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C. Dresler
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PLEN 01 - Lung Cancer Prevention and Screening (ID 50)
- Event: WCLC 2015
- Type: Plenary
- Track: Plenary
- Presentations: 3
- Moderators:C. Dresler, H.I. Pass
- Coordinates: 9/07/2015, 08:15 - 09:45, Plenary Hall (Bellco Theatre)
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PLEN01.01 - Lung Cancer Screening (ID 2038)
08:15 - 09:45 | Author(s): C. Berg
- Abstract
- Presentation
Abstract:
Screening of high risk individuals for lung cancer was shown to reduce lung cancer mortality by 20% in the National Lung Screening Trial (NLST) comparing low-dose helical computerized tomography (LDCT) to chest x-ray [1]. Implementation of lung cancer screening will be a serious challenge. Since the time of the IASLC meeting in Sydney in 2013 additional information from the NLST has provided guidance on many aspects of screening and informed public health policy in the United States. The United States Preventive Services Task Force (USPSTF) in December 2013 and the Centers for Medicare and Medicaid Services in February 2015 released decisions favorable to lung cancer screening [2, 3]. The USPSTF recommended it at a Grade B level which means under the terms of the Affordable Care Act (ACA), many insurance companies must reimburse without a deductible. The recommendations followed the NLST criteria but extended the age for screening to cover 55 to 80. CMS also followed NLST extending screening to age 77. The coverage includes a counseling and shared decision making visit with a written order for the procedure. Requirements also included radiologist credentials, image acquisition standards and participation in a CMS registry. The American College of Radiology Lung Cancer Screening Registry has been approved. Coverage decisions acknowledged the known drawbacks of high false-positive rates, overdiagnosis potential, radiation risk, psychosocial consequences, effect on smoking behavior and incidental findings. More efficient screening strategies may use different criteria than the NLST excluding those at lower risk while including those outside NLST criteria that are at identifiable high risk. Several risk prediction models exist. The PLCO~m2012~ model is the best-validated. Selected risk factors included age, race, ethnicity, education, body mass index, self-reported chronic obstructive pulmonary disease, personal and family history of lung cancer, and smoking variables. A risk threshold of 1.5% over 6 years was chosen as below this threshold there was no reliable evidence of screening benefit and much higher numbers needed to screen. Comparing this risk model threshold to the USPSTF criteria in the PLCO CXR arm demonstrates that the PLCO~m2012~ risk model approach is more efficient [4]. Table The American College of Radiology developed the Lung-RADS nodule classification system [5]. When applied retrospectively to NLST data (26,455 baseline scans and 48,671 incidence scans), Lung-RADS 1.0 substantially reduced the false-positive rate (12.8% versus 26.6% at baseline and 5.3% versus 21.8% at incidence scans respectively). However, the trade-off was reduced sensitivity compared to NLST criteria: 84.9% vs. 93.5% at baseline and 78.6% versus 93.8% for incidence scans [6]. Retrospective subset analyses while imperfect are useful, providing some information about potential variations in effectiveness in subgroups. Analysis of performance within the NLST was conducted by age, gender and smoking status with additional detail comparing those less than 65 and ≥ 65 [7]. The mortality risk ratios by age, < 65 and ≥ 65, were 0.82 and 0.87; gender, males and females, 0.92 and 0.73, and by smoking status, current versus former, 0.81 and 0.91. Reassuringly, ninety day postsurgical mortality rates in those less than and ≥ 65 were 1.8% and 1.0% respectively. An estimate of overdiagnosis within the NLST has been done [8]. Using follow-up data extended from that in the primary manuscript, a total of 1089 lung cancers occurred in the LDCT arm compared with 969 in the CXR arm, resulting in 120 additional lung cancer cases in the LDCT arm. Two estimates of the upper bound of overdiagnosis were calculated, 18.5% of the cases detected during screening and 11% of the cases overall. More follow-up would be helpful to determine the extent of continued catch-up in cases in the CXR arm. Current smokers in the Lung Screening Study portion of the NLST were evaluated for smoking cessation and results also analyzed by findings on LDCT [9]. Those with normal scans did show a decline in smoking prevalence that continued for the seven years of assessment. Those with abnormal scans had higher cessations rates; the more abnormal the scan the higher the rates. All lung cancer screening programs should incorporate proven smoking cessation strategies. The cost-effectiveness analysis from the NLST utilized data from medical record abstraction covering in exhaustive detail medical interventions delivered as a consequence of screening [10]. As compared with no screening, screening with low-dose CT cost an additional $1,631 per person and provided an additional 0.0316 life-years per person and 0.0201 Quality Adjusted Live Years (QALY) per person. The corresponding Incremental Cost Effectiveness Ratios were $52,000 per life-year gained and $81,000 per QALY gained but varied widely by underlying risk group. Information from the NLST continues to refine our understanding of lung cancer screening. This should prove invaluable in ensuring that screening is done at a high level to achieve optimal mortality reductions as programs are expanded. References 1. The National Lung Screening Trial Research Team. Reduced Lung-Cancer Mortality with Low-Dose Computed Tomographic Screening. N Engl J Med 2011; 365: 395-409. 