HPV-Cancer Relationship Could Uncover Treatment


An oncoprotein produced by the human papillomavirus results in cells that proliferate and do not die.

A new study discovered the underlying mechanisms of how human papillomavirus (HPV) can cause various types of cancer. The authors of the study published by Oncotarget suggest that a better understanding of the link could lead to novel treatment options for these cancers.

HPV is responsible for a majority of cervical cancers and a large number of head and neck and anal cancers, which is why current guidelines advise parents to vaccinate their children against the virus. The CDC recommends that children aged 11 to 12 years receive 2 doses of the HPV vaccine to protect against HPV-linked cancers. While most children receive the first dose, many do not receive the second.

Due to not completing the vaccine series or not starting it, many are at risk of contracting HPV and related cancers. Currently, treatment options for HPV-related cancers include surgery and non-specific chemotherapy, according to the authors.

In the study, the investigators discovered that E6, an oncoprotein created by HPV, communicates with cells to ensure that infected cells cannot die. Cancer results when these imperishable cells proliferate, according to the study.

“There is no targeted treatment now for these cancers since German virologist Harald zur Hausen, PhD, discovered in 1983 that HPV can cause cervical cancer,” said lead author, Xuefeng Liu, MD. “Recently, the numbers of HPV-linked head and neck cancers have increased in the US Now we have a chance to develop and test a very specific, potentially less toxic way to stop these cancers.”

Previously, the team of researchers discovered that the oncoprotein interferes with the p53 tumor suppressor protein to increase telomerase activity. This mechanism is used to lengthen the life of infected cells since telomerase allows a cell to multiply indefinitely.

The authors now discovered that E6 interacts with the myc protein, which is produced by the Myc gene that controls gene expression. These findings suggest that telomerase activity is contingent on E6-myc proteins binding, according to the study.

The authors hypothesize that by creating a small molecule that blocks E6 and myc from binding, it could inhibit the activation of telomerase to prevent cancer development.

The investigators are currently developing an investigational chemical to prevent the binding of E6 and Myc, according to the study.

“This small molecule would not be toxic to all normal cells or, importantly, to master stem cells, because myc would not be affected,” Dr Liu said. “It could be a unique treatment, targeted specifically to HPV cancers.”

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