Abstract:
The advancement of HIV treatment has led to increased life expectancy. However, people
living with HIV (PLWH) are at a higher risk of developing colorectal cancers. Chronic inflammation
has a key role in oncogenesis, affecting the initiation, promotion, transformation, and advancement
of the disease. PLWH are prone to opportunistic infections that trigger inflammation. It has been
documented that 15–20% of cancers are triggered by infections, and this percentage is expected to be
increased in HIV co-infections. The incidence of parasitic infections such as helminths, with Ascariasis
being the most common, is higher in HIV-infected individuals. Cancer cells and opportunistic
infections drive a cascade of inflammatory responses which assist in evading immune surveillance,
making them survive longer in the affected individuals. Their survival leads to a chronic inflammatory
state which further increases the probability of oncogenesis. This review discusses the key
inflammatory signaling pathways involved in disease pathogenesis in HIV-positive patients with
colorectal cancers. The possibility of the involvement of co-infections in the advancement of the
disease, along with highlights on signaling mechanisms that can potentially be utilized as therapeutic
strategies to prevent oncogenesis or halt cancer progression, are addressed.
