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R.J. Hopkins
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MINI 23 - Lung Cancer Risk: Genetic Susceptibility and Airway Biology (ID 135)
- Event: WCLC 2015
- Type: Mini Oral
- Track: Screening and Early Detection
- Presentations: 1
- Moderators:P.E. Postmus, R. Young
- Coordinates: 9/08/2015, 16:45 - 18:15, 401-404
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MINI23.02 - COPD Severity by GOLD Status and Lung Cancer Risk: Results from a Large Prospective Screening Study (NLST-ACRIN Cohort Analysis, N=18, 714) (ID 865)
16:45 - 18:15 | Author(s): R.J. Hopkins
- Abstract
Background:
Epidemiological studies consistently show that chronic obstructive pulmonary disease (COPD) is associated with an increased risk of lung cancer among smokers. However, debate exists as to whether there is a linear relationship between the severity of COPD and risk of lung cancer. The National Lung Screening Study (NLST) and it’s sub-study by the American College of Radiology and Imaging Network (ACRIN), provides the means to re-examine these findings. We examined the effect of spirometry-defined COPD (according to GOLD status at baseline), on the risk of lung cancer in the NLST-ACRIN cohort (according to lung cancer incidence), in a large prospective lung cancer screening study of high risk smokers.
Methods:
In the NLST-ACRIN cohort of 18,475 screening participants eligible for the NLST, 6,436 screening participants had COPD (35%) according to baseline pre-bronchodilator spirometry and were followed for a mean of 6.4 years. From this group, 401 lung cancer cases were identified. The 6,436 screening participants with COPD were sub-grouped according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) stages 1 (N=1607), 2 (N=3528), 3 (N=1083) and 4 (211). Lung cancer incidence at the end of follow-up was compared between the GOLD subgroups and those with normal spirometry (N=12,039).
Results:
Compared to those with normal spirometry, where the lung cancer incident rate was 4.63/1000 person years, the lung cancer incident rate was 7.58/1000 person years for GOLD 1, 9.43/1000 person years for GOLD 2, 12.7/1000 person years for GOLD 3 and 15.55/1000 person years for GOLD 4 (all P<0.0001). The lung cancer histology was significantly different, with more squamous and non-small cell cancers in those with COPD but more adenocarcinoma and Bronchoalveolar carcinoma in those with normal lung function (P<0.004). Figure 1
Conclusion:
In a large prospective study of unselected high risk smokers with and without COPD, we report a strong linear association between increasing severity of COPD and increasing lung cancer risk (incidence). This suggests that the risk of lung cancer is greatest in those with the most severe COPD and 3-4 fold greater than those with normal lung function. We also report that lung cancers of more aggressive histology were more common in those with COPD. Funding This study was funded by a grant from Johnson and Johnson and grants U01-CA-80098 and U01-CA-79778 to the American College of Radiology Imaging Network
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P1.06 - Poster Session/ Screening and Early Detection (ID 218)
- Event: WCLC 2015
- Type: Poster
- Track: Screening and Early Detection
- Presentations: 2
- Moderators:
- Coordinates: 9/07/2015, 09:30 - 17:00, Exhibit Hall (Hall B+C)
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P1.06-003 - Low-Dose CT Lung Cancer Screening in the Community: A Prospective Cohort Study Incorporating a Gene-Based Lung Cancer Risk Test (ID 879)
09:30 - 17:00 | Author(s): R.J. Hopkins
- Abstract
Background:
Following the publication of the National Lung Screening Trial (NLST) results in 2011, CT screening for lung cancer is now widely recommended in the US. However concerns remain with regards to patient selection according to risk level and overdiagnosis.Moreover adherence outside screening trials is typically about 50-60% and has been shown to be highly dependent on an individual's risk perception. This feasibility study explores the relevance of gene-based data on lung cancer risk assessment and adherence to screening, in a pilot screening program.
Methods:
This feasibility study was initiated in 2010 prior to NLST results being published. Following local media-based advertising, 157 current or former smokers (>50 years old with ≥20 pack year history), volunteered for lung cancer risk assessment and CT screening (using the IELCAP protocol). Participants were followed up for a mean of 2.4 years.At baseline CT screening, participants were assigned their lung cancer risk category according to a published and prospectively validated gene-based risk algorithm. This algorithm combines clinical risk variables with risk genotypes, derived from analysis of 20 risk single nucleotide polymorphisms (SNPS), to derive a composite lung cancer risk score categorised as moderate, high or very high.
Results:
SNP genotype results contributed to overall lung cancer risk in 88% of participants compared to the contribution from age = 68%, family history of lung cancer = 29% and self reported chronic obstructive pulmonary disease =15%. The SNP genotype results were the sole basis of risk in 18% of participants and contributed to risk in a further 70% of participants (total 88%). Adding SNP scores to the clinical risk score re-assigned screening participants into different risk categories in 28% (44/157) of participants (Figure 1). Importantly, timely adherence to the CT screening protocol was two-fold greater in those with a very high risk score compared to the high and moderate risk categories (71% vs 52% vs 52% respectively, OR =2.3, P<0.05). Figure 1
Conclusion:
In this feasibility study of a pilot community-based CT screening program we found gene-based risk assessment was of interest to all screening volunteers. As part of risk assessment, personalised SNP data made the greatest contribution to overall assignment of lung cancer risk in association with established clinical variables and significantly improved screening adherence. We conclude that gene-based risk stratification helps assign lung cancer risk and appears to improve adherence to screening.
