Virtual Library
Start Your Search
J. Jassem
Moderator of
-
+
ORAL 08 - Smoking Cessation, Tobacco Control and Lung Cancer (ID 94)
- Event: WCLC 2015
- Type: Oral Session
- Track: Prevention and Tobacco Control
- Presentations: 8
-
+
ORAL08.01 - The History of Tobacco Litigation in the United States (ID 795)
10:45 - 10:56 | Author(s): K.M. Cummings, A. Brown, R. Goldstein
- Abstract
- Presentation
Background:
This presentation reviews the history of tobacco litigation in the United States.
Methods:
Data for this study comes from industry business records available online through the UCSF Legacy Tobacco Documents Library, transcripts of court proceedings, and news and stock analyst reports on tobacco litigation.
Results:
Litigation against the tobacco industry began in 1954, corresponding to the emerging evidence linking smoking and disease. A total of 109 lawsuits were filed between 1954 and 1970, but only eight were tried and all ended in defense verdicts. Another 150 cases were filed between 1970 and 1985, but none went to trial. There was a second wave of cases filed during the mid-1980s that led to jury trials, but only one, Cipollone v. Liggett Group, was a plaintiff verdict. Cipollone was later overturned on appeal. A third wave of litigation followed in the early 1990s, with several plaintiffs’ verdicts. By 1999, juries were awarding punitive damages against the defendants. The state Attorney General cases against cigarette manufacturers resulted in the Master Settlement Agreement in 1998, which, among other things, required that the cigarette companies release millions of pages of business records. These documents have played a key role in fueling subsequent litigation and winning cases. The Engle v. Liggett Group class action verdict on behalf of injured smokers in Florida in the late 1990s helped to change the industry’s long held position that smoking was unproven as a cause of disease and that nicotine was not addictive. Decertification of the Engle class action lawsuit spawned several thousand individual lawsuits against the cigarette industry in Florida, which have resulted in dozens of verdicts favoring plaintiffs since 2009. Additional litigation against the tobacco industry continues nationwide on the “light” cigarettes fraud and on individual personal injury cases that have resulted in notable verdicts against the tobacco industry.
Conclusion:
In the United States, litigation against the cigarette industry began in 1954 and has accelerated over the past 60 years with a growing number of verdicts favoring plaintiffs since the mid-1990s. Litigation has proven to be a powerful tool for tobacco control efforts helping to change public sentiment about the industry and its products, increasing the costs of cigarettes, and forcing the industry to accept responsibility, in front of a jury, for its deceptive practices.
Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.
-
+
ORAL08.02 - Interest in Smoking Cessation Treatment among Patients in a Community-Based Multidisciplinary Thoracic Oncology Program (ID 2886)
10:56 - 11:07 | Author(s): K.D. Ward, S. Kedia, N. Faris, F.E. Rugless, M. Sheean, C. Foust, K.S. Roark, L. McHugh, C. Fehnel, R.U. Osarogiagbon
- Abstract
- Presentation
Background:
Cigarette smoking is the major cause of lung cancer. Many adults smoke at the time of a lung cancer diagnosis and continue to smoke during treatment although doing so adversely affects treatment response, quality of life, and survival time. While authoritative bodies recommend that tobacco use be addressed in lung cancer care, few patients receive effective treatment. The coordinated multidisciplinary model of care delivery, in which patients, their caregivers, and key specialists concurrently develop evidence-based care, offers an ideal setting to integrate high quality cessation treatment. To assess the need for and acceptability of cessation services, we surveyed patients about their smoking status, interest in quitting, and willingness to participate in a clinic-based cessation program.
Methods:
The study was conducted in the Multidisciplinary Thoracic Oncology Program at Baptist Cancer Center, Memphis TN. One-hundred eight consecutive new patients, seen between 7/31/13 and 9/24/14, completed a social history questionnaire. From this history, we extracted data related to sociodemographic characteristics (age, gender, race, marital status), smoking status, age of smoking initiation, and tobacco dependence (using the Heaviness of Smoking Index, consisting of cigarettes smoked per day and time of first cigarette of the day). Current smokers reported their level of interest in quitting, and how likely they would be to participate in a cessation program (‘I would not participate’; ‘I might participate but am not sure’; ‘I would participate’). Chi square tests were used to compare characteristics of those who would participate in the stop-smoking program vs. those who would not or were unsure whether they would participate.
Results:
Average age of patients was 65 years (range: 29-91), 41% were men, 58% were white, 39% black, and 15% had graduated college. Patients’ cancer stage broke down to stage I (16%), stage II (9%), stage III (18%), stage IV (28%), and undetermined (29%). 84% of patients had ever smoked cigarettes, 35% currently smoked, and 11% had quit smoking within the past year. Among current smokers, 71% (n=27) were “very interested” in quitting smoking in the next month and of these, 74% reported that they would be willing to participate in a smoking cessation program in the clinic. Willingness to participate in a cessation program was associated with greater interest in quitting (χ[2][1]= 13.3, p=.0003), but was not associated with sociodemographic characteristics, cancer stage, or smoking-related characteristics (amount smoked, age at smoking initiation, or dependence).
Conclusion:
Nearly half (46%) of patients in a community-based multidisciplinary thoracic oncology program were current cigarette smokers or had quit within the previous year, indicating a considerable need for cessation and relapse-prevention support. Encouragingly, a majority of current smokers were highly motivated to make a quit attempt in the next month, and most indicated that they would take advantage of a clinic-based cessation program. Willingness to participate in a cessation program was similar across a broad range of sociodemographic, cancer stage, and nicotine dependence levels. There is considerable need for, and interest in, smoking cessation services in the setting of community-based multidisciplinary lung cancer care.
Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.
