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According to the World Health Organization, approximately 240 million people worldwide are infected with the hepatitis B virus (HBV)
Recently, a study in "Nature-Communications" found that HBV quietly promotes the growth and survival of cancer cells.
The researchers obtained 296 hepatocellular carcinoma sample data from the sample database of the Whole Genome Pan-Cancer Analysis Project
The analysis results show that the integration of viral DNA is random and can occur on any chromosome
▲The gene of HBV may be integrated in any position (picture source: reference [2])
Many previous studies have found that mutations in the TERT gene are associated with increased risk of a variety of cancers.
Other oncogenes (gene coding region and vicinity) modified by HBV integration include KMT2B and CCNE1, which are located on chromosome 19q
In addition to direct gene insertion, HBV may also cause more serious gene loss of large fragments.
Further analysis found that this virus integration event basically appeared in the early stage of tumor development, and could even be traced back many years before the patient was diagnosed with hepatocellular carcinoma
This kind of telomere deletion often occurs in the process of HBV recombination.
▲Tumor suppressor genes may be damaged (picture source: reference [2])
In total, out of the 23 hepatocellular carcinoma samples with telomere deletion alone, about 244 genes listed as related to tumor suppression were missing or became loss-of-function genes
HBV, as one of the few viruses that can establish a connection with cancer, has been determined to cause large fragments of damage in the genome
Note: The original text has been deleted
Reference materials:
[1] Hepatitis B virus can trigger genetic changes in liver cells years before cancer diagnosis.
[2] Eva G.