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C. Zhou

Moderator of

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    O06 - Cancer Control and Epidemiology I (ID 135)

    • Event: WCLC 2013
    • Type: Oral Abstract Session
    • Track: Prevention & Epidemiology
    • Presentations: 8
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      O06.00 - Nationwide Quality Improvement in Lung Cancer Care: The Role of the Danish Lung Cancer Group and Registry. (ID 1014)

      E. Jakobsen, A. Green, K. Oesterlind, T. Riis Rasmussen, M. Iachina, T. Palshof

      • Abstract
      • Presentation
      • Slides

      Background
      In order to improve prognosis and quality of lung cancer care the Danish Lung Cancer Group has developed a strategy consisting of national clinical guidelines and a clinical quality and research database. In 1998 the first edition of guidelines was published and a registry was opened for registrations in the year 2000. This abstract describes the methods used and the result obtained through the collaborative work and discusses how to improve the quality of lung cancer care through the development and monitoring of indicators.

      Methods
      A wide range of indicators was established, validated and monitored. By registration of all lung cancer patients since the year 2000, more than 40.000 patients have been included in the database. Results are reported periodically and submitted to formal auditing on an annual basis.

      Results
      Improvements in all outcome indicators are documented and statistical significant. Thus the one year overall survival has between 2003 and 2011increased from 36.6 % to 42.7 %; the 2 year survival from 19.8 % to 24.3 % and the 5 year survival from 9.8 % to 12.1 %. 5 year survival after surgery has increased from 39.5 % to 48.1 %. Improvements in waiting times, accordance between cTNM and pTNM and in resection rates are documented.

      No Indicator Threshold (%) 2003 (%) 2004 (%) 2005 (%) 2006 (%) 2007 (%) 2008 (%) 2009 (%) 2010 (%) 2011 (%) 2012 (%)
      Ia Patients surviving 1 year from date of diagnosis 42 36,6 37,4 37,3 37,2 39,3 38,2 38,3 40,2 42,7
      Ib Patients surviving 2 years from date of diagnosis 22 19,8 20,5 20,7 20,9 22,9 21,8 23,0 24,3
      Ic Patients surviving 5 years from date of diagnosis 12 9,8 9,6 10,4 10,5 12,1
      IIa Patients surviving 30 days from date of operation 97 93,7 98,4 96,9 96,7 96,8 97,5 97,8 98,0 99,0 99,0
      IIb Patients surviving 1 year from date of operation 75 73,8 76,4 79,7 80,7 83,8 82,2 86,1 85,9 88,6
      IIc Patients surviving 2 years from date of operation 65 60,5 58,9 64,3 67,2 70,6 66,6 73,6 75,5
      IId Patients surviving 5 years from date of operation 40 39,5 38,8 44,5 46,9 48,1
      IIIc Rate of patients starting chemo within 42 days after referral 85 62,9 51,1 50,3 56,0 59,8 73,4 72,7 74,7 80,8 82,9
      IV Rate of patients with accordance between cTNM and pTNM 85 68,2 70,2 77,0 72,7 79,8 77,6 80,1 83,3 86,4 91,3
      V Rate of patients with NSCLC who had a resection 20 18,7 18,9 19,8 20,4 19,8

      Conclusion
      The Danish experience shows that a national quality management system including national guidelines, a database with a high degree of data quality, frequent reports, audit and commitment from all stakeholders can contribute to improve clinical practice, improve core results and reduce regional / geographic differences.

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      O06.01 - Lung cancer risks, beliefs, and healthcare access among the underprivileged (ID 2113)

      J. Morere, J. Viguier, C. Touboul, X. Pivot, J. Blay, Y. Coscas, C. Lhomel, F. Eisinger

      • Abstract
      • Presentation
      • Slides

      Background
      One goal of the current French National Cancer Plan is to reduce health inequities in cancer control. In this study, an underprivileged population was investigated to analyze exposure to lung cancer risk factors and health care access in order to highlight ways to improve lung cancer control in that population.

      Methods
      Within the nationwide observational study EDIFICE 3, conducted by phone interviews among a representative sample of 1603 subjects aged between 40 and 75 years old, we used the “EPICES” validated questionnaire to examine the association of underserved status with lung cancer risk factors, beliefs, and health care access.