-
+
ORAL08.03 - Smoking Cessation Before the Initiation of Chemotherapy in Metastatic NSCLC: Impact on Overall Survival (ID 1746)
11:07 - 11:18 | Author(s): S. Chiasson, M. Lelièvre, B. Fortin, J. Dionne
- Abstract
- Presentation
Background:
It is well documented that active smoking affects the overall mortality in lung cancer. Smoking cessation has been associated with better prognostic outcomes in patients with early stage non-small cell lung carcinoma (NSCLC) and limited stage small cell lung carcinoma (SCLC). Smoking cessation impact in advanced stage NSCLC is less well characterized. We studied the benefit of smoking cessation, before the initiation of chemotherapy, on overall survival (OS) in advanced NSCLC.
Methods:
We retrospectively reviewed the clinical data of 306 patients with stage IV SCLC and NSCLC between 2008 and 2014 in our centre. The 237 NSCLC patients treated with at least one cycle of chemotherapy are the subjects of this study. Smoking status and smoking cessation duration at the chemotherapy initiation time, number of packs/years, comorbidities, histology, sites of metastases, type and number of cycles of chemotherapy were all collected. Never-smokers were defined by a smoking history of < 100 cigarettes during their entire lifetime. Survival curves were calculated by the Kaplan-Meier method and compared using log-rank test. Cox proportional hazard models were used for multivariable analyses.
Results:
Smoking cessation before the initiation of chemotherapy is associated with a better median overall survival of 16 vs 10 months (p=0.007). This is even seen in heavy smokers of > 30 pq/year, with a median OS of 15 vs 8 months (p=0.008). The multivariable analysis confirms that active smoking is an independent negative factor on survival (51% increase in the risk of death) after adjustment for gender, heart or vascular disease, diabetes, high blood pressure, ECOG performance status, histology, site of metastases (brain, liver, adrenals, lungs and bones). Figure 1
Conclusion:
Smoking cessation, before the initiation of chemotherapy, is associated with a better overall survival in chemotherapy treated stage IV NSCLC patients, even in previously heavy smokers and after adjustments for comorbidities. This retrospective analysis demonstrates the possible magnitude of the effect of smoking cessation on treatment efficacy with a potential gain of 6 months in median overall survival. Efforts to encourage smoking cessation are likely beneficial even among this population of patients.
Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.
-
+
ORAL08.04 - Discussant for ORAL08.01, ORAL08.02, ORAL08.03 (ID 3316)
11:18 - 11:28 | Author(s): J. Ostroff
- Abstract
- Presentation
Abstract not provided
Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.
-
+
ORAL08.05 - Impact of an Inpatient Tobacco Cessation Service (ID 1557)
11:39 - 11:50 | Author(s): K.M. Cummings, G. El Nahhas, V. Talbot, D. Wilson, D. Woodard, K. Cartmell, G.W. Warren, B. Toll
- Abstract
- Presentation
Background:
Cigarette smoking is responsible for 85% of all lung cancers and about 1/3rd of all cancer deaths. Quitting smoking reduces the risk of getting lung cancer and other serious health problems. In 2012, the Joint Commission (JC) which sets quality standards for hospitals in the United States recommended that all current smokers identified upon hospitalization receive tobacco cessation services as an inpatient and be followed up after hospital discharge. However, few hospitals implement JC standards due to extra costs, the voluntary nature of the standards, and the lack of evidence demonstrating financial benefits to the hospital and insurers. In 2014, the Medical University of South Carolina (MUSC), a major tertiary care hospital in South Carolina, implemented an automated in-hospital smoking cessation program using interactive voice recognition (IVR) technology to follow-up with patients after discharge consistent with JC standards. This study reports on the results of the program over the first 12 months of operation between February 17, 2014 and January 31, 2015.
Methods:
Descriptive statistics are used to report on the number of patients screened, number of tobacco using patients seen by a bedside tobacco counselor while hospitalized, the number of tobacco using patients followed-up 3, 14, and 30 days after discharge, and the rate of unplanned hospital readmissions within a month of discharge.
Results:
A total of 30,846 patients aged 18 and older were screened for tobacco on hospital admission and 18% were identified current smokers. Of the 5,546 identified smokers, 2008 (36%) were approached by a single bedside counselor while hospitalized; 29% were unavailable for counseling for various reasons (e.g., discharged, too sick, not in room, deceased), 11% refused counseling, and 3% reported to the bedside counselor that they were non-tobacco users. A total of 4,197 tobacco using patients were enrolled into the automated telephone follow-up to assess smoking status and offer triage to the state quitline for those who wanted help. A total of 1,378 (33%) responded to at least one of the follow-up calls by one month, with 31% reporting that they were not smoking (10% classified as not smoking if non-responders are counted as smoking). The one month nonsmoking rate was 44% (19% based on intent to treat) in those seen by the bedside counselor compared to 24% (7% based on intent to treat) in those merely followed by phone. Unplanned 30-day hospital readmission rates were 9.1% for patients seen by the bedside counselor as compared with 15.7% for patients who did not receive bedside counseling based on the first 6 months of the program.
Conclusion:
An opt-out inpatient tobacco cessation service is feasible, can reduce relapse back to using tobacco after hospital discharge, and may reduce unplanned hospital readmissions.
Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.
-
+
ORAL08.06 - Introducing Smoking Cessation Across Ontario's Cancer Treatment System: Early Successes and Continuing Challenges (ID 537)
11:28 - 11:39 | Author(s): W.K. Evans, R. Presutti, M. Haque, R. Truscott, M. Bassier-Paltoo, A. Peter, L. Rabeneck
- Abstract
- Presentation
Background:
Smoking cessation (SC) has rarely been recommended by oncologists in Ontario’s cancer centres. Many believe it is too late to matter or perceive that patients will not be receptive to SC. However, a growing body of literature has identified substantial health benefits from SC in cancer patients including improved general health, improved all-cause and cancer-specific mortality, reduced toxicity, greater response to treatment and decreased risk of disease recurrence and second primaries. Based on this evidence, Cancer Care Ontario (CCO) undertook an initiative to support SC for new ambulatory cancer patients in its Regional Cancer Programs (RCPs) in 2013.