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P1.06-019 - A Comparison of Demographic Risk Variables for Lung Cancer in New Zealand Europeans and Maori: Are Maori More Susceptible to the Effects of Smoking? (ID 867)
09:30 - 17:00 | Author(s): R.J. Hopkins
- Abstract
Background:
Lung Cancer is the leading cause of cancer death among New Zealand (NZ) Maori. Over the past twenty years lung cancer incidence has decreased in New Zealand for non-Maori but has increased for Maori, and is recognised to be the highest in the world of any ethnic group. Nationally, the incidence of lung cancer in Maori is 3.5 times higher than that in New Zealand Europeans, and lung cancer mortality in Maori males and females respectively, is 2.4 and 4.2 times higher than NZ Europeans. Maori have a higher incidence of lung cancer than countries with similar smoking rates. This suggests that there are additional factors other than smoking that predispose Maori to this disease. In the current study demographic and the well-established clinical risk variables for lung cancer were compared between New Zealand Maori and Europeans residing in the greater Auckland region and who were diagnosed between January 2004-January 2015.
Methods:
A retrospective review of patient clinical notes for those identified as being of NZ Maori ethnicity who were diagnosed with lung cancer (n=473) between January 2004 and January 2015 and treated within the greater Auckland region. Data extracted included histological type, smoking history, spirometry and basic demographics. This data was then compared with an established cohort of NZ European patients n= 417, with similar recruitment criteria over the period 2004-2008.
Results:
Despite comparable smoking exposure histories, NZ Maori patients were diagnosed on average 6 years younger than NZ European lung cancer patients (P<0.0001). At diagnosis, current smoking rate was 2 fold greater in NZ Maori compared to NZ Europeans (69% vs 36%, P<0.0001). Although NZ Maori patients had similar rates of COPD (≈64%), they had a trend towards less GOLD 1 (mild stage disease, P=0.08) and significantly greater airflow obstruction (worse COPD, FEV~1~%predicted 64% vs 73% in NZ Europeans, P<0.001). At lower smoking exposure (≤10 pk yrs), COPD rates in Maori with lung cancer were 2 fold greater than in NZ Europeans (64% vs 32% respectively, P<0.05). NZ Maori lung cancer patients had a lower prevalence of adenocarcinoma than in NZ Europeans (32% vs 43%, P=0.002) and a higher proportion of more aggressive lung cancer subtypes (squamous, non-small cell and small cell cancers) than NZ Europeans (61% vs 52%, P<0.0007).
Conclusion:
These results show that lung cancer in NZ Maori is associated with younger age at diagnosis, worse lung function and more aggressive histological subtypes compared to NZ Europeans. These results suggest that NZ Maori may have a greater inherent susceptibility to lung cancer compared to NZ Europeans. This greater susceptibility to lung cancer in Maori, along with socio-cultural factors, may contribute to their considerably greater mortality. These results suggest that for the future management of lung cancer, prevention measures (such as smoking cessation and tobacco control), risk assessment (such as lung function testing) and early diagnostic approaches (such as computed tomography screening) should be prioritised in high risk groups, particularly those with NZ Maori ancestry.
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P3.06 - Poster Session/ Screening and Early Detection (ID 220)
- Event: WCLC 2015
- Type: Poster
- Track: Screening and Early Detection
- Presentations: 1
- Moderators:
- Coordinates: 9/09/2015, 09:30 - 17:00, Exhibit Hall (Hall B+C)
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P3.06-002 - Favourable Stage-Shift Limited to Screening Participants with COPD in a Biomarker Sub-Study of the National Lung Screening Trial (NLST) (ID 873)
09:30 - 17:00 | Author(s): R.J. Hopkins
- Abstract
Background:
Based on a 20% reduction in lung cancer deaths in participants of the National Lung Screening Trial (NLST), CT screening for lung cancer is now widely recommended in the US. However concerns remain regarding the cost-benefits of screening due to overall low detection rates, over-diagnosis and high false-positive rates. Using the spirometric data available from the ACRIN-biomarker sub-study of the NLST (n=18,714), we examined the effect of Chronic Obstrucitve Pulmonary Disease (COPD) status on lung cancer detection in the NLST screening participants. Specifically we compared lung cancer incidence, histology and stage shift in those with and without COPD based on baseline pre-bronchodilator spirometry.
Methods:
Baseline spirometry results were available for 18,475 (99%) of the total cohort of 18,714, (6,436 with COPD and 12,039 with no COPD). Spirometry results were available for 758 (99%) of the 768 histology-confirmed lung cancer cases diagnosed over the 7 year follow-up period. After lung cancer cases were sub-grouped by spirometry-defined COPD (GOLD 1-4, n=401) and no baseline COPD (n=357) it was possible to compare the number of cancers, histology and stage according to screening arm. Differences in lung cancer incidence rates were compared by incident rate ratios, while prevalence, histology and stage shift, were compared by chi-square frequency tables.
Results:
In this NLST-ACRIN Biomarker sub-study, we found the demographic variables were comparable to those from the full NLST study. Regardless of screening interval, we found the lung cancer incidence was 2 fold greater in those with COPD compared to no COPD (P<0.0001). In those with COPD, we found a signficant reduction in adenocarcinomas and bronchioloalveolar carcinomas. After stratification by COPD status, when comparing CT versus CXR screening arms, we found no excess lung cancers and comparable lung cancer histology. However, a clinically significant stage shift favouring increased early stage (+17) and reduced late stage cancers (-23) was found (P=0.05). In contrast, in cancer cases with no COPD, we found an 18% excess of lung cancers in the CT arm (+29) which were of a BAC/AC histology. After correction for this overdiagnosis from these excess cancers, the stage shift no longer favoured early stage over late stage. Figure 1
Conclusion:
These data suggest that in those with COPD at baseline, CT screening (vs CXR) was associated with no excess cancers, no histology shift but a clinically significant stage shift favouring early over late stage cancers. In those with no COPD, CT was associated with excess cancers and a marginal stage shift.