      Results
      Based on the EPICES score, underserved subjects represented 33% of the sample. These subjects subjectively perceived a higher risk of cancer compared to subjects in the served population (21% vs. 14% respectively, p<0.01). Among people with cancer, underserved subjects have a higher rate of lung cancer (10% of cancers vs. 1%, p<0.05). They also have more cancer risk factors: a high BMI (26.0 vs. 24.8, p<0.01), are active smokers (38% vs. 23%, p<0.01) with a higher consumption of cigarettes (16.0 cigarettes/day vs. 10.1, p<0.01) and for a longer period (29.4 years vs. 26.3, p<0.01), and also practice less sport (42% vs. 77%, p<0.01). They have more comorbidities: on average (2.2 vs. 1.8, p<0.01), at least one (76% vs. 65%, p<0.01), hypertension (24% vs. 19%, p<0.05), cardiovascular disease (13% vs. 9%, p<0.05) and respiratory disease (13% vs. 7%, p<0.01). Access to healthcare is not an issue (consultations with a general practitioner are more frequent for the underserved group: 5.4 vs. 3.7 per year, p<0.01). They trust the national health system less (an average score from 1 to 10; 6.0 vs. 6.3, p <0.05). However, 85% of underserved subjects think that lung cancer can be efficiently screened vs. 78% of the served population (p<0.01).

      Conclusion
      In order to reduce inequities in lung cancer control, the effort of upstream interventions should be focused on prevention, as healthcare access does not discriminate. Underserved subjects have a high level of trust in lung cancer screening but a riskier behavior in terms of smoking. This constitutes new targets for specific communication campaigns and Health authorities’ interventions.

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      O06.02 - Statin Use and Reduced Lung Cancer-Related Mortality (ID 1535)

      R.P. Young, R.J. Hopkins, G.D. Gamble

      • Abstract
      • Presentation
      • Slides

      Background
      Lung cancer results from the combined effects of smoking exposure and genetic predisposition. Recent studies have shown that susceptibility to chronic obstructive pulmonary disease (COPD) is also relevant to a predisposition to lung cancer. The latter may be mediated in part through exaggerated systemic inflammation secondary to smoking exposure and the innate response to smoking in genetically susceptible people. Recently a large population based study reported that statin therapy was associated with a reduction in mortality from cancer (Nielsen et al. Statin Use and Reduced Cancer-Related Mortality, NEJM 2012; 367: 1792-1802). The aim of this study was to examine the cancer specific effect of statins on mortality.

      Methods
      Using the raw data from the Nielsen study, we calculated the estimated number of lives saved from statin therapy use according to type of cancer and then estimated the absolute numbers of lives saved.

      Results
      When we examined the raw data showing hazard ratios according to statin use in each of the cancers described, we found that except for lymphoma, the mortality reductions were significant for smoking related cancers (lung, pharynx, oesophagus, urinary) and obesity-related cancers (colon, prostate, breast - see Figure 1). When we calculated the number of lives saved according to specific cancer type, we found that of all lives saved, 43% could be attributed to a reduction in lung cancer deaths (Table 1). Importantly, mortality for many of these cancers (lung, colon, breast and prostate) has been associated, in large prospective studies, to elevation of the C-reactive protein, a marker of systemic inflammation. Figure 1Figure 2

      Conclusion
      We conclude that the reduction in cancer mortality attributed to statin therapy by Nielsen et al. is seen almost exclusively in cancers where smoking and/or systemic inflammation is thought to be of significant pathogenic importance. Significantly, the single largest reduction can be attributed to lung cancer where both smoking and systemic inflammation are strongly implicated. We suggest that a reduction in systemic inflammation by statins may be one mechanism underlying the reduction in mortality reported by Nielsen and colleagues.

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      O06.03 - DISCUSSANT (ID 4002)

      M.A. Steliga

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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      O06.04 - The association between having a first-degree family history of cancer and smoking status (ID 1191)

      H. Poghosyan, J.G. Joseph, J. Bell, M.E. Cooley

      • Abstract
      • Presentation
      • Slides

      Background
      Smokers with a family history of cancer are at higher risk for developing cancer. A diagnosis of cancer within the family may provide an opportunity for smokers to adopt health-promoting behavior. This study examined associations between having a first-degree family history of cancer and smoking status.

      Methods
      Data from the 2009 California Health Interview Survey (CHIS) on 47,331 adults were used in this cross-sectional study. Sample weights were applied to account for the complex survey design with results generalizable to non-institutionalized adults in California (27.4 million). Smoking status was classified as current, former, or never-smoker. Family cancer history was defined as blood relatives that include biological father or mother, full brothers or sisters, or biological sons or daughters. Demographic characteristics included age, gender, race/ethnicity, marital status, poverty level, education level and health insurance coverage. General health status, physical activity, body weight status and binge drinking status were also included. CHIS defined binge drinking status as ≥5 alcoholic drinks for males or ≥4 alcoholic drinks for females in a single episode in the past year. Body weight status was defined by body mass index as underweight <18.5 kg/m2, normal = 18.5–24.9 kg/m2, overweight = 25.0–29.9 kg/m2, and obesity ≥30.0 kg/m2. Multinomial logistic regression was used to analyze the association between first-degree family history of cancer and smoking status.

