Inflammation

Cancer and inflammation are closely related, with research showing that chronic inflammation can significantly contribute to the development and progression of various cancers. This connection is crucial in the field of oncology and has implications for prevention, diagnosis, and treatment strategies.

The Link Between Inflammation and Cancer

Inflammation is the body's response to injury or infection, involving immune cells, blood vessels, and molecular mediators. In the context of cancer, inflammation plays a dual role. On one hand, it can help fight against tumor cells; on the other hand, prolonged inflammation can lead to a tumor-promoting environment.

Chronic Inflammation: Cancer can arise from persistent infections (like CPV or FPC), autoimmune diseases (such as IBD progressing to LSA), or chronic exposure to irritants (such as household use of insecticides and herbicides). Chronic inflammation is characterized by the ongoing presence of inflammatory cells and signaling molecules, which can lead to DNA damage and promote mutations that drive cancer development

Cytokines and Chemokines: These are signaling proteins released by cells in the inflamed area. Certain cytokines and chemokines can promote tumor growth and survival, enhance blood vessel formation (angiogenesis), and suppress anti-tumor immune responses. For example, interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) are known to enhance tumor cell proliferation and survival.

Project-29 investigates how routine inflammatory surveillance may help to prevent cancer

Mechanisms of Inflammation Driven Carcinogenesis

Genetic Mutations

Inflammatory cells can produce reactive oxygen and nitrogen species that damage DNA, leading to mutations.

Tissue Remodeling and Angiogenesis

Inflammatory cells release factors that promote tissue remodeling and angiogenesis, creating an environment conducive to tumor growth.

Epigenetic Mutations

Inflammation can also lead to changes in gene expression without altering the DNA sequence, affecting tumor suppressor genes and oncogenes.

Immune Suppression

Chronic inflammation can induce an immunosuppressive microenvironment that allows tumor cells to evade the immune system.

C-reactive Protein

C-reactive protein (CRP) is classified as an acute-phase reactant, which means its levels increase significantly and rapidly in response to inflammation. The acute-phase response is a part of the early defense or innate immunity that occurs soon after tissue injury, infection, or other inflammatory stimuli. The levels of CRP can begin to rise within 6 to 8 hours after the onset of inflammation, and its concentration in the blood can increase as much as 1000-fold compared to baseline levels. Because of these properties, CRP is widely used in clinical practice to assess the presence and intensity of inflammation.

Cancer can drive an increase in CRP levels through several mechanisms associated with both the tumor itself and the body's response to the tumor:

Tumor-Induced Inflammation

Many cancers induce a local inflammatory response. Tumor cells and the surrounding stroma can produce inflammatory cytokines such as interleukin-6 (IL-6), interleukin-1 (IL-1), and tumor necrosis factor-alpha (TNF-alpha), which are potent inducers of the acute-phase response in the liver. IL-6, in particular, has a direct stimulatory effect on the liver to produce CRP.

Tissue Damage and Necrosis

As tumors grow, they can outstrip their blood supply, leading to areas of hypoxia (low oxygen) and subsequent necrosis (cell death). This damage triggers an inflammatory response, further increasing CRP levels.

Infection and Complications

Patients with cancer are often immunocompromised, either due to the cancer itself or as a result of treatments such as chemotherapy. This increases susceptibility to infections, which can also lead to elevated CRP levels.

Metastasis and Widespread Disease

Advanced cancers, especially those that metastasize to distant organs, are associated with higher levels of systemic inflammation, again reflected in higher CRP levels.

Data now shows that in cancer inflammation (and CRP) have a relationship with both cellular respiration and tumor proliferation.

Implications for Treatment and Prevention

Understanding the relationship between inflammation and cancer can more precisely define a prevention and treatment plan:

Anti-inflammatory Drugs: Nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin, have been found to lower the risk of certain cancers, such as colorectal cancer, by reducing inflammation.

Targeted Therapies: Therapies targeting specific components of the inflammatory process, like cytokines or their receptors (e.g., inhibitors of IL-6 or TNF-alpha), are being developed.

Lifestyle Changes: Addressing underlying causes of chronic inflammation, such as obesity, poor diet, and heavy metal accumulation, can help reduce cancer risk.

This relationship between cancer and inflammation underscores the importance of a holistic approach to cancer management, integrating strategies to modulate inflammation alongside conventional treatments.