Methods:
A steering committee of experts recommended a framework for SC in 2012 based on the Ottawa Model for Smoking Cessation. The CCO executive leadership and Regional Vice-Presidents supported the initiative which was then piloted in all 14 health regions in Ontario in 2014. Regional SC “champions” participated in monthly web meetings, data calls and in-person meetings led by a secretariat at CCO. Presentations on the health benefits of SC were made to physicians and other health care providers (HCPs) at regional cancer treatment centres and through the Ontario Telehealth Network. Presentations emphasized short, repeated oncologist scripts on the benefits of SC with referral to other HCPs for in-depth SC advice. New ambulatory cancer patients are screened, advised and referred to internal or external SC services dependent on regional resources. A minimum data set of standardized performance metrics is captured by CCO with patient-level data aggregated at the RCP level, presented as a provincial average, and reviewed with the RCPs in quarterly performance management sessions.
Results:
During Q1-Q3 of the 2014/15 fiscal year, 52.9% of all new ambulatory cancer cases were screened for smoking status. Of those screened, 21.3% were current or recent (within the last 6 months) tobacco users. Approximately three-quarters of these individuals were advised of the benefits of SC; a referral for cessation services was recommended in nearly 50%; of these patients, 66.7% accepted the referral to SC services. Of those accepting a referral, 50.4% chose referrals internal to the cancer treatment facility, 32.3% chose external referrals and the remainder (17.2%) used a combination of both referral resources. As part of this initiative a standardized cancer patient resource on SC in a print-ready format has been recently developed in both French and English and will be adapted for Ontario’s Aboriginal population.
Conclusion:
CCO’s centralized yet collaborative approach has led to province-wide implementation of a standardized intervention in a relatively short timeframe with limited financial resources. Ongoing barriers to implementation and sustainability experienced by RCPs include financial constraint, limited SC training resources, reluctant physician buy-in, strained staff and system capacity, and suboptimal inter-departmental communication. Nonetheless, there has been substantial progress. Framing SC as a quality of care issue has been critical to the success to date. Sustainability of the initiative will be dependent on continued committed leadership, buy-in from front-line staff, funding for dedicated SC counselors and other resources, and evidence of program cost-effectiveness.
Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.
-
+
ORAL08.07 - Primary Prevention of Lung Cancer in Poland - Successes and Challenges (ID 2398)
11:50 - 12:01 | Author(s): J. Jassem, K. Przewoźniak, W. Zatonski
- Abstract
- Presentation
Background:
In the 1990s Poland was among countries with the highest tobacco exposure and catastrophically high lung cancer mortality. Within the past two decades this situation has dramatically improved as a result of comprehensive national tobacco-control programs. We present the current tobacco exposure and
Methods:
Data on trends in cigarette consumption, smoking rates and lung cancer mortality were analyzed using the per capita sale of manufactured cigarettes, results of nation-wide questionnaire surveys conducted in adult (15+) population, and standardized mortality rates from lung cancer, respectively.
Results:
Between 1995 and 2013 annual cigarette sales in Poland decreased from 101 billion to 47 billion. The proportion of smokers among men dropped from 65% in 1980 to 28% in 2013, and among women from 32% to 18%, respectively. If this trend continues, the cigarette consumption per capita in Poland in 2040 will fall to the level of the 1920s. The age-standardized mortality rates per 100,000 from lung cancer in men declined from 71.1 in 1990 to 56.2 in 2010. The pattern of changes in lung cancer mortality among young Polish men became similar to that observed two decades earlier in the Unites States (Figure). However, Poland is still facing several challenges. Between 2003 and 2012 tobacco production in Poland increased by 90%, of which around two-thirds is exported. There is a persistently high proportion of smoking women, with almost a gender parity in the 35-44 age bracket (34% and 32% in women and men, respectively). Polish middle-aged women belong to the most common smokers in the European Union. The mortality rates from lung cancer among women are still on the rise. Since 2010 lung cancer has become the leading cause of death among women in Poland. Today, differences in smoking rates and lung cancer mortality are mainly generated by education and financial status, and not by gender. Figure 1
Conclusion:
There is an apparent need for further tobacco control efforts in Poland, including enforcement of the effective legislative measures (pictorial health warnings, plain cigarette packages, banning the sale of aromatic and ‘slim’ cigarettes) and implementation of tailored population-based preventive programs for women and socially unprivileged populations.
Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.
-
+
ORAL08.08 - Discussant for ORAL08.05, ORAL08.06, ORAL08.07 (ID 3329)
12:01 - 12:11 | Author(s): E. Stone
- Abstract
- Presentation
Abstract not provided
Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.
-
+
ORAL 23 - Prevention and Cancer Risk (ID 121)
- Event: WCLC 2015
- Type: Oral Session
- Track: Prevention and Tobacco Control
- Presentations: 8
-
+
ORAL23.01 - A Randomized Phase IIb Trial of Myo-Inositol in Smokers with Bronchial Dysplasia (ID 856)
10:45 - 10:56 | Author(s): S. Lam, S. Mandrekar, K. Allen Ziegler, D. Seisler, D. Midthun, J. Mao, M.C. Aubry, A. McWilliams, D. Sin, T. Shaipanich, A. Spira, D. Ionescu, J. Mayo, J.E. Yi, H. Tazelaar, W. Harmsen, J. Smith, P. Limburg, E. Szabo
- Abstract
- Presentation
Background:
Previous preclinical studies and a phase I clinical trial suggested myo-inositol may be a safe and effective lung cancer chemopreventive agent. We conducted a randomized, double blind, placebo-controlled, phase IIb study to determine the chemopreventive effects of myo-inositol in smokers with bronchial dysplasia.
