECH) and the tumorlets whose role in the neuroendocrine carcinogenesis are yet to be fully clarified. PNETs represent about 25% of all lung cancers, most of them represented by SCLC. Thymic NETs (NeuroEndocrine Thymic Tumors, NETT) are considered as a subgroup of thymic carcinoma, although in most series they are classified separately, and are further classified as well-differentiated NETT (typical carcinoid), moderately-differentiated NETT (atypical carcinoid) and poorly-differentiated NETT (Large cell and small cell neuroendocrine carcinoma). NETTs are exceedingly rare and represent about 5% of all thymic tumors. The present lecture will focus on PNETs and NETTs, with a particular insight in the surgical management of these tumors. 1, Pulmonary NETs. The most recent TNM staging classifications of lung cancer (7[th] and 8[th] edition) suggest that PNETs should be staged similarly to Non-Small Cell Lung Cancer (NSCLC). Surgical indications largely depend on histology and stage. Bronchial carcinoids (BCs) represent about 10% of PNETs. The vast majority are typical carcinoids (TC, well-differentiated neuroendocrine tumors); they are usually located centrally in the lung parenchyma/airways (70%), and they are frequently confined to the lung without evidence of loco-regional or distant spread, which occur in about 5-10% of the cases. Atypical carcinoids (AT) share most of the characteristics of typical carcinoids, although they present a higher rate of mytoses and necrosis. They are more aggressive than TCs and they present with lymphnodal metastatic involvement in 30%-50% of the cases. LCNEC are usually diagnosed after resection, since a preoperative characterization on small biopsies is challenging. They are aggressive tumors, and more than 50% of the patients present with an advanced disease at diagnosis, for whom surgery is not indicated. As for SCLC, the vast majority of the patients present at an advanced stage, with hematogenous spread. The role of surgery in the treatment of PNETs is similar to what is currently employed for NSCLC. BCs are often amenable to surgery, due to the early stage at presentation. Anatomical resections (segmentectomy, lobectomy or more extended resections) offer the best outcome, while sublobar wedge resection should be avoided in fit patients, and should be reserved only for patients not amenable to anatomical resections. Parenchymal-sparing techniques (bronchial/vascular sleeve resection) should be employed whenever possible to avoid pneumonectomy in centrally-located tumors. Lymphadenectomy should be carried out according to the current guidelines (IASLC/ESTS), including a minimum of 6 nodes/stations of which 3 mediastinal including the subcarinal one. Endoscopic resection may have a role only in case of lobar/lung atelectasis to restore the bronchial patency before definite surgical resection Endobronchial resection is also employed with palliative intent in unresectable disease. Survival after resection of BCs is excellent, with more than 90% of the patients with typical carcinoids alive at 10 years, and 70% and 50% with atypical carcinoids alive at 5 and 10 years. The role of adjuvant therapy after complete resection of BCs is not fully determined and it is often discussed on an individual basis in a multidisciplinary tumour board setting. LCNEC are poor candidates for surgery, because of the loco-regional and distant spread at presentation. Anatomical resections, including extended resection to neighboring organs are needed in order to achieve a complete resection. Despite this, local recurrence and distant metastases are frequent after surgery. Adjuvant therapy (chemotherapy or chemoradiotherapy) is almost always needed after surgery for the disease control. SCLC has customarily been considered nonsurgical because of the high aggressiveness and the chemosensitivity of this neoplasm. However, in carefully selected patients with limited disease (T1-T2N0) surgery as part of a multidisciplinary protocol (chemoradiotherapy) may be proposed after a careful assessment of loco-regional (including mediastinal) and distant spread. 2, Thymic NETs. Thymic NETs (NETTs) are usually aggressive thymic tumors, very often presenting atypical features (atypical carcinoid). They express somatostatin receptors which may justify the use of Octreotide scintigraphy for the diagnosis and follow-up. About 30-40% have metastases at presentation and in some cases they are associated with endocrinopaties (Cushing syndrome, MEN-1 syndrome, etc). The staging system for NETTs has traditionally been the Masaoka system. The 7[th] edition of the TNM of thymic tumors included also the NETTs. As for other thymic malignancies, surgery is the treatment of choice for local and loco-regional disease (Stage I/II and selected Stage III). The resectability rate for NETTs is far lower than that of thymoma, ranging between 30% and 100% in most series. Complete (R0) resection is the most important prognostic factor. Median sternotomy and open surgical approaches are the optimal accesses for NETTs. The role of minimally-invasive techniques (MIT) in the treatment of NETT is extremely limited, due to the aggressive nature of the tumor. The role of induction and adjuvant treatments (radiotherapy or chemotherapy) has not been established yet, due to the rarity of the condition. 3, The collaborative effort. As for many rare diseases, also for NETs a collaborative, multi-Institutional, society-based effort is the single most important factor that can provide a real advancement in the research and management of this condition. The European Society of Thoracic Surgeons (ESTS) launched in 2012 a Neuroendocrine Tumors Working Group with the aim of collecting data from interested Institutions across the world. An amazing database collating more than 2100 patients has been designed which represents a tremendous opportunity for the study of these rare conditions. A number of studies have been published so far which constitute a solid backbone for the management of NETs.

