Targeting inflammation may help control polycythemia vera

Inflammation plays a key role in the progression of polycythemia vera (PV), making it an important potential treatment target.

In a new Perspective article, three scientists in Italy reviewed available research on inflammation in PV and its implications for treatment. The paper, “The bidirectional relationship between JAK2V617F allele burden and inflammation in polycythaemia vera: Insights from interferon and ruxolitinib therapy,” was published in HemaSphere.

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Inflammation may help drive PV progression

PV is a form of blood cancer marked by the abnormal growth of blood cells. Abnormally growing blood cells harbor genetic mutations that drive their uncontrolled growth; mutations in the JAK2 gene account for about 98% of cases. This review focuses on a specific JAK2 mutation called JAK2V617F.

Genetic mutations that trigger abnormal blood cell growth are essential for the development of PV. However, these mutations alone don’t explain how the disease progresses: inflammation also plays an important role.

“Although these mutations are central to disease initiation, accumulating evidence indicates that chronic inflammation plays a pivotal role in disease progression and clinical manifestations, making it a relevant therapeutic target,” the researchers wrote.

Inflammation is part of the body’s normal response to infection or injury and helps protect and repair tissues. But when inflammation becomes chronic, it can contribute to disease.

Available data suggest a two-way relationship between inflammation and the expansion of blood cells carrying the JAK2V617F mutation. Inflammatory conditions can give these mutant cells a growth and survival advantage, while the expanding mutant cells can further increase inflammation, creating a self-perpetuating cycle.

“Collectively, the body of evidence supports the concept that inflammation is not merely [a byproduct] but rather a central [disease] driver that establishes a permissive microenvironment for [mutant cell expansion] and sustained disease evolution. Consequently, inflammation represents a rational and actionable therapeutic target,” the researchers wrote.

Besremi, Jakafi may act differently on PV biology

Currently available PV treatments include Besremi (ropeginterferon alfa-2b-njft) and Jakafi (ruxolitinib). The researchers noted that, based on available biomarker data from clinical studies, both treatments have anti-inflammatory effects but appear to affect PV differently. Besremi reduces inflammation while also suppressing the mutant cell population, whereas Jakafi primarily targets the inflammatory environment. As such, these two medications “appear complementary rather than interchangeable,” the researchers wrote.

“[Besremi] combines [mutant cell] suppression with immune modulation, whereas [Jakafi] primarily targets the inflammatory milieu, highlighting inflammation as a key determinant of [changes in the mutant cell population] and therapeutic response,” they added.

Based on these findings, the researchers called for greater consideration of inflammation in PV care, including in risk assessment and as a treatment target.

“Conventional risk stratification should evolve toward integrated models combining [the pattern and burden of genetic mutations] with quantitative inflammatory markers,” they wrote. “Together, these advances support a shift from blood count control toward biology-directed therapy, in which simultaneous targeting of [changes in the mutant cell population over time] and inflammation may ultimately modify the natural history of PV,” they added.