In a new study from the Perelman School of Medicine at the University of Pennsylvania, scientists noticed that patients whose HER2-positive breast cancer had recurred showed a much weaker T cell response than patients still in remission to HER2 (human epidermal growth factor receptor 2), a gene that is overexpressed and causes uncontrolled cell growth in 25 percent of breast cancers (BreastCancer.org). Their results were published in JAMA Oncology this week.
"The thinking is that the patient's anti-HER2 T cells somehow become exhausted and die or otherwise stop responding," said Brian J. Czerniecki, MD, PhD, and senior author of the study. "We're trying to determine the mechanism, but we already know that we can 'fill the tank' with vaccines to restore that specific responsivity to HER2."
Czerniecki’s “fill the tank” notion comes from revitalizing T cell ability to recruit killer lymphocytes to attack growing tumor cells with stimulatory vaccines. HER2-positive breast cancers are not the only abnormally growing cells to inhibit the immune system in order to evade detection or attack.
To test the ability of immune cells from cancer patients with recurrent HER2-positive breast cancer with the cells of patients still in remission, Czerniecki and his team observed in vivo the T cell response of 95 isolated immune cells when HER2 is injected. Results showed the recurrent cancer patients’ T cells “had only about a tenth of the anti-HER2 responsivity” compared to the T cells of patients whose cancer had not returned.
The team from the University of Pennsylvania is continuing studies on the change in immune response to HER2 over time as well as doing clinical trials with a HER2-targeted vaccine.
To learn more about how HER2 can promote cancer cell growth, watch the following video. Source: University of Pennsylvania