| Literature DB >> 33377150 |
Shuang Qiu1, Zheng An1, Renbo Tan1, Ping-An He2, Jingjing Jing3, Hongxia Li3, Shuang Wu4, Ying Xu5.
Abstract
Data from the SEER reports reveal that the occurrence rate of a cancer type generally follows a unimodal distribution over age, peaking at an age that is cancer-type specific and ranges from 30+ through 70+. Previous studies attribute such bell-shaped distributions to the reduced proliferative potential in senior years but fail to explain why some cancers have their occurrence peak at 30+ or 40+. We present a computational model to offer a new explanation to such distributions. The model uses two factors to explain the observed age-dependent cancer occurrence rates: cancer risk of an organ and the availability level of the growth signals in circulation needed by a cancer type, with the former increasing and the latter decreasing with age. Regression analyses were conducted of known occurrence rates against such factors for triple negative breast cancer, testicular cancer and cervical cancer; and all achieved highly tight fitting results, which were also consistent with clinical, gene-expression and cancer-drug data. These reveal a fundamentally important relationship: while cancer is driven by endogenous stressors, it requires sufficient levels of exogenous growth signals to happen, hence suggesting the realistic possibility for treating cancer via cleaning out the growth signals in circulation needed by a cancer.Entities:
Keywords: cancer occurrence rate; cancer risk; cervical cancer; testicular cancer; triple negative breast cancer
Year: 2021 PMID: 33377150 PMCID: PMC8294564 DOI: 10.1093/bib/bbaa349
Source DB: PubMed Journal: Brief Bioinform ISSN: 1467-5463 Impact factor: 11.622