2. Moyer VA. Screening for lung cancer: U.S. Preventive Services Task Force recommendation statement. Ann Int Med 2014; 160: 330-338. 3. Centers for Medicare and Medicaid Services. Decision Memo for Screening for Lung Cancer with Low Dose Computed Tomography (LDCT) (CAG-00439N). http://www.cms.gov/medicare-coverage-database/details/nca-decision-memo.aspx?NCAId=274 (accessed February 22, 2015). 4.Tammemagi MC, Church TR, Hocking WG et al. Evaluation of the Lung Cancer Risks at Which to Screen Ever- and Never-Smokers: Screening Rules Applied to the PLCO and NLST Cohorts. PLoS Medicine 2014; 11: e10001764. 5. American College of Radiology ACR-STR Practice Guideline for the Performance and Reporting of Lung Cancer Screening Thoracic Computed Tomography http://www.acr.org/~/media/ACR/Documents/PGTS/guidelines/LungScreening.pdf (accessed February 22, 2015). 6. Pinsky PF, Gierada DS, Black W et al. Performance of Lung-RADS in the National Lung Screening Trial. Ann Intern Med [Epub ahead of print 10 February 2015] doi:10.7326/M14-2086. 7. Pinsky PF, Gierada DS, Hocking W et al. National Lung Screening Trial Findings by Age: Medicare-Eligible Versus Under-65 Population. Ann Intern Med 2014; 161: 627-633. 8. Patz EF, Pinsky P, Gatsonis CG et al. Overdiagnosis in Low-Dose Computed Tomography Screening for Lung Cancer. JAMA Intern Med 2014: 174: 269-274. 9. Tammemagi MC, Berg CD, Riley TL et al. Impact of Lung Cancer Screening Results on Smoking Cessation. J Natl Cancer Inst 2014;106: dju084. 10. Black WC, Gareen IF, Soneji SS et al. Cost-Effectiveness of CT Screening in the National Lung Screening Trial. N Engl J Med 2014; 371: 1793-1802. TABLE Comparison of PLCO~M2012~, NLST and USPSTF [4]
[1] Estimated lung cancer risk over six yearsPLCO~M2012 ~vs. NLST PLCO~M2012~ vs. USPTF PLCO~M2012~ NLST PLCO~M2012 ~ USPSTF Selection criteria >1.3455%[1] Age 55-74, current/former smoker ≥30 PY ≥ 1.51%1 Age 55-80, current/former smoker ≥30 PY Validation cohort 14,144 PLCO trial screening arm smokers 14,144 PLCO trial screening arm smokers who met NLST criteria 37,327 PLCO trial screening arm smokers 37,327 PLCO trial screening arm smokers who met USPSTF criteria Sensitivity, % (95% CI) 83.0 71.1 80.1 (76.8–83.0) 71.2 (67.6–74.6) Specificity, % (95% CI) 62.9 62.7 66.2 (65.7–66.7) 62.7 (62.2–63.1) Positive Predictive Value, % (95% CI) 4.0 3.4 4.2 (3.9–4.6) 3.4 (3.1–3.7)
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PLEN01.02 - Epidemiology of Lung Cancer/Smoking in the World (ID 2039)
08:15 - 09:45 | Author(s): D. Christiani
- Abstract
- Presentation
Abstract:
Lung cancer remains the most common cancer in the world. Worldwide, the leading cause of cancer mortality in men and the second leading cause in women. 1.8 million new cases were diagnosed in 2012. About 58% of lung cancer cases occurred in low and middle income countries. Although by far not the only known or suspected lung carcinogen, cigarette smoking remains the principal cause of lung cancer and is estimated to be responsible for 85% of all types of this cancer. The major risk factors and risk modifiers for lung cancer include: Cigarette Smoking Secondhand Smoke (SHS) Air Pollution Radon Occupational Exposures (e.g., asbestos, silica, Chromium, radon) Lung Cancer Susceptibility Genes Aspirin/NSAIDs Use (protective) Dietary vitamin D (protective) HRT – possibly protective. I will cover updates on our understanding of the major risk factors for lung cancer in the USA and globally. Smoking Smoking causes an estimated 170,000 cancer deaths in the U.S. every year (American Cancer Society) and the incidence among women is rising. Lung cancer now surpasses breast cancer as the number one cause of death among women. Globally, cigarette consumption has changed over the decades, with China now the number one consumer (44%) of cigarettes in the world, while the USA is consumes about 5%. In the USA, “Second Hand Smoke” is the third leading cause of lung cancer and responsible for an estimated 3,000 lung cancer deaths every year. Globally, the number of SHS related cancer deaths is unknown, but surely rising. SHS is also referred as ‘environmental tobacco smoke (ETS)’, ‘passive smoking’ or ‘involuntary smoking’. IARC has deemed SHS is “carcinogenic to humans”, with an increased risk of 20% for women and of 30% for men among never smokers who are exposed to SHS (i.e., environmental tobacco smoke) from their spouse. Ambient Air Pollution IARC has classified outdoor air pollution - as a whole - as “carcinogenic to humans (Group 1)”. Outdoor air pollution has been shown to cause lung cancer and bladder cancer, pointing to the role of overlapping carcinogen exposure to compounds such as polycylic aromatic compounds (PAC). The