      Results
      In 2009, 13.6% (3.7 million) of the 27.4 million adults were current-smokers, 23.0% (6.3 million) former-smokers and 63.4% (17.4 million) never-smokers. Thirty-five percent (9.6 million) had a first-degree family history of cancer (Table 1). Among those with a first-degree family history of cancer, 13.5% (1.3million) were current-smokers, 29.7% (2.8 million) were former-smokers and 56.8% (5.4 million) were never-smokers. Adults with a first-degree family history of cancer were more likely to be former-smokers compared with adults without a first-degree family history of cancer (29.7% vs. 19.3%, p<.001). Controlling for demographic factors and other risk characteristics (binge drinking, obesity, physical activity), having a first-degree family history of cancer was significantly related to being a current-smoker (OR=1.16; 95% CI=1.01-1.34) and former-smoker (OR=1.17; 95% CI 1.05-1.30).

      Table 1: Characteristics of California Health Interview Survey participants, 2009
      Characteristics Unweighted sample size Weighted percentages (95% CI)
      Smoking Status
      Current smokers 5,528 13.6 (12.8-14.4)
      Former Smokers 14,487 23.0 (22.1-23.8)
      Never smokers 27,317 63.4 (62.5-64.3)
      Family Cancer History
      Yes 22,286 35.0 (34.1-35.8)
      No 25,045 65.0 (64.1-65.8)
      Age
      18-25 2,826 16.0 (15.6-16.4)
      26-34 3,446 15.6 (15.0-16.0)
      35-49 10,484 30.2 (29.7-30.5)
      50+ 30,575 38.2 (38.1-38.2)
      Gender
      Male 19,280 49.0 (49.0-49.1)
      Female 28,051 51.0 (50.0-51.0)
      Race/Ethnicity
      Hispanic 8,281 32.5 (32.4-32.5)
      Non-Hispanic White 30,951 46.4(46.4-46.5)
      Non-Hispanic Black 1,839 5.6 (5.6-5.7)
      Non-Hispanic Asian 4,833 12.8 (12.8-13.0)
      Non-Hispanic Other 1,427 2.6 (2.5-2.6)
      Marital Status
      Married 27,079 61.3 (60.5-62.2)
      Not-married 20,252 38.6 (37.8-39.5)
      Federal Poverty Level (FPL)
      < 100% FPL 5,747 16.0 (15.3-16.8)
      100-199 % FPL 7,950 18.0 (17.2-18.7)
      200-299 % FPL 6,478 13.7 (13.0-14.5)
      ≥ 300% FPL 27,156 52.2 (51.3-53.1)
      Education Level
      < High-school 4,795 16.3 (16.1-16.4)
      High-school graduate 10,345 26.0 (25.8-26.0)
      Some college 12,858 23.7 (23.0-24.5)
      College or more 19,333 34.0 (33.3-34.7)
      Health Insurance
      Currently insured 42,186 82.0 (81.0-82.8)
      Not insured 5,145 18.0 (17.1-19.0)
      General Health
      Excellent/Very Good 24,554 52.0 (51.0-52.8)
      Good 13,588 29.8 (28.4-30.8)
      Fair/Poor 9,189 18.2 (17.4-19.0)
      Body Weight Status
      Underweight 1,051 2.2 (2.0-2.5)
      Normal 19,689 41.3 (40.4-42.3)
      Overweight 16,078 33.7 (32.8-34.5)
      Obese 10,513 22.7 (21.8-23.5)
      Physical Activity
      Sedentary 16,936 34.6 (33.6-35.7)
      Some activity 20,838 43.4 (42.3-44.5)
      Regular activity 9,557 21.8 (21.0-22.7)
      Binge drinking status
      Yes 11,049 31.4 (30.5-32.3)
      No 36,282 68.5 (67.6-69.4)

      Conclusion
      In California, many adults with a first-degree family history of cancer still smoke which places them at higher risk for poor health outcomes. Smokers with a first-degree family history of cancer may be an important target population for smoking cessation interventions.

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      O06.05 - Multidisciplinary smoking cessation model in a specialist oncology hospital - our 5 year experience (ID 2106)

      M. Alexander, I. Plueckhahn, J.D. Mellor, S.W. Kirsa

      • Abstract
      • Presentation
      • Slides

      Background
      Australia established its first national quitline service in 1997 as part of the Australian National Tobacco Campaign (NTC). In 2005 our hospital, an Australian tertiary specialist cancer centre, commenced a multidisciplinary smoking cessation program which included the provision of counselling and behaviour techniques as well as free access to pharmacological smoking cessation agents. In 2007 the hospital went totally smoke free and in 2009 all new patient registrations included collection of information pertaining to smoking behaviours. Cancer patients are known to withhold and underreport details regarding current and previous smoking behaviours however there is limited data on the impact of non-disclosure on the ability to implement interventional smoking cessation programs in the oncology setting. Five years after initiation of an interventional smoking cessation program we present previously uncollected and unreported hospital wide smoking behaviour data (prevalence, magnitude and willingness to report) of cancer patients. We also evaluate our multidisciplinary smoking cessation model including recruitment and quit rates for cancer patients at a specialist oncology centre.

