Background and aim Lung cancer is increasingly affecting women. The aim of this study was to identify sex-specific trends in lung cancer incidence and survival. Methods Complete national data on 40 118 cases from the Cancer Registry of Norway sampled from 1988 to 2007 are presented, with incidence rates, 1-and 5-year relative survival in 5 year intervals and multivariate HRs adjusted for covariates, each with 95% CIs. Results Lung cancer incidence increased by 64%, with an age-adjusted annual average increase of 4.9% in women and 1.4% in men in this period. Relative survival was lower in men than in women in all time periods, and men had an increased risk of dying within 5 years of diagnosis compared with women (HR 1.14, 95% CI 1.11 to 1.17), adjusted for covariates. Adenocarcinoma is now the most frequent histological group in men and women, yet the risk of dying was higher in men in all histological subtypes except squamous cell carcinoma. A higher proportion of women than men were diagnosed with localised disease, and the risk of dying was significantly higher in men among all stages, most apparent in localised disease (HR 1.25, 95% CI 1.18 to 1.33). Conclusion The findings highlight important characteristics of the lung cancer epidemic; despite a rising incidence of female lung cancer cases, women are diagnosed with less advanced disease than men; when adjusted for covariates, men have an increased risk of excess death at 5 years compared with women, irrespective of stage, age, period of diagnosis and selected histological subgroups.

Background: TP53 mutations are among the most common mutations found in lung cancers, identified as an independent prognostic factor in many types of cancers. The purpose of this study was to investigate the frequency and prognostic impact of TP53 mutations in never-smokers and in different histological subtypes of lung cancer.Methods: We analyzed tumor tissue from 394 non-small cell carcinomas including adenocarcinomas (n = 229), squamous cell carcinomas (n = 112), large cell carcinomas (n = 30), and others (n = 23) for mutations in TP53 by the use of Sanger sequencing (n = 394) and next generation sequencing (n = 100).Results: TP53 mutations were identified in 47.2% of the samples, with the highest frequency (65%) of mutations among squamous cell carcinomas. Among never-smokers, 36% carried a TP53 mutation, identified as a significant independent negative prognostic factor in this subgroup. For large cell carcinomas, a significantly prolonged progression free survival was found for those carrying a TP53 mutation. In addition, the frequency of frameshift mutations was doubled in squamous cell carcinomas (20.3%) compared to adenocarcinomas (9.1%).Conclusion: TP53 mutation patterns differ between the histological subgroups of lung cancers, and are also influenced by smoking history. This indicates that the histological subtypes in lung cancer are genetically different, and that smoking-induced TP53 mutations may have a different biological impact than TP53 mutations occurring in never-smokers.

The frequency of EGFR mutations is lower in our cohort than among Asian lung cancer patients and present in both men and women and smokers and never-smokers. However, the frequency is significantly higher among women and never-smokers and among patients with adenocarcinomas.

Background. Unlike cervical, anogenital and oropharyngeal cancers, where high-risk human papillomavirus (hrHPV) has long been known to play a major role, a causative link between HPV and lung cancer has been investigated for decades with discrepant results. Methods. Lung cancer patients eligible for surgical treatment were tested for the presence of HPV-DNA in excised, fresh frozen lung tumor tissue. Patients that tested positive were further examined for the presence of HPV-DNA in adjacent normal lung parenchyma. HPV detection and genotyping was performed using a polymerase chain reaction (PCR)-based approach and allowed the typing of 13 " high-risk " -HPV-types and 2 " low-risk " -HPV-types. Results. Of the 334 tumor-DNA samples tested, 13 (3.9%) showed presence of HPV-DNA, of which 12 were of a high-risk HPV type (16,33, 66). In those tested positive, HPV-DNA was not found in adjacent normal lung tissue. No correlation with smoking or EGFR/KRAS mutation status was seen, and only one of 84 squamous cell carcinomas was HPV-positive. Conclusion. We conclude that HPV is rarely associated with lung cancer in a Northern European population and in those tested positive, more functional studies are required to determine the role HPV plays in lung cancer oncogenesis.

The proportion of carcinomas NOS has increased to 19% of all lung cancer cases. This histological entity is associated with older age and poor survival.