MedImmune Scientists Publish New Findings in ‘American Journal of Respiratory and Critical Care Medicine’
The human body is an exquisitely interconnected ecosystem, one where even the slightest change can cause cascading effects in the way the body handles the progression and treatment of disease.
For example, there is ample evidence to show that certain diseases can increase the likelihood of a developing other conditions.
But what happens once a patient develops a second disease? Could the condition that made someone more susceptible also impact their response to treatment?
Or, even more surprisingly, could it actually make them more responsive to available treatments?
In the case of chronic obstructive pulmonary disease (COPD) and lung cancer, new research published by MedImmune scientists and their collaborators in the American Journal of Respiratory and Critical Care Medicine suggests it may do precisely that.
The COPD-Cancer Connection
Both COPD and lung cancer pose significant global health threats, due in large part to the rapidly increasing rates of smoking throughout the 20th century. Although each can lead to significant and even fatal complications in isolation, data has shown that patients with COPD have a high risk of also developing lung cancer.
The underlying connection between COPD and lung cancer is primarily due to the immune system’s strong involvement in the establishment of chronic inflammation in COPD, believed to promote the earliest stages of carcinogenesis through an increased expression of genes involved in cell proliferations and survival.
What’s more, once tumors have progressed to malignancy, COPD has shown to worsen the survival of patients with early stage lung cancer.
Identifying an Opportunity
So how could a condition that increases prevalence and worsens survival ever be leveraged in treatment? The answer lies in the connectivity of the human body.
Just as the immune system is heavily involved in the establishment of COPD related inflammation, it also plays a central role in controlling tumor burden. This strong epidemiological link led researchers to explore how COPD may impact the immune microenvironment of non-small cell lung cancer (NSCLC).
What they found was a positive correlation between COPD severity and increasing exhaustion of CD8 T cells, identified by the coexpression of immune checkpoint receptors PD-1 and TIM-3. Although both receptors inhibit the function of CD8 T cells, their coexpression is considered one of the hallmarks of severe T cell dysfunction and tumor progression.
Leveraging the Link
The next question is: How can the identified correlation between COPD and tumor microenvironment of Lung Cancer benefit patients?
This elevated expression means that the coexistence of COPD and NSCLC appears to help better align the tumor microenvironment with emerging therapies. As a result, patients with COPD might be more sensitive and responsive to immuno-oncology treatments such as anti-PD-1 therapies.
The discovery is leading researchers to explore other chronic inflammatory diseases to see if similar benefits may be found.
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