      Methods
      For the two year period 2009-2011 self-reported smoking behaviors were obtained from hospital registration datasets. A retrospective single arm cohort study, including patients with a cancer diagnosis who accessed the smoking cessation program within the same two year period, was also conducted. Patients and family members are recruited to the program via a multidisciplinary referral system and have access to nurse led counselling and behaviour modification consultations as well as provision of free pharmacological smoking cessation aids. Evaluation of the program was undertaken through and audit of medical and pharmacy records for all patients who participated in the program (n=312) and by phone interviews with a subset of patients (n=30) and compared to data from a previously published study at our institution[1].

      Results
      50% (n=10,401) of patients newly registered to the hospital identified as having ever smoked with 12% (n=2448) current smokers. Recruitment of self-identified active smokers into the smoking cessation program was low (7.3%). 43% (n=134) of patients enrolled into the program had not disclosed their smoking status at hospital registration. Magnitude of smoking was high; average pack-years of patients who have ever smoked was 22.6 and for current smokers was 27.8; 155 patients reported smoking magnitude as greater than 100 pack years. Provision of free pharmacotherapy equated to a net expenditure of AUD$22,042. Point prevalence smoking cessation rate among patients who participated in follow-up interviews (n=30) was similar to that previously reported following participation in our multidisciplinary smoking cessation program, 33% compared to 37%[1]. 66% of patients reported successful outcomes (cessation or reduction in consumption).

      Conclusion
      Patient-reported smoking behaviours were grossly underreported impacting on the ability to actively enrol patients into established interventional cessation programs. Despite low recruitment rates and high magnitude of smoking, the multidisciplinary model was able to achieve successful outcomes at minimal cost in this vulnerable patient cohort. Improving disclosure practices may enable future targeted recruitment of patients by health-care professionals and increase the participation of smokers in proven healthcare interventions.

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      • Abstract
      • Presentation
      • Slides

      Background
      Lung cancer screening programs provide unique opportunities to facilitate smoking cessation in smokers who participate in these programs. However, the effects of screening on motivation to quit might be mediated or modified by other variables. Identifying the participants more likely to quit will allow rapid application of smoking cessation resources to these participants, while those least likely to quit can be afforded experimental interventions. The aim of our study was to assess the impact of lung cancer screening on smoking cessation in current smokers at the time of enrollment and to identify factors that were associated with quitting smoking in this screening population.

      Methods
      Using data collected from the Pan-Canadian Study of Early Detection of Lung Cancer, both univariate and multivariable logistic regression analysis was used to identify predictors of smoking cessation among current smokers at enrolment. Smoking cessation was defined as quitting for at least a 6 month period, occurring anytime after enrolment.

      Results
      We analyzed baseline and follow-up questionnaires of 2320 participants, of which 1419 were current smokers. Of these 1419 patients, 392 (27.8%) met the definition of smoking cessation during a median of two annual follow-up visits. In both univariate and multivariable (MV) analysis, greater smoking cessation was associated with four factors: (i) having a diagnosis of lung cancer at any time during the screening process, with a MV Odds ratio (OR) of quitting of 2.4 (95%CI: 1.1-5.0); (ii) lower and medium nicotine addiction as assessed by the Fagerström Nicotine Dependence Scale Score, with MV-ORs of 3.2 (95%CI: 2.2-4.6) and 1.4 (95%CI: 0.9-2.0), respectively; (iii) having higher education, with MV-OR: 1.4 (95%CI: 1.1-1.9); and (iv) having an earlier age of onset of regular alcohol intake, with MV-OR of 1.11 (95%CI: 1.02-1.21) per 5 year decrease in age. Smoking cessation was also associated with (i) previous attempts of quitting [UV-OR 1.8 (95%CI: 1.2-2.7)], willingness to quit smoking within the next month (at baseline screening) [UV-OR 2.2 (95%CI: 1.8-2.9)] or within the next 6 months after baseline screening [UV-OR 1.8 (95%CI: 1.3.-2.4)]. Second-hand smoking exposure, including exposure as a child, or as an adult at work, at home, privately with friends, or in public settings, or a cumulative index of these different exposures, was not associated with smoking cessation. Presence of potential index symptoms for lung disease, including shortness of breath, cough (both dry and productive), hoarseness, audible wheezing or even chest pain, was not associated with an increased chance of smoking cessation.

