| Literature DB >> 34127738 |
Clara Domingo-Sabugo1, Elizabeth Starren1, Saffron A G Willis-Owen1, Liming Liang2,3, Maxim B Freidin1,4, Madeleine Arseneault5, Youming Zhang1, Shir Kiong Lu1, Sanjay Popat6,7, Eric Lim8, Andrew G Nicholson1,9, Yasser Riazalhosseini5,10, Mark Lathrop5, William O C Cookson11, Miriam F Moffatt12.
Abstract
Lung cancer is the most frequent cause of cancer death worldwide. It affects more men than women, and men generally have worse survival outcomes. We compared gene co-expression networks in affected and unaffected lung tissue from 126 consecutive patients with Stage IA-IV lung cancer undergoing surgery with curative intent. We observed marked degradation of a sex-associated transcription network in tumour tissue. This disturbance, detected in 27.7% of male tumours in the discovery dataset and 27.3% of male tumours in a further 123-sample replication dataset, was coincident with partial losses of the Y chromosome and extensive autosomal DNA hypomethylation. Central to this network was the epigenetic modifier and regulator of sexually dimorphic gene expression, KDM5D. After accounting for prognostic and epidemiological covariates including stage and histology, male patients with tumour KDM5D deficiency showed a significantly increased risk of death (Hazard Ratio [HR] 3.80, 95% CI 1.40-10.3, P = 0.009). KDM5D deficiency was confirmed as a negative prognostic indicator in a further 1100 male lung tumours (HR 1.67, 95% CI 1.4-2.0, P = 1.2 × 10-10). Our findings identify tumour deficiency of KDM5D as a prognostic marker and credible mechanism underlying sex disparity in lung cancer.Entities:
Year: 2021 PMID: 34127738 DOI: 10.1038/s41598-021-91907-8
Source DB: PubMed Journal: Sci Rep ISSN: 2045-2322 Impact factor: 4.379