Methods:
Smokers with ≥1 site of dysplasia identified by autofluorescence bronchoscopy-directed biopsy were randomly assigned to receive oral placebo or myo-inositol, 9 g once/day for two weeks, and then twice/day for 6 months. The primary endpoint was change in dysplasia rate after six months of intervention on a per participant basis. Other trial endpoints reported herein include Ki-67 labeling index and pro-inflammatory, oxidant/anti-oxidant biomarker levels in blood and bronchoalveolar lavage fluid (BAL).
Results:
Seventy four (n=38 myo-inositol, n=36 placebo) participants with a baseline and 6-month bronchoscopy were included in all efficacy analyses. The complete response and the progressive disease rates were 26.3% versus 13.9% and 47.4% versus 33.3%, respectively, in the myo-inositol and placebo arms (p=0.76). The mean percent change in Ki67 labeling index in bronchial biopsies with dysplasia was -22.8% and -6.2%, respectively, in the myo-inositol and placebo arms (p=0.34). Compared with placebo, myo-inositol intervention significantly reduced IL-6 levels in BAL over 6 months (p=0.03) and had borderline significant effects on BAL myeloperoxidase (p= 0.06) level.
Conclusion:
The heterogeneous response to myo-inositol suggests a targeted therapy approach based on molecular alterations is needed in future clinical trials to determine the efficacy of myo-inositol as a chemopreventive agent.
Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.
-
+
ORAL23.02 - Pioglitazone for the Chemoprevention of Lung Cancer (ID 2419)
10:56 - 11:07 | Author(s): R.L. Keith, P.J. Blatchford, M.K. Jackson, W.A. Franklin, P.A. Bunn, Jr, B. Bagwell, D.T. Merrick, Y.E. Miller
- Abstract
- Presentation
Background:
Prior clinical studies have shown that the oral prostacyclin agonist iloprost improves bronchial dysplasia in former smokers. Prostacyclin is a PPAR gamma agonist, and epidemiologic and pre-clinical studies suggest PPAR gamma agonists like pioglitazone may chemoprevent lung cancer. Based on these promising results, a double-blind, placebo controlled, phase II trial of pioglitazone in subjects at increased risk for lung cancer was sponsored by the Department of Veterans Affairs.
Methods:
Subjects were selected for the trial if they met one the following criteria: current or former smoker (> 10 pack years); biopsy proven endobronchial dysplasia; airflow obstruction (FEV1/FVC < 0.70); or at least mild sputum cytologic atypia. Fluorescent bronchoscopy was performed with biopsy of 6 standard endobronchial sites and all other abnormally appearing areas. Subjects also had pulmonary function testings and quantitative high resolution CT scans at the start and completion of the trial. Subjects were then randomized to oral pioglitazone or placebo for 6 months and then a second fluorescent bronchoscopy with repeat biopsy of all the central airway areas sampled on the first bronchoscopy. The endobronchial biopsies were scored on a 1-8 scale based on WHO criteria. The primary endpoint for the study is change in maximum (worst) endobronchial histology.
Results:
A total of 90 subjects (46 pioglitazone, 44 placebo) have been enrolled in the trial, with 76 completing both bronchoscopies. Subjects are well matched in terms of age, gender, tobacco exposure, and sputum cytology. No significant differences in lung function were observed between the treatment groups. While the investigators remain blinded in regards to treatment group, aggregate data is available. Overall, mild dysplasia or worse was seen in 26% of the initial biopsies. Similar to prior studies, current smokers exhibited more dysplasia at baseline compared to former smokers (32.4% vs. 16.6%) and also had more angiogenic squamous dysplasia (11.7% vs. 3.2%). Our primary endpoint is change in maximum histology, and histologic scores from matched biopsies in all participants showed a change of at least 1 grade in 50.2% (25.9% improved, 24.3% progressed). More histologic changes were observed in current smokers (59.2%) than former smokers (41.7%). Summary data for the non-normal biopsy pairs (ie those with a histologic score of at least 2 on baseline biopsy) showed that the majority of pairs (73.7%) changed by at least one grade. Current smokers exhibited more progression (29.3%) compared to former smokers (14.6%).
Conclusion:
The pioglitazone lung cancer chemoprevention trial is currently in progress. The treatment has been well tolerated and histologic changes were observed in many of the subjects.
Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.
-
+
ORAL23.03 - Role of Inflammatory Infiltrates in Promoting Persistence or Regression of Bronchial Dysplasia (ID 3026)
11:07 - 11:18 | Author(s): D.T. Merrick, E.J. Donald, D. Olson, M.C. Okeefe, M.G. Edwards, W.A. Franklin, L. Dwyer-Nield, D. Orlicky, R.L. Keith, Y.E. Miller, M. Tennis, A.E. Barón, X. Lu, A. Van Bokhoven, H. Malinowski, P.A. Bunn, Jr, M.W. Geraci, R. Nemenoff
- Abstract
- Presentation
Background:
Inflammatory infiltrates show differing capacities to eliminate malignant cells. This capacity is related to the polarization of key inflammatory cells in tumor infiltrates. A pathway analysis of genes that are differentially expressed between persistent and regressive bronchial dysplasia (BD) identified 13 pathways associated with persistence of which 8 were related to inflammation. We have hypothesized that differences in inflammatory infiltrate polarization may contribute to lung carcinogenesis and have employed gene expression and in situ analyses to characterize differences in inflammatory infiltrates related to persistence and regression of pre-malignant BD.
