Can differences in genomic immune system signatures detect lung cancer before it takes hold?
There’s aspirin for colorectal cancer and statins for cardiovascular disease, but for the leading cause of cancer deaths globally — lung cancer — there’s no tool in the doctor’s arsenal to arrest or prevent the fatal disease (apart from smoking abstinence). But a new study suggests genomic immune system disparities may play a crucial role in the development of lung cancer, setting the stage for fresh therapeutics that could arm the immune system to better fight cancerous cells from anchoring in the lungs.
Killing roughly 160,000 Americans annually, lung cancer has a higher death toll than colorectal, pancreatic, breast, and prostate cancer combined. This is partly due to the fact that it is typically only detected in its later stages, which makes treatment difficult and puts a cure out of contention.
Although lung cancer can occur in non-smokers — exposure to cigarette smoke creates a field of injury throughout the entire respiratory tract by inducing a variety of genomic alterations that can lead to an at-risk airway where premalignant lesions (PMLs) and lung cancers develop. So researchers from Boston University School of Medicine; University of California, Los Angeles; the Roswell Park Comprehensive Cancer Center and J&J’s Janssen unit conducted a study, evaluating, via biopsies, former and current cigarette smokers that presented these early pre-cancerous lesions in the airway and lungs over several years to check whether their lesions progressed toward lung cancer.
Their study, published in Nature Communications on Tuesday, found biological characteristics within the lesions that indicated a higher risk of progressing to lung cancer, and that the progressive lesions had a paucity of immune cells.
“(I)t shows that the presence or absence of immune cells in lung pre-cancerous lesions may provide critical information as to whether that lesion will progress towards invasive lung cancer,” said Avrum Spira, who serves as global head of J&J’s Lung Cancer Initiative and Alexander Graham Bell professor at Boston University, in a statement. “This information could one day underpin strategies to identify individuals who are incubating lung cancer and intercept the development of manifested invasive disease.”
In addition, the study indicated that changes in aggressive pre-cancerous lesions could be diagnosed by employing a flexible brush to amass cells from the airway through the catheter of a bronchoscope, versus the traditionally invasive lung or airway biopsy. This could culminate in the development of diagnostics for early-stage disease and identify patients who could benefit from medical intervention.
J&J has been taking steps to expand its offerings to manage lung cancer — one of the most lucrative pharmaceutical fields — from diagnosis to intervention. In February, the US drugmaker agreed to a $3.4 billion deal to buy Auris Health, a privately held developer of robotic tools for lung cancer to beef up its arsenal of surgical, interventional and diagnostic products.