      Conclusion
      The diagnosis of a new lung cancer had a major positive impact on screening participants quitting smoking, as were factors such as lower nicotine dependence, higher education, earlier starting alcohol drinking age, and willingness to quit. Whether a new lung cancer diagnosis triggered additional efforts by clinicians to help the person quit will be explored further. Individual lung symptoms and secondhand smoke exposure were not associated with smoking cessation. (Geoffrey Liu and Martin Tamemmagi are co-senior authors)

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      O06.07 - DISCUSSANT (ID 4003)

      J.K. Cataldo

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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    PL04 - How Can We Stop the Epidemic of Lung Cancer? (ID 75)

    • Event: WCLC 2013
    • Type: Plenary Session
    • Track: Prevention & Epidemiology
    • Presentations: 5
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      PL04.0 - N/A - Chair Intro (ID 637)

      • Abstract

      Abstract not provided

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      PL04.1 - Risk Reduction by Stopping Smoking (ID 638)

      V. Beral, K. Pirie, R. Peto

      • Abstract
      • Slides

      Abstract
      Smoking is the most important cause of lung cancer and of death and morbidity from a wide range of causes. In most of Europe, North America and Australia recent results show that two-thirds of all deaths among male and female smokers in their 50s, 60s and 70s are caused by smoking. Smokers lose at least 10 years of lifespan. It takes decades for the full effects of smoking to emerge in a population. The hazards of smoking have been well described in men, but only recently have sufficiently large numbers of women in western countries been smoking for long enough for the full effects to be evident. For example, in the Million Women Study, a prospective study of 1.3 million UK women, lung cancer death rates in smokers were 20 times higher than in never smoker. Even in women who smoked fewer than 10 cigarettes per day, lung cancer rates were increased 10 fold, whereas among women who smoked about 25 cigarettes per day the risk was increased almost 40 fold. Risks were greater the younger women were when they started smoking. In western countries women began smoking in large numbers more than 50 years ago, and it is only now that results show clearly that when women smoke as much as men their risk of lung cancer and other conditions are similar. In Asia the full effects of smoking are still not evident, since large proportions of the population smoking began only a few decades ago. Stopping smoking substantially reduces the risks of lung cancer and of other conditions that would have occurred with continued smoking. Stopping at any age is beneficial. In the Million Women Study stopping at age 40 years was associated with a 3 fold increase in lung cancer, thus avoiding about 90% of the 20-fold excess mortality from lung cancer caused by continued smoking. Stopping smoking at around age 30 avoided about 97% of the excess risk of lung cancer. Similar findings have been reported from the USA and elsewhere. The avoidance of most of the excess risk of lung cancer and other adverse effects of continuing smoking by quitting before about age 40 years has major public health implications. It is estimated that during the 20th century smoking caused about 100 million deaths worldwide, but that it will cause ten times as many - 1000 million deaths - in the 21st century if current smoking patterns continue. If current smoking patterns continue almost all the smoking-related excess lung cancers and deaths in the next 50 or so years will occur in people who are already smoking. Much of the predicted epidemic of smoking-related deaths in the next 50 could be avoided if people who now smoke stopped, preferably before age 40.

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      PL04.2 - Risk Factors for Lung Cancer in Never-Smokers (ID 639)

      C. Chen

      • Abstract
      • Slides

      Abstract not provided

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      PL04.3 - A Critical Review of CT Lung Cancer Screening (ID 640)

      E. Quoix

      • Abstract
      • Slides

      Abstract not provided

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      PL04.4 - Biomarker-Driven Programs for Lung Cancer Screening (ID 641)

      P.P. Massion

      • Abstract
      • Slides

      Abstract
      The purpose of this presentation is to define a potential role for biomarkers 1) in the risk assessment of lung cancer among individuals considered for screening and 2) in the diagnostic evaluation of screening detected lung nodules. We will distinguish types of biomarkers design for the screening of lung cancer and their desired performance characteristics. We will describe current front runner candidates biomarkers and discuss how one could envision using those in the clinic. Suggested reading: The state of molecular biomarkers for the early detection of lung cancer. Hassanein M, Callison JC, Callaway-Lane C, Aldrich MC, Grogan EL, Massion PP. Cancer Prev Res (Phila). 2012 Aug;5(8):992-1006.

