cancer and infectious disease

There could be much to learn from the field of infectious diseases when it comes to the treatment of cancer.

That is the perspective of a group of scientists from the University of California, Berkeley, in an article published in Science Immunology.

The researchers suggest that cancer could be thought of as a chronic infectious disease. They say that the “foreign-ness” of tumor cells is similar to “invader” signals caused by infectious diseases that the immune system can recognize and fight.

An understanding of the shared immunological processes, the researchers say, could assist in the improvement of existing cancer immunotherapies as well as facilitating the development of new treatments that can be used in both the fields of infectious disease and cancer.

David Raulet, Ph.D., Esther and Wendy Schekman Chair in basic cancer biology, professor of immunology and pathogenesis at U.C. Berkeley, and co-author of the article, told Healthline collaboration between the fields of cancer research and infectious disease research is essential for progress in both areas.

“We often hear the complaint that researchers live in their little boxes and don’t benefit sufficiently from the perspectives of other scientists. For far-flung fields that may be understandable, but it is troubling that cancer immunologists and infectious disease immunologists are quite isolated from each other for historical and cultural reasons,” Raulet said.

“The two fields are dramatically intertwined … and have much to learn from each other. More interactiveness is likely to fuel major strides in both fields,” he added.

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Understanding the immune system

An immune response to infections depends on two factors.

The first is that the pathogen (a bacterium, virus, or microorganism that can cause disease) is foreign to the host, and the second being that the pathogen displays features that mark it as dangerous.

Raulet explains that until recently, it was not well established that cancer met either criteria.

However, it has become apparent that cancer cells are also foreign and, like a pathogen with features marked as dangerous, tumors mimic features of infection and cause inflammation.

Put another way, cancer cells can induce immune responses just as infectious diseases do.

In both the cases of tumors and infections, Raulet says, the immune cells are inhibited and rendered ineffective.

“The similarities are significant because it means that potentially protective immune responses are ongoing but inhibited. And that means that if the inhibitory interaction can be blocked, the protective immune response may be restored,” Raulet said.

This is how a class of immunotherapy drugs, called checkpoint blockers, was developed. The drugs work by blocking the inhibitory interaction and restoring the immune response.

Checkpoint blockers were first shown to be effective in mice with persistent infections. Then, the therapy was tried on animals with cancer.

From there, the drugs were put into clinical trials and were successful.

“The drugs are FDA approved and have shown remarkable long-term remissions, possibly cures, in an appreciable fraction of patients with various cancers that were previously incurable,” Raulet said.

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Spurring new treatments

Checkpoint blockers are just some of the cancer therapies that came about due to the study of infectious diseases.

Raulet says the success of the treatments can benefit both fields.

“The remarkable success of these therapies has spurred greater efforts to apply similar approaches to infections. So the success of cancer therapies has certainly provided motivation for similar approaches in infections,” he said.

Another area the researchers say has an “obvious overlap” between infectious disease and cancer is in the development of vaccines.

Most of the vaccines for infectious disease are prophylactic, in which healthy people are vaccinated to prevent an infection. In cancer treatments, however, most are therapeutic and are received by patients after a diagnosis.

“To date, prophylactic vaccines to prevent cancer are limited to instances where tumors are caused by pathogens and the vaccine targets the pathogen,” the authors write in the article.

“Important examples are the HPV and hepatitis B virus vaccines, which strongly reduce the risk of cervical cancer and hepatocellular carcinoma, respectively. Prophylactic vaccines against cancers that are not pathogen-induced remain an ambitious goal.”

Raulet says it will likely be a long time before such a vaccine is developed.

“There are many challenges, both scientific and societal. But it is a worthy undertaking, and would have enormous societal impact. I believe we should pursue it,” he said.

Even so, Raulet and his co-authors hope that coordination between scientists in both fields will lead to therapies that may be “double-dipped” and facilitate advancement in the treatment of both infectious diseases and cancer.

“One of the problems with immunotherapy approaches is toxicity. The very responses that cure us in the long term may, and often do, make us sick in the short term. Efforts to better counter these toxic effects without blunting the efficacy of the treatments will be critical going forward,” he said.

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