Methods:
Normalized gene expression levels (Affymetrix Hu 1.0) of selected genes related to inflammatory cell polarization features were analyzed to find differences associated with follow-up histology for BD. Validational analyses of these relationships were undertaken in studies of baseline biopsies selected to represent persistent (n=43) and regressive BD (n=39). These biopsies were analyzed by quantitative immunohistochemistry and dual immunofluorescence studies to characterize the overall proportion of subsets of T-lymphocytes and macrophages in each of the groups. Image analysis tools (Aperio) were used to characterize the density of inflammatory cell subsets in the stromal and epithelial compartments of biopsy tissue within defined areas.
Results:
Analysis of expression levels for a subset of inflammatory cell related genes assessed in a global gene expression analysis indicated significantly higher levels of expression of macrophage M1 markers HLA-DRA (p=0.01) and inducible nitric oxide synthetase (iNOS; p=0.02) and T-helper lymphocyte marker CD4 (p=0.04) in regressive BD compared to persistent BD. There was also a trend toward higher expression of cytotoxic T-lymphocyte marker CD8 in regressive BD (p=0.25). Expression of B-lymphocyte and neutrophil markers were not different between regressive and persistent BD. CD68 immunohistochemical stains (IHC) demonstrated a trend toward an increase in macrophages per area of combined dysplastic epithelium and underlying stroma with a mean increase in IHC positivity of 1.75-fold in regressive versus persistent BD (p=0.08). CD4 and CD8 IHC showed 1.36- and 1.19-fold increases, respectively, in regressive BD but these changes were not statistically significant (p=0.36 and p=0.43 respectively). Dual immunofluorescence was undertaken to determine if polarization specific subsets of macrophages correlated with regression or persistence of BD. Analysis of a preliminary subset of regressive (n=3) and persistent (n=3) BD demonstrates a wide range of M1 to M2 ratios (range = 0.84 – 4.82 for ratio of HLA-DRA-CD68 dual positive M1 to CD206-CD68 dual positive M2 macrophages per high power field, 400X). Additional analyses of macrophages are ongoing to determine if the polarization status is related to regression or persistence of BD, and analysis of markers of T-helper lymphocyte subsets are planned.
Conclusion:
Gene expression analyses indicate that increased expression of markers of M1 macrophages and T-helper lymphocytes are associated with regression, and in situ analyses suggest that differences in the amount of inflammatory cell subsets may be related to outcome in BD. These studies could have implications for predicting the behavior of premalignant disease and manipulating inflammatory activity in preventing progression of BD to invasive lung cancer.
Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.
-
+
ORAL23.04 - Discussant for ORAL23.01, ORAL23.02, ORAL23.03 (ID 3357)
11:18 - 11:28 | Author(s): E. Szabo
- Abstract
- Presentation
Abstract not provided
Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.
-
+
ORAL23.05 - Increased Proportion of Female and Young Mesothelioma Cases Are Indicators of Environmental Exposure to Carcinogenic Mineral Fibers in Nevada (ID 959)
11:28 - 11:39 | Author(s): F. Baumann, B.J. Buck, R.V. Metcalf, B.T. McLaurin, D. Merkler, M. Carbone
- Abstract
- Presentation
Background:
Inhalation of asbestos and other carcinogenic mineral fibers cause malignant mesothelioma (MM) and lung cancer. Occupational exposure leads to a MM male to female (M:F) sex-ratio of 4-8:1, with a mean age of diagnosis of 74 years old because of the 30-50 years latency between initial exposure and MM development. In places where people are only environmentally exposed to carcinogenic fibers, the M:F sex-ratio is about 1:1 and the mean age of diagnosis is 50-60 years. In places where both types of exposure exist, the M:F sex ratio decreases and the proportion of young (<55 years old) cases increases, compared to places with occupational exposure only. Therefore, incidence rates cannot distinguish between occupationally- and environmentally-caused mesotheliomas.
Methods:
In order to detect areas with possible environmental exposure to carcinogenic fibers, we studied the geology of Nevada. We compiled and integrated known presence of fibrous minerals in Nevada from published sources. We used the CDC 2006-2010 cancer data to study MM incidence and death rates by state and by gender. We also analyzed MM mortality data from the CDC in different Nevada Counties, per sex and age group, for the 1999-2010 period.
Results:
Several fibrous minerals were identified in Nevada, including actinolite asbestos, other amphiboles such as magnesioriebeckite, winchite and richterite that caused an epidemic of asbestos-related disease in Libby, Montana, and the highly carcinogenic erionite. For the 2006-2010 period, Nevada has a global MM age-standardized incidence rate of 10 cases per million inhabitants-year (95% confidence interval (CI): 8-12), similar to the average MM rate in the US (10 per million; 95% CI: 10-10). We discovered that Clark and Nye counties in southern Nevada had higher proportion of young (<55 years) MM cases (11.28%) and lower M:F sex-ratio (2.69:1), compared with other Nevada counties (M:F sex-ratio=6.33:1, p=0.04; proportion of young MMs=9.09%, p=0.80) and with the US (M:F sex-ratio=4.97:1, p=0.04; proportion of young MMs=6.21%, p=0.02).
Conclusion:
The significant decrease of MM M:F sex-ratio and increase of young cases are indicators of possible environmental exposure to carcinogenic fibers in southern Nevada. In this arid region, naturally occurring asbestos minerals are present in urban and rural areas where people use to enjoy outdoor activities including horseback riding, running, hiking, bicycling, and off-road vehicle (ORV) recreation. Airborne dust is common due to wind erosion. Asbestos fibers have been found in air and dust samples in Clark County. Further research should be conducted in this area to help identify sources of environmental exposure to these mineral fibers, activities that lead to the release of these carcinogenic fibers into the air, and measures to reduce the consequent risk of MM and other cancers.
Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.