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    MTE 18 - Treatment for Squamous Cell Carcinoma (Sign Up Required)

    • Type: Meet the Expert
    • Track: Advanced NSCLC
    • Moderators:
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      MTE 18.01 - Treatment for Squamous Cell Carcinoma

      07:00 - 08:00  |  Presenting Author(s): Paul K. Paik

      • Abstract

      Abstract:
      Squamous cell lung cancers (SQCLC) account for between 15-25% of non-small cell lung cancer (NSCLC) cases. They are, biologically, quite distinct from lung adenocarcinomas, though this remains a fact that has had little positive effect to date in the management of this disease. Indeed, despite the FDA approval of a handful of new drugs for patients with SQCLCs since 2014, progress has been, for most, limited, reflecting the modest gains in survival achieved by these new agents. Navigating the treatment landscape has been, by turns, straight-forward and frustrating. This is most evident in the first-line setting where, apart from patients whose tumors exhibit high expression of PD-L1, a variety of platinum-based chemotherapy options are available, all with more or less equivalent efficacy as shown in Table 1:

      cisplatin + gemcitabine + necitumumab(1) cisplatin + gemcitabine(1) carboplatin + nab-paclitaxel(2) carboplatin + paclitaxel(2) cisplatin + docetaxel(3)
      ORR (%) 31 29 41 24 37
      Median PFS (mo) 5.7 5.5 5.6 5.7 -
      Median OS (mo) 11.5 9.9 10.7 9.5 11.3
      Second-line therapy is dictated then largely through exclusion. Patients who received pembrolizumab as first-line treatment will cycle through platinum-based chemotherapy. Patients who received platinum-based chemotherapy will, by and large, cycle through any one of a number of FDA-approved PD-1/PD-L1 antibody therapies, all with equivalent efficacy (pembrolizumab, nivolumab, atezolizumab). Docetaxel +/- ramucirumab is thus relegated to the de facto third-line option. There are, arguably, few clinically meaningful therapeutic options beyond this; the data behind these options will be discussed in further detail. Most recently, attempts have been made to target putative oncogenic drivers in this disease, based on larger scale genomic analyses and pre-clinical experiments generated TCGA and others.(4-6) Three relatively large-frequency signaling pathways and targets have been tested in early phase trials, including FGFR1 amplification, PI3K pathway alterations, and G1/S checkpoint aberrations both by individual groups and SWOG (LUNG-MAP, S1400). In short, there has been modest to no efficacy in targeted therapy trials to date. These studies are summarized in Table 2:
      Target Frequency Drug ORR
      FGFR1 amplification Up to 20% AZD4547(7) 8%
      BGJ-398(8) 15%
      Dovitinib(9) 11.5%
      PI3K pathway Up to 50% BKM120(10) 0%
      GDC-0032(ASCO 2017) 5%
      G1/S checkpoint Up to 50% Abemaciclib(11) 17%