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    CALC - Chinese Alliance Against Lung Cancer Session (ID 79)

    • Event: WCLC 2013
    • Type: Other Sessions
    • Track: Other Topics
    • Presentations: 2
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      CALC.03 - Pathogenesis and Pathology of Never Smoking Lung Cancer (ID 3867)

      C. Zhou

      • Abstract
      • Slides

      Abstract
      Lung cancer (LC) is the leading cause of cancer deaths in the world. While smoking is universally accepted as the major cause of lung cancer in tobacco users, lung cancer in lifetime never smokers (LCNS) is among the 10 major causes of cancer deaths. LCNS is a very different disease than LC arising in ever smokers (LCES), and these differences are discussed in this Abstract. Because LCNS is highly influenced by gender and ethnicity, we put special emphasis on LCNS arising in East Asians. The reader is referred to several recent review articles on this subject [1-5] Etiology: Unlike LCES, the etiology of LCNS is not fully elucidated. The suspected factors include exposure to environmental tobacco smoke (ETS), exposure to industrial or domestic carcinogens including coal smoke and volatile cooking oils, radon exposure, viruses including HPV, and genetic factors. While these factors may individually or in combination contribute to the pathogenesis of LCNS, none of them is likely to be the major causative factor. Further investigation of causation is required. Clinico-patholgoical differences. While adenocarcinoma is the predominant form of NSCLC, the vast majority of LCNS are of adenocarcinoma histology, or large cell carcinomas (which may represent poorly differentiated adenocarcinomas). Squamous cell histology is rare and small cell carcinomas almost never occur. A retrospective study from Singapore identified significantly better performance status, younger age at diagnosis, and higher proportion of females (68.5% vs. 12-13%) and more advanced stage at diagnosis in never smokers compared with current and former smokers [6]. The disease stage variation at diagnosis might be explained by late presentation of symptoms and delayed diagnosis by physicians. The survival outcome of never smokers was significantly better than smokers, with the 5-year overall survival rate of LCES, respectively [6]. The differences in the treatment response and survival outcome between never smokers and smokers with lung cancer may be attributed to the differences in molecular pathogenesis and tumor biology (see below). Genetics: While lung cancer prone families have been well described, the risk of affected subjects is greatly increased after smoke exposure. Recently the interest has focused on single nucleotide polymorphisms (SNPs). Genome wide association studies (GWAS) identified a locus in chromosome region 15q25 that was strongly associated with lung cancer. The association region contains several genes, including three that encode nicotinic acetylcholine receptor subunits [7]. Such subunits are expressed in neurons and other tissues, including alveolar epithelial cells, pulmonary neuroendocrine cells and lung cancer cell lines, and they bind to potential lung carcinogens. Thus variants in this region undoubtedly code for increased susceptibility to smoke and are unlikely to be associated with LCNS. Not unexpectedly, GWAS studies indicate different patterns of susceptibility for Asians and never smokers and possibly related to gender [8, 9]. Molecular differences: The molecular differences between LCES and LCNS show marked differences and characteristic patterns. While TP53 mutations are common to all types of lung cancer, the mutational spectra are very different [10]. KRAS mutations are largely limited to LCES, and, along with TP53, show the typical smoking associated characteristic G to T transversions. In addition, the total numbers of non-synonymous and synonymous mutations in LCES tumors are much higher than that in LCNS, indicating that tobacco exposure results in in widespread genomic instability. Paradoxically, some of the most responsive currently available or potential molecular targets for precision medicine are more frequent in never smokers, including EGFR, BRAF and HER2 mutations and ALK translocations. Therapeutic options and precision medicine: While the overall treatment strategy is the same for LCES and LCNS, the differences in molecular profiles dictate differences in precision medicine and, response to targeted agents and overall survival. These factors are also influenced by gender and ethnicity. For instance, one study found that the frequency of driver mutations (EGFR, HER2, ALK, KRAS, or BRAF) in lung adenocarcinoma from female never-smokers in China was over 87% [11]. Summary: The differences between LCES and LCNS are major, and cover etiologic factors, clinic-pathological changes, genetic susceptibility genes, mutational and molecular changes and precision medicine. These differences are vast enough so that we can regard lung cancers arising in ever and never smokers as two different diseases. References: 1. Rudin CM, Avila-Tang E, Harris CC, et al. Lung cancer in never smokers: molecular profiles and therapeutic implications. Clin Cancer Res 2009;15(18):5646-61. 2. Sun S, Schiller JH, Gazdar AF. Lung cancer in never smokers - a different disease. Nat Rev Cancer 2007;7(10):778-90. 3. StatBite lung adenocarcinoma in smoker vs. never smokers. J Natl Cancer Inst 2010;102(10):674. 4. Lee YJ, Kim JH, Kim SK, et al. Lung cancer in never smokers: change of a mindset in the molecular era. Lung Cancer 2011;72(1):9-15. 5. Subramanian J, Govindan R. Lung cancer in never smokers: a review. J Clin Oncol 2007;25(5):561-70. 6. Toh CK, Gao F, Lim WT, et al. Never-smokers with lung cancer: epidemiologic evidence of a distinct disease entity. J Clin Oncol 2006;24(15):2245-51. 7. Hung RJ, McKay JD, Gaborieau V, et al. A susceptibility locus for lung cancer maps to nicotinic acetylcholine receptor subunit genes on 15q25. Nature 2008;452(7187):633-7. 8. Shiraishi K, Kunitoh H, Daigo Y, et al. A genome-wide association study identifies two new susceptibility loci for lung adenocarcinoma in the Japanese population. Nat Genet 2012;44(8):900-3. 9. Lan Q, Hsiung CA, Matsuo K, et al. Genome-wide association analysis identifies new lung cancer susceptibility loci in never-smoking women in Asia. Nat Genet 2012;44(12):1330-5. 10. Pfeifer GP, Besaratinia A. Mutational spectra of human cancer. Hum Genet 2009;125(5-6):493-506. 11. Zhang Y, Sun Y, Pan Y, et al. Frequency of driver mutations in lung adenocarcinoma from female never-smokers varies with histologic subtypes and age at diagnosis. Clin Cancer Res 2012;18(7):1947-53