-
+
ORAL23.06 - Radon Gas Exposure and Lung Cancer in a Cohort of Lung Cancer Patients Who Never Smoked (ID 2859)
11:39 - 11:50 | Author(s): C. Egan, A. D'Silva, J. Macklow, G. Bebb, D. Morris
- Abstract
- Presentation
Background:
Radon is a naturally occurring radioactive gas produced by the breakdown of uranium and uranium progeny in soil and rocks. This colourless and odourless gas moves easily through bedrock and foundations to accumulate within homes (basements) and buildings. Once inhaled, radon gas can decay to solid radionucleotides that deposit within tissue of the airways and lungs and continue to emit alpha particle radiation over the course of >25 years. Exposure to radon gas is thought to be a major epidemiological risk for the development of lung cancer in people who have never smoked, but the precise relationship between exposure and molecular alterations associated with lung cancer are poorly described. In order to explore the relationship between domestic radon gas levels and lung cancer incidence in never-smokers, we set out to identify a cohort of Alberta lung cancer patients who have never smoked and measure radon gas levels of in their homes.
Methods:
The Glans-Look Database, comprised of clinicopathological and outcome data for over 5000 patients with non-small cell lung cancer (NSCLC) consulted at the Tom Baker Cancer Centre between 1999 and 2010, was searched for patients who had developed NSCLC but never smoked. Follow-up information was obtained to determine if the patients or their family members still lived at the address provided at diagnosis. Initial letters of contact were sent explaining the study. Patients and their family members will be notified by mail of the levels of radon gas in their homes, and how best to mitigate levels if high. Radon concentration was examined as a continuous variable and as a dichotomous variable, using the cut point value of 200 Bq/m[3] suggested by Health Canada guidelines. Statistical analysis of data utilizes Cox proportional hazard regression models to examine the independent effects of radon exposure on patient outcome, utilizing IBM SPSS Statistical Package version 19. The model addresses the possible confounding variables of exposure to second hand smoke, type and age of dwelling, family history of lung cancer, profession and hours spent within the home.
Results:
A cohort of 317 patients was identified, 189 of whom met study criteria requirement. As of March 2015, 42 patients or their family members agreed to participate in this study. 30 long term testing radon monitors have been placed in the homes where patients lived for at least five years before developing NSCLC. These monitors are being collected by the study team by: all will be retrieved by June 30, 2015, three months after initial placement.
Conclusion:
This study will contribute significantly to our understanding of residential radon gas exposure in NSCLC, and in the short term, alert patients and their families to potential risk of high level radon gas exposure. In the longer term, as this will be the first study of its type in Alberta, the findings may be seminal in forming the basis of a health program for improved testing for radon gas in the home and educating the public with respect to the dangers of radon gas exposure.
Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.
-
+
ORAL23.07 - Interactions Between Smoking and the Dietary Inflammatory Index in Relation to Lung Cancer in the Prostate Lung Colorectal and Ovarian Trial (ID 1220)
11:50 - 12:01 | Author(s): A. Shoaibi, N. Shivappa, M. Wirth, S. Vyas, J. Houston, J. Hebert
- Abstract
- Presentation
Background:
Chronic inflammation can influence the process of lung carcinogenesis. Dietary factors can modulate inflammation and may modify the effect of tobacco smoke. In this study, we aim to investigate the association between the inflammatory potential of usual diet, as assessed by the novel Dietary Inflammatory Index (DII), and lung cancer and to assess the interactions between the DII and tobacco use.
Methods:
Existing data from the Prostate Lung Colorectal and Ovarian Cancer (PLCO) screening trial was used to test the hypothesis that DII influences lung cancer and modifies the effect of tobacco smoke. PLCO participants were enrolled between 1993 and 2001 and randomized to a control arm or screening arm for four target cancers. Data were collected on cancer diagnoses and deaths from all causes that occurred through December 31, 2009. The baseline DII score for each subject was calculated from self-reports via food frequency questionnaires. A proportional hazards model was used to assess the association between the DII and DII-smoking interaction in relation to the probability of developing lung cancer. To investigate the association between DII and lung cancer prognosis, we explored the distribution of the lung cancer stage by the DII quintiles
Results:
Of 110,317 participants who met our eligibility criteria, 1850 (1.68%) developed lung cancer. The median follow-up time was 8.38 years. The association between DII and C-reactive protein was significant (beta coefficient of Quintile5 vs. Quntile1 =0.45, p-value<0.01). Results from the proportional hazards model show that those at the higher DII quintiles were at higher risk of lung cancer. The risk of lung cancer among Participants at the 5[th] quintile was 1.28 times higher the risk among these at 1[st] quintile (HR~Q5vsQ1~ = 1.28, 95 % CI 1.09–1.51, and P~trend~ <0.03, after controlling for possible confounders (demographics, smoking, family history, intervention and others) . An interaction was observed between DII score and tobacco smoke in relation to lung cancer (p-value for the interaction =0.01). Among current and former smokers combined HR~Q5vs.Q1~ was 2.00, 95 % CI 1.6-2.36 ( P~trend~ <0.001) compared to 0.82, 95 % CI 0.48-1.41 among never smokers. Table 1 shows the distribution of the lung cancer stage. Cases with worse prognosis were more likely to be in the higher DII quintile. Figure 1
Conclusion:
Overall, more pro-inflammatory diets are associated with increased risk of lung cancer, particularly for former and current smokers, suggesting that dietary-mediated inflammation plays an important role in lung carcinogenesis
Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.
-
+
ORAL23.08 - Discussant for ORAL23.05, ORAL23.06, ORAL23.07 (ID 3563)
12:01 - 12:11 | Author(s): M. Carbone
- Abstract
- Presentation
Abstract not provided
Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.
