An enzyme that protects human cells from viruses may contribute to cancer development. Source: Cornell University.
In the study, researchers used a bladder cancer cell model to examine the role of the enzyme APOBEC3G in the progression of the disease. They found that APOBEC3G significantly increased the number of mutations in tumor cells, expanded the genetic diversity of the tumor, and accelerated lethal outcomes. The APOBEC3 family can induce RNA or DNA mutations by chemically altering the cytosine nucleotide. Normally, this enzyme fights retroviruses such as HIV by interfering with viral replication, which it achieves by mutating cytosines in viral genetic material. Source: Cornell University.
There are several safeguards in the body designed to prevent damage to its own DNA. Yet experiments showed these mechanisms are not reliably protective. In the study, scientists modified animals to produce human APOBEC3G and then exposed them to a bladder cancer–promoting chemical that simulates cigarette smoke carcinogens. Source: Cornell University.
The results revealed a striking difference. Animals expressing APOBEC3G had a much higher likelihood of developing this cancer type, with 76 percent affected compared with 53 percent in mice that did not produce APOBEC3G. After 30 days of observation, nearly one third of the APOBEC3G-expressing mice died from cancer, while all members of the control group survived. Source: Cornell University.
These findings lead the authors to propose that blocking the action of APOBEC3G could lay the groundwork for a new approach to anticancer therapy. Though the work centers on bladder cancer, the implications resonate for broader cancer research and treatment strategies in North America, including the United States and Canada. Researchers emphasize that understanding how APOBEC3G controls mutation rates in tumor cells may guide the development of targeted interventions that reduce genetic diversity in cancers and slow disease progression. Source: Cornell University.
For readers in North America, these insights underscore the delicate balance between innate antiviral defenses and potential risks when those defenses interact with cancer pathways. Ongoing investigations aim to translate this knowledge into therapies that minimize collateral genetic changes in healthy tissue while targeting malignant cells. The evolving science invites clinicians and patients to watch for advances that could improve prognosis in bladder cancer and related cancers across the United States and Canada. Source: Cornell University.