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      CALC.08 - Targeted Therapies for Adenocarcinoma, Now and Future (ID 3875)

      C. Zhou

      • Abstract
      • Slides

      Abstract
      Lung cancer remains as the most fatal disease world-wide.Non-small cell lung cancer (NSCLC) accounts for about 80% of all lung cancers. Incidence of pulmonary adenocarcinoma has been increasing in most countries and becomes a major histology. We had, up to the recent past, treated patients with chemotherapy without any clinical or biological selection. Unfortunately, the improvement in overall survival (OS) with platinum-based doublets is modest, although statistically significant when compared to best supportive care. We now, however, understand that adenocarcinoma could be divided into several subsets according to oncogenic drivers and each subset of adenocarcinoma has a different biology. So, targeted therapies against these drivers have been extensively studied and will play more and more important roles in treatment of advanced adenocaricnoma of the lung. Oncogenic drivers Adenocarcinoma is different in oncogenic drivers between East Asian and Caucasian patients. East Asian patients have more frequent epidermal growth factor receptor (EGFR) mutation but less frequent KRAS mutation. Incidence of EGFR mutation is about 50% - 78.8% but of KRAS mutation about 1.9% to 12%. Other oncogenic drivers include ALK or ROS1 rearrangement, BRAF mutation, HER2 amplification or mutation, c-MET amplification, etc, and arecomparable in their incidencesbetween Asian and Caucasian patients. These oncogenic drivers are mutually exclusive in majority cases. EGFR TKI Several phase II/III studies have investigated the efficacy of EGFR tyrosine kinase inhibitors (TKI) as front-line therapy of patients with advanced NSCLC. EGFR TKI is not appropriate for front-line therapy in unselected populations, in those without EGFR mutation, or those with unknown EGFR mutation status. Improvement in PFS with EGFR TKI is confined to those with EGFR mutation. In fact, first-line EGFR TKI seems to have a detrimental effect in those without an EGFR mutation. Clinical characteristics alone are not sufficient to correctly predict benefit from EGFR TKIs. Treatment with EGFR TKI in EGFR mutant NSCLC patients has also been found to be associated with improvement of progression-free survival (PFS) and quality of life and less toxicity profile. Both first-generation and second-generation EGFR TKIs are effective. Treatment of patients with acquired resistance to EGFR-TKI is wildly being studied. Switching to standard chemotherapy, continuation of an EGFR TKI beyond disease progression and/or plus local therapy, afatinib plus cetuximab are some options of treatment. ALK inhibitors Crizotinib proves effective in adenocarcinoma with ALKorRos1 rearrangement. Several studies (Profile 1001, 1005 and 1007) investigated crizotinib in advanced NSCLC with ALK rearrangement. Tumor response is about 51-61% and PFS 41.9-48.1 weeks. Second-line crizotinib was found more effective than chemotherapy in terms of tumor response rate and PFS. The compound was also found to be effective in those with ROS1 rearrangement. Among 35 patients, its tumor response rate was 60% and PFS was not reached. LDK 387 is a second-generation ALK inhibitor. Phase I study showed its promising efficacy in the patients with ALK rearrangement. It could overcome acquired resistance of NSCLC to crizotinib. Antiangiogenicagents Bevacizumab is approved to be combined with doublet chemotherapy as 1[st] line treatment of non-squamous NSCLC. The combination significantly improves tumor response, PFS and OS. But up to now, there is no biomarker for selection of non-squamous NSCLC patients to receive bevacizumab therapy. Many small molecular anti-angiogenicinhibitors plus standard chemotherapy have been investigated but failed in improvement of OS. Recently, LUME-Lung 1 trials suggested ninetedanib plus docetaxelsignificantly improved PFS and OS of patients with advanced adenocarcinoma of the lung in second line setting compared with docetaxel + placebo. KRAS inhibitors Some compounds are being investigated in those with KRAS mutation. Selumetinib, MKE1/2 inhibitor, combined with docetaxel significantly improved tumor response (37% vs 0%) and PFS (5.2 months vs 2.1 months, HR 0.58), compared with docetaxel alone.Trametinib plus second line chemotherapy produced about 12 to 28% of tumor response rate and 2.9 to 4.1 months of PFS. BRAF inhibitor Dabrafenib has been approved for treatment of melanoma harboringBRAF V600E mutation. Incidence of BRAF V600E mutation is about 1% in NSCLC. A phase II study investigated dabrafenib in adenocarcinoma of the lung withBRAF V600E mutation. Preliminary results in 20 patients showed 40% of tumor response rate and 60% of disease control rate with the compound. c-MET inhibitors c-METamplification is one of major mechanisms for acquire resistance of NSCLC to EGFR TKI. Several small molecular inhibitors of cMET and monoclonal antibodies against cMET are under clinical development. METmab plus erlotinib significantly improved PFS than erlotinib in those with MET high patients in the phase II trial. Crizotinib led to tumor shrinkage in a patient with MET amplification. HER2 inhibitors HER2 mutation and amplification are not frequently observed in adenocarcinoma of the lung. Mazieres and the colleagues reported that HER2-targeted therapies in additional lines of treatment produced 50% of overall response rate, 82% of disease control rate and 5.1 months of PFS. The disease control rate was 96% with trastuzumab-based therapies and 100% with afatinib monotherapy. The relative efficacy of these compounds deserves prospective evaluation in larger international clinical trials. Inhibitors of other oncogenic drivers Many inhibitors of other drivers including PDGFR, FGFR, RET rearrangement, PI3K, mTOR, MEK, AKT, STAT3, etc are under clinical development. We are just waiting for their results of clinical trials. In summary, EGFR TKI and ALK inhibitors are important agents for EGFR mutant and ALK or ROS1 rearranged adenocarcinoma of the lung, respectively. They become standard 1[st] line therapy for these patients. Bevacizumab plus doublet chemotherapy could be 1[st] line therapy for those with advanced adenocarcinoma harboring no oncogenic drivers. Many inhibitors of other oncogenic drivers are under clinical development and will become standard therapy for these patients in near future.