Author of
-
+
MINI 34 - RNA and miRNA (ID 162)
- Event: WCLC 2015
- Type: Mini Oral
- Track: Biology, Pathology, and Molecular Testing
- Presentations: 1
- Moderators:C. Mascaux, L.(. Wang
- Coordinates: 9/09/2015, 18:30 - 20:00, 205+207
-
+
MINI34.14 - Biological Role of Prognostic MicroRNAs (MiRNAs) in Squamous Lung Cancer Cell Lines (ID 1171)
19:45 - 19:50 | Author(s): J. Jassem
- Abstract
- Presentation
Background:
The benefit from postoperative chemotherapy in non-small cell lung cancer (NSCLC) is modest and there are no reliable tools allowing for individual selection of high-risk patients for this management. We earlier demonstrated that overexpression of three miRNAs: miR-662, -192 and -192* may correlate with the risk of distant relapse in squamous cell lung cancer (SCC) patients undergoing pulmonary resection (Skrzypski et al. 2014, Br J Cancer). However, the role of these miRNAs in maintaining aggressive phenotype and/or chemoresistance of SCC is unknown. The aim of this study was to assess the biological role of three abovementioned miRNAs in SCC cells in vitro.
Methods:
In the search for appropriate in vitro model we screened by reverse transcription quantitative PCR 11 NSCLC cell lines (H1703, H520, H662, SK-MES-1, A549, H23, H1975, HCC 827, PC9, H460 and Calu-6) for miRNA expression profiles and analyzed their phenotypic features including migration, invasion and clonogenic potential. H520 and H1703 SCC cell lines were transfected with locked nucleic acid miRNA inhibitors. The sensitivity of transfected and wild type cells to cisplatin and etoposide was compared using cytotoxic MTT test. Soft agar colony formation assay was performed to assess the clonogenic potential of transfected vs. non-transfected cells.
Results:
Among the analyzed NSCLC cell lines, H520 cells showed natural overexpression of miR-662, -192 and -192*. These cells were resistant to both chemotherapeutics and exhibited an ability to form colonies in soft agar. The inhibition of miR-662 and miR-192 sensitized these cells to etoposide (p=0.004 and 0.016, respectively) but not to cisplatin. Similar results were obtained for H1703 cells (p=0.002 and 0.02, respectively). H520 cells treated with miR-192 and miR-662 inhibitors, compared to negative control, also demonstrated reduced number of colonies in soft agar (p<0.001).
Conclusion:
We developed and optimized a cellular model for in vitro studies of biological role of three prognostic miRNAs in SCC. Genes regulated by miR-662 and/or miR-192 may be involved in maintaining the chemoresistance and clonogenic potential of SCC, and these features may be inhibited in a miR-dependent specific manner. Further studies may elucidate predictive value of these genes and a possibility of their targeting with novel therapeutics.
Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.
-
+
MTE 32 - Treatment of Early Stage SCLC (Ticketed Session) (ID 84)
- Event: WCLC 2015
- Type: Meet the Expert (Ticketed Session)
- Track: Small Cell Lung Cancer
- Presentations: 1
- Moderators:
- Coordinates: 9/09/2015, 07:00 - 08:00, 703
-
+
MTE32.01 - Treatment of Early Stage SCLC (ID 2022)
07:00 - 07:30 | Author(s): J. Jassem
- Abstract
Abstract:
SCLC constitutes about 15% of all lung cancers and occurs almost exclusively in smokers. Clinical features of SCLC include rapid growth and the early development of metastases. The vast majority of SCLC patients present with either locally advanced or metastatic disease. Owing to high metastatic potential of SCLC, a careful mediastinum staging, along with brain, bone and abdomen imaging, is indicated to identify patients amenable to curative approaches. Traditionally, SCLC patients have been divided into limited stage (LS), defined as tumor confined to the ipsilateral hemithorax and regional nodes, and extensive stage disease, defined as tumor beyond these boundaries. In 2007, the International Association for the Study of Lung Cancer (IASLC) recommended TNM staging for SCLC similarly to NSCLC, and this change was incorporated in 2010 into the AJCC/UICC 7[th] edition. Chemotherapy remains the mainstay of treatment in all SCLC patients. The current standard of care for LS-SCLC patients includes 4 cycles of chemotherapy consisting of cisplatin and etoposide. Carpoplatin can be substituted to cisplatin if contraindicated or in patients with poor tolerance to cisplatin. In LS-SCLC patients chemotherapy should be accompanied by thoracic radiotherapy. The metaanalysis of randomized studies comparing chemotherapy with or without radiotherapy showed apparently increased local tumor control and increased overall survival in favor of combined treatment (relative risk of death 0.86 [95% CI, 0.78 to 0.94; p=0.001], corresponding to a an absolute benefit of 5.4% at 3 years), at the expense of slightly increased early toxicity.[1] Radiotherapy concurrent to chemotherapy is preferred to sequential approach, despite higher incidence of severe pneumonitis and oesophagitis.[2 ]Early introduction of radiotherapy (with 1 or 2 cycle of chemotherapy) may increase treatment outcome.[3 ]A critical factor in chemoradiation for LS-SCLC is a short time from to the start of any therapy to the end of radiotherapy.[4] The optimal dose of radiotherapy for patients with LS-SCLC remains a matter of debate. Hyperfractionated radiotherapy including 45 Gy in 3 weeks (1.5 Gy twice daily) has been shown to be superior to 45 Gy in 5 weeks (1.8 Gy daily),[5 ]and is currently used as an alternative to standard regimens (60-70 Gy, 2 Gy daily). The volume of thoracic radiotherapy should be defined based on CT or (whenever possible) PET/CT scan, obtained within 4 weeks before treatment, and on CT scan obtained in the therapeutic position at the time of radiotherapy planning. The target to be irradiated should include all gross disease present at the time of radiation planning (postchemotherapy volume), and all nodal regions involved at the time of initial diagnosis (prechemotherapy volume). The use of traditional larger fields including also elective nodal sites is currently not recommended. With more effective therapy of LS-SCLC and a decreased risk of a thoracic relapse, the brain has emerged as one of the main sites of relapse, with a cumulative incidence at 2 years higher than 50%. Owing to limited penetration of cytotoxic drugs through the blood-brain barrier, the brain is considered a pharmacologic sanctuary site. This observation led to the development of prophylactic cranial irradiation (PCI) aiming at prevention of clinically overt brain metastases. Several randomized trials showed that PCI in patients who achieved a complete remission with chemotherapy significantly decreases the incidence of brain metastasis. The metaanalysis of these studies also demonstrated a small but significant overall survival improvement with PCI (the relative risk of death in the PCI vs. non-PCI group was 0.84 [95% CI: 0.73–0.97, p=0.01]), corresponding to a 5.4% increase in the rate of survival at 3 years.