de Magalhães has shown recently that most human genes have several papers in PubMed mentioning cancer, leading the author to suggest that every gene is associated with cancer, a conclusion that contradicts the widely held view that cancer is driven by a limited number of cancer genes, whereas the majority of genes are just bystanders in carcinogenesis. We have analyzed PubMed to decide whether publication metrics supports the distinction of bystander genes and cancer genes. The dynamics of publications on known cancer genes followed a similar pattern: seminal discoveries triggered a burst of cancer-related publications that validated and expanded the discovery, resulting in a rise both in the number and proportion of cancer-related publications on that gene. The dynamics of publications on bystander genes was markedly different. Although there is a slow but continuous time-dependent rise in the proportion of papers mentioning cancer, this phenomenon just reflects the increasing publication bias that favors cancer research. Despite this bias, the proportion of cancer papers on bystander genes remains low. Here, we show that the distinctive publication dynamics of cancer genes and bystander genes may be used for the identification of cancer genes.
Keywords: bystander gene; cancer gene; confirmation bias; funding bias; passenger gene; publication bias; tumor essential gene.