      Most of these studies have lacked detailed molecular analyses of patient tumor samples, hampering our ability to determine why these targeted efforts have largely failed. One exception is the study of AZD4547 in FGFR1 amplified SQCLCs, where correlative tests demonstrated that focal amplification of FGFR1 in the 8p11 amplicon does not occur in the majority of cases, commensurate with relatively low mRNA and protein expression of the gene.(7) Overall, heterogeneity with regard to aberrations in overlapping signaling pathways and clonal diversity remains a concern. The rationale for and data from other studies will also be discussed, including early data from combination chemotherapy plus PD-1/L1 inhibition trials as well as potential future directions for research. References 1. Thatcher N, Hirsch F, Luft A, Szczesna A, Ciuleanu T, Szafranski W, et al. A randomized, multicenter, open-label, phase III study of gemcitabine-cisplatin (GC) chemotherapy plus necitumumab (IMC-11F8/LY3012211) versus GC alone in the first-line treatment of patients (pts) with stage IV squamous non-small cell lung cancer (sq-NSCLC). J Clin Oncol. 2014:abstr 8008. 2. Socinski MA, Bondarenko I, Karaseva NA, Makhson AM, Vynnychenko I, Okamoto I, et al. Weekly nab-Paclitaxel in Combination With Carboplatin Versus Solvent-Based Paclitaxel Plus Carboplatin as First-Line Therapy in Patients With Advanced Non–Small-Cell Lung Cancer: Final Results of a Phase III Trial. Journal of Clinical Oncology. 2012;30:2055-62. 3. Kubota K, Watanabe K, Kunitoh H, Noda K, Ichinose Y, Katakami N, et al. Phase III Randomized Trial of Docetaxel Plus Cisplatin Versus Vindesine Plus Cisplatin in Patients With Stage IV Non-Small-Cell Lung Cancer: The Japanese Taxotere Lung Cancer Study Group. Journal of Clinical Oncology. 2004;22:254-61. 4. TCGA Network. Comprehensive genomic characterization of squamous cell lung cancers. Nature. 2012;489(7417):519-25. 5. Paik PK, Shen R, Won H, Rekhtman N, Wang L, Sima CS, et al. Next-Generation Sequencing of Stage IV Squamous Cell Lung Cancers Reveals an Association of PI3K Aberrations and Evidence of Clonal Heterogeneity in Patients with Brain Metastases. Cancer Discovery. 2015;5:610-21. 6. Kim Y, Hammerman PS, Kim J, Yoon J-a, Lee Y, Sun J-M, et al. Integrative and Comparative Genomic Analysis of Lung Squamous Cell Carcinomas in East Asian Patients. Journal of Clinical Oncology. 2014;32:121-8. 7. Paik PK, Shen R, Berger MF, Ferry D, Soria J-C, Mathewson A, et al. A Phase 1b Open Label Multicentre Study of AZD4547 in Patients with Advanced Squamous Cell Lung Cancers. Clinical Cancer Research. 2017. 8. Nogova L, Sequist LV, Garcia JMP, Andre F, Delord J-P, Hidalgo M, et al. Evaluation of BGJ398, a Fibroblast Growth Factor Receptor 1-3 Kinase Inhibitor, in Patients With Advanced Solid Tumors Harboring Genetic Alterations in Fibroblast Growth Factor Receptors: Results of a Global Phase I, Dose-Escalation and Dose-Expansion Study. Journal of Clinical Oncology. 2017;35:157-65. 9. Lim SH, Sun J-M, Choi Y-L, Kim HR, Ahn S-M, Lee JY, et al. Efficacy and Safety of Dovitinib in Pretreated Advanced Squamous Non-small Cell Lung Cancer with FGFR1 Amplification: A Single-arm, Phase II Study. Cancer. 2016. 10. Vansteenkiste JF, Canon J-L, De Braud F, Grossi F, De Pas T, Gray JE, et al. Safety and Efficacy of Buparlisib (BKM120) in Patients With PI3K Pathway-Activated Non-Small Cell Lung Cancer (NSCLC): Results From the Phase II BASALT-1 Study. Journal of Thoracic Oncology. 2015;Publish Ahead of Print. 11. Patnaik A, Rosen LS, Tolaney SM, Tolcher AW, Goldman JW, Gandhi L, et al. Efficacy and Safety of Abemaciclib, an Inhibitor of CDK4 and CDK6, for Patients with Breast Cancer, Non–Small Cell Lung Cancer, and Other Solid Tumors. Cancer Discovery. 2016.