Reproducibility of Major Diagnoses in a Binational Study of Lung Cancer in Uranium Miners and Atomic Bomb Survivors

1994 ◽  
Vol 101 (4) ◽  
pp. 478-482 ◽  
Author(s):  
Robert Keehn ◽  
Oscar Auerbach ◽  
Shigeru Nambu ◽  
Darryl Carter ◽  
Yukio Shimosato ◽  
...  
2021 ◽  
Vol 46 (3) ◽  
pp. 83-97
Author(s):  
Kazumasa Shimada ◽  
Michiaki Kai

Background: The lifetime risk of lung cancer incidence due to radiation for nonsmokers is overestimated because of the use of the average cancer baseline risk among a mixed population, including smokers. In recent years, the generalized multiplicative (GM)-excess relative risk (ERR) model has been developed in the life span study of atomic bomb survivors to consider the joint effect of radiation and smoking. Based on this background, this paper discusses the issues of radiation risk assessment considering smoking in two parts.Materials and Methods: In Part 1, we proposed a simple method of estimating the baseline risk for nonsmokers using current smoking data. We performed sensitivity analysis on baseline risk estimation to discuss the birth cohort effects. In Part 2, we applied the GM-ERR model for Japanese smokers to calculate lifetime attributable risk (LAR). We also performed a sensitivity analysis using other ERR models (e.g., simple additive (SA)-ERR model).Results and Discussion: In Part 1, the lifetime baseline risk from mixed population including smokers to nonsmokers decreased by 54% (44%–60%) for males and 24% (18%–29%) for females. In Part 2, comparison of LAR between SA- and GM-ERR models showed that if the radiation dose was ≤200 mGy or less, the difference between these ERR models was within the standard deviation of LAR due to the uncertainty of smoking information.Conclusion: The use of mixed population for baseline risk assessment overestimates the risk for lung cancer due to low-dose radiation exposure in Japanese males.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Lingling Li ◽  
Xinan Zhang ◽  
Tianhai Tian ◽  
Liuyong Pang

Abstract Genomic instability plays a significant role in lung cancer. Although substantial research has been conducted using both clinical and theoretical studies, it is still a hotly debated issue to whether genomic instability is necessary or whether genomic instability precedes oncogenes activation and tumor suppressor genes inactivation for lung cancer. In response to this issue, we come up with a mathematical model incorporating effects of genomic instability to investigate the genomic instability pathway of human lung cancer. The presented model are applied to match the incidence rate data of lung cancer from the Life Span Study cohort of the atomic bomb survivors in Nagasaki and Hiroshima and the Surveillance Epidemiology and End Results registry in the United States. Model results suggest that genomic instability is necessary in the tumorigenesis of lung cancer, and genomic instability has no significant impact on the net proliferation rate of cells by statistical criteria. By comparing the results of the LSS data to those of the SEER data, we conclude that the genomic instability pathway exhibits a sensitivity to radiation exposure, more intensive in male patients.


Sign in / Sign up

Export Citation Format

Share Document