Immunotherapy Outcomes Prediction: Scientists Discover Methods for Anticipating Responses
In the world of cancer treatment, one of the latest weapons developed is immunotherapy. This innovative approach leverages the body's immune system to combat the deadly disease.
Unfortunately, not every person and cancer type responds positively to immunotherapy. Researchers are constantly striving to understand the underlying reasons for its success or failure.
Recently, a team from Johns Hopkins University made a significant breakthrough. They found a specific subset of mutations in cancer tumors that hint at how receptive they might be to immunotherapy. This finding could help doctors better choose immunotherapy patients and more accurately predict its effectiveness.
Their research was published in the journal Nature Medicine.
A brief overview of immunotherapy
Immunotherapy is a treatment that harnesses the body's immune system to fight disease. Typically, cancer cells develop mutations that allow them to hide from the immune system. Immunotherapy boosts the immune system's power, making it better at finding and destroying these cancer cells.
There are several types of immunotherapy, including checkpoint inhibitors, CAR-T cells, and vaccines.
The importance of mutations
Currently, doctors use the total number of mutations in a tumor, known as the Tumor Mutational Burden (TMB), to guess how well a tumor will respond to immunotherapy.
Dr. Valsamo Anagnostou, a senior author of the study and an associate professor of oncology at Johns Hopkins, explains, "Tumor mutational burden is the number of changes in a tumor's genetic material or DNA sequence. A large number of mutations clearly distinguishes cancer cells from normal cells, making them more visible to the immune system and improving the chances of longer clinical outcomes with immunotherapy."
Persistent mutations and their role
In this study, Anagnostou and her team discovered a specific subset of persistent mutations within the overall TMB. These mutations stay constant as cancer evolves, keeping the tumor visible to the immune system and enhancing the body's ability to locate and eliminate it.
According to Anagnostou, "Persistent mutations are always present in cancer cells and may render the cancer cells continuously visible to the immune system, which leads to an immune response. This response is amplified with checkpoint inhibitors, enabling the immune system to continue eliminating cancer cells containing these persistent mutations over time, resulting in sustained immunologic tumor control and long survival."
Paving the way for the future
Dr. Kim Margolin, a medical oncologist, praised the study, saying, "The study demonstrates that the collaborative group has gone beyond the concept of tumor mutational burden and defined persistent mutations, loss of mutation-containing sequences, and the immune response in a new light."
In the future, scientists believe high-throughput, next-generation sequencing techniques will allow them to study patients' mutational spectrum, categorize patients by their likelihood of responding to immunotherapy, and predict the benefits of immunotherapy for disease-free patients.
Ultimately, these findings may help doctors tailor immunotherapy to specific mutational profiles, improve treatment efficacy, and save countless lives.
- For cancer patients seeking immunotherapy, the discovery of specific persistent mutations within their tumors could help doctors make more informed decisions, potentially enhancing the treatment's effectiveness.
- The science behind immunotherapy continues to evolve, with researchers now focusing on persistent mutations that stay constant as cancer evolves, making the cancer cells more visible to the immune system.
- In the future, medical-conditions such as cancer may be treated more accurately with immunotherapy, following advancements in health-and-wellness that allow doctors to analyze a patient's mutational spectrum and predict the benefits of immunotherapy for each individual based on their unique immune system response.