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    P1.10 - Poster Session 1 - Chemotherapy (ID 204)

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Medical Oncology
    • Presentations: 1
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      P1.10-008 - Clinical Significance of Hyperpigmentation due to Pemetrexed Treatment in Advanced Non-Squamous Non-small cell lung cancer in China (ID 719)

      C. Zhou

      • Abstract

      Background
      Previous publications have demonstrated the efficacy of pemetrexed (PEM) as first-line, second-line and maintenance therapy in advanced non-small cell lung cancer (NSCLC). A recent study found skin toxicities compromised continuation of PEM treatment. The purpose of this study is to investigate the clinical significance of hyperpigmentation (HP) in advanced non-squamous (NS) NSCLC receiving PEM-based therapy in China.

      Methods
      Medical records of patients with advanced NS NSCLC who received PEM-based treatment in our hospital were retrospectively studied. Chi-square test, Pearson’s test as well as Kaplan-Meier method and Cox Proportional Hazards model were performed for statistical analysis.

      Results
      A total of 101 patients were collected with a median age of 58 years old. Among them, 53 (52.5%) were female and 65 (64.4%) were nonsmokers. 52 (51.5%) patients received first-line treatment. Presence of HP was associated with better ORR (22% vs 7.1%, p=0.043), higher DCR (84.7% vs 54.8%, p=0.001), and had longer PFS (186 days versus 96 days, p<0.0001). There were no significant differences according to grade of HP in ORR, DCR and PFS. There was a higher incidence of hyperpigmentation in patients who received first-line treatment (73.1%% vs 42.9%, p=0.023) and doublet chemotherapy (43.1% vs 74.0%, p=0.002). However,multivariate analysis demonstrated HP was not an independent factor for better clinical outcomes (vs absence, Hazard Ratio [HR] 0.417, 95% Confidential Interval [CI] 0.255-0.690, p=0.493).

      Conclusion
      HP due to PEM is frequent in advanced NS NSCLC receiving PEM. It might be a predictive factor for better clinical outcomes in Pemetrexed-treated advanced NS NSCLC in China.