[6 ]Based on these results, PCI is currently recommended as a routine part of management in LS-SCLC patients who achieve a response to initial therapy. The dose of PCI has long been a matter of debate. Results of the randomized study comparing a standard (25 Gy in 10 fractions) vs. higher dose (36 Gy in 18 fractions) of PCI in LS-SCLC showed no significant difference in the 2-year incidence of brain metastases between two groups, and a lower overall survival in the higher-dose group.[7] In consequence, 25 Gy in 10 fractions remains the standard of care in LS-SCLC. In summary, current management in patients with LD-SCLC and good performance status includes the combination of cisplatin and etoposide, along with early thoracic radiotherapy (45 Gy in 3 weeks, 2 fractions daily, or 60-70 Gy in 6-7 weeks, one fraction daily), followed by PCI (25 Gy in 10 fractions) in those who achieved response to initial chemotherapy. References 1. Pignon JP, Arriagada R, Ihde DC, et al. A meta-analysis of thoracic radiotherapy for small-cell lung cancer. N Engl J Med 1992;327:1618-24. 2. Takada M, Fukuoka M, Kawahara M, et al. Phase III study of concurrent versus sequential thoracic radiotherapy in combination with cisplatin and etoposide for limited-stage small-cell lung cancer: results of the Japan Clinical Oncology Group Study 9104. J Clin Oncol 2004;22:4837-45. 3. Pijls-Johannesma M, De Ruysscher D, Vansteenkiste J, et al. Timing of chest radiotherapy in patients with limited stage small cell lung cancer: A systematic review and meta-analysis of randomised controlled trials. Cancer Treat Rev 2007: 33: 461–473 4. De Ruysscher D, Pijls-Johannesma M, Bentzen SM, et al. Time between the first day of chemotherapy and the last day of chest radiation is the most important predictor of survival in limited-disease small-cell lung cancer. J Clin Oncol 2006;24:1057-63. 5. Turrisi AT 3rd, Kim K, Blum R, et al. Twice-daily compared with once-daily thoracic radiotherapy in limited small-cell lung cancer treated concurrently with cisplatin and etoposide. N Engl J Med 1999;340:265-71. 6. Aupérin A, Arriagada R, Pignon JP, et al. Prophylactic cranial irradiation for patients with small-cell lung cancer in complete remission. Prophylactic Cranial Irradiation Overview Collaborative Group. N Engl J Med 1999;341:476-84. 7. Le Péchoux C, Dunant A, Senan S, et al. Standard-dose versus higher-dose prophylactic cranial irradiation (PCI) in patients with limited-stage small-cell lung cancer in complete remission after chemotherapy and thoracic radiotherapy (PCI 99-01, EORTC 22003-08004, RTOG 0212, and IFCT 99-01): a randomised clinical trial. Lancet Oncol 2009;10:467-74. The author declares no relevant conflict of interest.
-
+
ORAL 08 - Smoking Cessation, Tobacco Control and Lung Cancer (ID 94)
- Event: WCLC 2015
- Type: Oral Session
- Track: Prevention and Tobacco Control
- Presentations: 1
-
+
ORAL08.07 - Primary Prevention of Lung Cancer in Poland - Successes and Challenges (ID 2398)
11:50 - 12:01 | Author(s): J. Jassem
- Abstract
- Presentation
Background:
In the 1990s Poland was among countries with the highest tobacco exposure and catastrophically high lung cancer mortality. Within the past two decades this situation has dramatically improved as a result of comprehensive national tobacco-control programs. We present the current tobacco exposure and
Methods:
Data on trends in cigarette consumption, smoking rates and lung cancer mortality were analyzed using the per capita sale of manufactured cigarettes, results of nation-wide questionnaire surveys conducted in adult (15+) population, and standardized mortality rates from lung cancer, respectively.
Results:
Between 1995 and 2013 annual cigarette sales in Poland decreased from 101 billion to 47 billion. The proportion of smokers among men dropped from 65% in 1980 to 28% in 2013, and among women from 32% to 18%, respectively. If this trend continues, the cigarette consumption per capita in Poland in 2040 will fall to the level of the 1920s. The age-standardized mortality rates per 100,000 from lung cancer in men declined from 71.1 in 1990 to 56.2 in 2010. The pattern of changes in lung cancer mortality among young Polish men became similar to that observed two decades earlier in the Unites States (Figure). However, Poland is still facing several challenges. Between 2003 and 2012 tobacco production in Poland increased by 90%, of which around two-thirds is exported. There is a persistently high proportion of smoking women, with almost a gender parity in the 35-44 age bracket (34% and 32% in women and men, respectively). Polish middle-aged women belong to the most common smokers in the European Union. The mortality rates from lung cancer among women are still on the rise. Since 2010 lung cancer has become the leading cause of death among women in Poland. Today, differences in smoking rates and lung cancer mortality are mainly generated by education and financial status, and not by gender. Figure 1
Conclusion:
There is an apparent need for further tobacco control efforts in Poland, including enforcement of the effective legislative measures (pictorial health warnings, plain cigarette packages, banning the sale of aromatic and ‘slim’ cigarettes) and implementation of tailored population-based preventive programs for women and socially unprivileged populations.
Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.