most recent data from the Global Burden of Disease (GBD) Project indicate that in 2010, 3.2 million deaths worldwide resulted from air pollution alone, including 223,000 from lung cancer. Radon Radon is an odorless, colorless, radioactive gas that causes lung cancer. IARC classifies radon and its progeny as “carcinogenic to humans” (Class I), and the US EPA lists radon as the second leading cause of lung cancer in the US and the number one cause of lung cancer among non-smokers. Originally described as a risk factor in underground miners (among both smokers and non-smokers, with synergistic interaction with smoking), the U.S. EPA estimates that 1 of 15 homes in the US (as many as 1 of 3 homes in some states)-about 7 million homes-have high radon levels. Occupational Exposures: Asbestos In North America, and most other high income countries, asbestos has been the most prevalent occupational lung carcinogen exposure. All forms of asbestos have been classified as a known human carcinogen (by the U.S. Department of Health and Human Services, EPA, and the IARC). About 125 million people in the world are exposed to asbestos at the workplace. According to WHO estimates, more than 107,000 deaths each year are attributable to occupational exposure to asbestos. Exposure to asbestos, including chrysotile, causes cancer of the lung, larynx and ovaries, and also mesothelioma. Co-exposure to tobacco smoke and asbestos fibers substantially increases the risk for lung cancer (multiplicative interaction). Heritable Factors: Common Genetic Variants GWAS provide novel insights into the development of LC. Genetic factors are increasingly recognized to be important in the etiology of LC: 15q25.1 (CHRNA5-CHRNA3-CHRNB4) 5p15.33 (TERT-CLPTM1) 6p21.33 (BAT3-MSH5) Follow up studies that pool data international as part of a large consortium (International Lung Cancer Consortium - ILCCO) have identified other common variants at multiple loci influencing LC risk, and these include BRACA1. Studies of pleiotropy are well underway. Additionally, GWAS studies globally, such as one from China, have identified unique, population-specific, risk loci. COPD and Lung Cancer risk COPD and LC are the 4[the] and 7[th] leading causes of death worldwide. The coexistence of COPD is an important marker of future risk of LC among smokers. Epidemiologic studies have shown that 50-70% of LC patients have co-existing impaired lung function or COPD. And, not surprisingly, 90% of combined LC and COPD cases are attributable to cigarette smoking. Recently, we have found that the co-existence of COPD with lung cancer also negatively influences survival among patients with all stages. Conclusion Lung cancer remains the number one cancer threat to the world’s populations. Lung cancer epidemiology continues to evolve and as we understand more about the origins and behavior of lung cancer, the more opportunities we will have for prevention and control of this deadly disease.
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PLEN01.03 - Smoking by Lung Cancer Patients: Clinical, Biologic and Behavioral Considerations (ID 2040)
08:15 - 09:45 | Author(s): G. Warren
- Abstract
- Presentation
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Smoking is the largest preventable risk factor for the development of lung cancer. Continued smoking by cancer patients and survivors causes adverse outcomes including an increase in overall mortality, cancer specific mortality, risk for second primary cancer, and associated increases in cancer treatment toxicity. Significant evidence demonstrates the biologic mechanisms of cancer initiation and progression caused by cigarette smoke, but relatively few studies have evaluated the effects of smoking on cancer biology and therapeutic response to cytotoxic agents. Most oncologists believe smoking causes adverse outcomes and that smoking cessation treatment should be a standard part of cancer care. However, most oncologists do not regularly provide cessation support to cancer patients. Moreover, tobacco assessments and cessation support are not regularly incorporated into clinical trials design or analysis. Recently released guidelines from several national and international organizations advocate for addressing tobacco use by cancer patients. This session will discuss the clinical and biologic effects of smoking on cancer, present the current state of tobacco assessments and cessation in clinical practice and research, and discuss methods to improve access to cessation support for cancer patients. Discussion will further detail deficits in the current understanding of the effects of smoking on cancer treatment outcomes and highlight areas of needed improvement.
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HOD 02 - Highlights of the Previous Day: Biology, Pathology, Molecular Testing, Prevention, Tobacco Control, Screening and Early Detection (ID 241)
- Event: WCLC 2015
- Type: Highlights of the Day
- Track: Biology, Pathology, and Molecular Testing
- Presentations: 1
- Moderators:
- Coordinates: 9/08/2015, 07:00 - 08:00, Four Seasons Ballroom F3+F4
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HOD02.02 - Prevention, Tobacco Control (ID 3396)
07:00 - 08:00 | Author(s): C. Dresler
- Abstract
Abstract not provided
