The doctors of the National Health Institutes have discovered a new cause of skin cancer, according to a case report published Wednesday at the New England Journal of Medicine.
The culprit is a type of human papilloma (HPV) that is found regularly on the skin. For a long time it is believed that he plays a role in the development of skin cancer, but it was not believed to be a direct cause.
Skin cancer is caused by DNA damage in skin cells. The most common source of that damage is the ultraviolet radiation of the sun. HPV can help DNA damaged by UV rays in cells and become cancerous. However, in the new case report, doctors found that the virus itself could cause cancerous injuries.
The discovery was made in a 34 -year -old woman with a weakened immune system; Experts said it is very unlikely that HPV can play the same role in causing skin cancer in a person with a healthy immune system.
“The virus was replicated in a somewhat uncontrolled way and ended up being integrated into the skin cells and once they did, they became cancerous,” said Dr. Andrea Lisco, head of section of the mucosa and cutaneous viral immunopathogenesis unit in the National Institute of Allergies and Infectious, part of the NIH. Lisco was the woman’s doctor and also the main author of the case report.
The woman had 4 3 -style cutaneous cell carcinoma spots, the second most common type of skin cancer, after melanoma, on her face, hands and legs. He underwent surgery to eliminate cancers and immunotherapy, but cancer returned. When Lisco and his team biopsy several of his new tumors, they discovered that women’s skin cancer was being driven by something they had not seen before: a HPV group called Beta VPV.
About 90% of people carry a Beta VPV strain. Usually, the virus lives in the skin and is not integrated into the DNA of skin cells.
“We shake hands and take those viruses, but if our immune systems are under control, we are fine,” Lisco said.
It is a different group of HPV strains, Alpha VPVs, which are linked to a variety of cancers. ALFA HPV live in mucus membranes and can be integrated into DNA, causing cancers of the cervix, anus, head and neck.
The woman in the case report had a genetic condition that weakened her T cells (an immune cell type), leaving her immunocompromised. This allowed Beta VPV to live in his skin to behave more like Alpha VPV, integrating his DNA into his skin cells and replicating not disturbed, turning the cancer cells.
“You don’t know how much a patient’s information can apply directly to the wide variety of patients,” said Dr. Anthony Oro, a dermatology professor at Stanford Medicine, who was not involved in the case.
However, “it suggests that, in case the immune system’s T -system arm is not doing their job, beta type HPV viruses could contribute to skin cancer, and perhaps also other types of cancers,” he said.
The patient needed a stem cell transplant, which replaced his defective T cells with T cells that could prevent HPV from replicating.
“We needed to give this patient a new new immune system,” Lisco said. It worked. Three years after transplantation, women’s skin cancer has not returned.
“It gives us good information on how HPV interaction and the immune system work,” said Dr. Anthony Rossi, a dermatologist and surgeon of Mohs in the Moan Kettering memorial center, who was not involved in the case of women either.
Doctors have long known that some beta vpv causes skin changes, such as warts in the hands and feet.
“HPV can integrate and cause changes in the cell cycle, especially in people with suppressed immune systems,” Rossi said. “What was novel about this is that they discovered that it was a beta VPV that was integrated into the DNA.”
Other researchers have speculated that this was a possibility based on mice studies, but the new report shows that it can occur in humans. It is still unknown how many people could be at risk.
“This is just a patient, and they have this unique situation of an immune condition that allows Beta VPV to replicate without control,” Oro said.
Other biopsies of scamming skin cancers have not detected HPV, which means that not all cases are caused by viruses. Lisco said that the original notion, that HPV contributes passively to the carcinoma of squamous cutaneous cells by helping skin cells to damage skin cells, but does not actively help cancer, remains the probable explanation for many people.
For them, “protection against UV rays would be prevention,” Lisco said, with sunscreen and covering his skin from the sun, adding that immunocompromised people must be monitored more closely. People with weakened immune systems have up to 100 times more likely to develop squamous cell carcinoma.
The Gardasil HPV vaccine protects against nine strains of Alpha VPV and it has been shown that the rates of cervical cancers and head and neck decrease. It is not clear how much cross protection, if any, it provides the vaccine against other HPV strains, including Beta VPV.
“Even if this strain is not in the vaccine, there is some theory that there is a cross conversation between HPV strains,” Rossi said.
Most people will get HPV in their lives. Until now, scientists have identified around 200 unique virus strains. Alpha-HPV, with its well-established links with cancer, so far it has been the main research topic.
“This suggests that this other side of the family could also be important in situations in which our immune system is not doing its job,” Oro said.
