Inflammation and Cancer: How It Could Be Fueling Disease

What if the same process that fights off an infection could also be quietly fueling one of the world’s deadliest diseases?

Research has revealed that chronic inflammation can create the perfect environment for cancer to develop and spread. In fact, a 2024 study published in Frontiers estimates that 20% (1 in 5) of cancer worldwide is linked to chronic inflammation processes. This connection is especially significant in regions where infection-related cancers remain high, making inflammation not just a personal health concern but a global public health challenge.

In this article, you’ll learn the relationship between cancer and inflammation, what factors trigger this process, and what you can do to mitigate it.

What Is Inflammation? Understanding the Body’s Defense Mechanism

Inflammation is an immune response by the body that could present in the form of redness, heat, swelling, pain, or loss of function. When inflammation occurs, the blood vessels dilate and increase blood vessel permeability, allowing for the increased flow of blood to the injured site. This process is mediated by inflammatory agents, including histamine, bradykinin, cytokines, and lysosomal compounds. The normally selective capillary wall permits water and small molecules but keeps out proteins/, becomes more permeable during inflammation, allowing protein-rich exudates to enter the tissues. This exudate carries components such as clotting factors that help localize and prevent the spread of infectious agents.

Another important aspect of the inflammation-related program of the body is phagocytosis. In this process, white blood cells known as phagocytes migrate to the site of injury, where they engulf bacteria and other foreign particles. Within about 12-24 hours, monocytes arrive and mature into macrophages, which further populate the injured site and continue the defense.

These macrophages play a critical role in cleaning up cellular debris, dead neutrophils, and any remaining pathogens. In addition to their scavenging function, they release signaling molecules called cytokines that help orchestrate tissue repair and recruit other immune cells.

Factors that can stimulate the inflammatory response include:

• Microorganisms;
• Physical agents;
• Chemicals;
• Inappropriate immunological responses;
• Tissue death;

An inflammatory response may be short-lived, lasting only a few days, in which case it is referred to as acute inflammation. This type is usually protective and beneficial. However, when the response persists for a longer period, it becomes chronic inflammation, and not specific to one location of the body, it become systemic and has been linked to the development of various disease conditions.

The Inflammation-Cancer Connection: Key Biological Mechanisms

Inflammation contributes to tumorigenesis and is often present throughout its stages- from cancer initiation to cellular proliferation and malignant transformation. Often described as a hallmark of cancer, it plays a central role in tumor growth mechanisms, driving tumor progression and facilitating the transition to a malignant phenotype. In essence, inflammation influences nearly every stage of cancer development.

Key biological mechanisms through which inflammation drives cancer progression include:

• Activation of transcription factors: Inflammatory signals activate factors like NF-kB, STAT3, and HIF-1alpha, which drive cancer-supporting processes.
• Blocking cell death (anti-apoptosis): NF-kB stimulates genes such as BCL-XL and BCL-2, helping cancer cells survive when they should normally die.
• Fueling cytokine production: It boosts inflammatory cytokines (TNF-alpha, IL-1beta, IL-6, IL-8), which maintain a chronic inflammatory environment that favours tumor growth.
• Increasing inflammatory enzymes: Enzymes like iNOS and COX-2 promote further inflammation, DNA damage, and tumor progression.
• Supporting metastasis: Inflammatory activation increases adhesion molecules and matrix metalloproteases (MMPs), which help cancer cells detach, invade tissues, and spread.

In addition, chronic inflammation fuels cancer by pushing cell proliferation, as it activates key cell cycle genes such as c-MYC and cyclin D1, leading to uncontrolled cell division. At the same time, it promotes angiogenesis by releasing factors like VEGF and angiopoietin, which stimulate the formation of new blood vessels to feed the growing tumor with oxygen and nutrients. Understanding these pathways has opened new frontiers in cancer therapy approaches, with scientists now exploring anti-inflammatory agents as possible treatment strategies for cancer.

How Chronic Inflammation Can Lead to Tumor Development

Tumor initiation begins when a normal cell develops genetic changes that give it a growth and survival advantage over surrounding cells. However, one mutation alone is usually not enough to cause cancer. Most malignancies result from the stepwise accumulation of several genetic alterations, often occurring in long-lived stem cells or short-lived progenitor cells that survive long enough to acquire multiple successful mutations.

Chronic inflammation-whether caused by chronic infections, persistent irritants, or autoimmune diseases–plays an active role in tumor development by shaping a microenvironment that favors genetic damage and abnormal cell growth. Inflammatory immune cells generate reactive oxygen species (ROS) and reactive nitrogen intermediates (RNS), which induce DNA damage, genomic instability, and epigenetic changes that increase the mutation rate.

Chronic inflammation induces immune suppression and creates an enabling environment for neoplastic progression. The tumor microenvironment (TME) often contains inflammatory cells such as neutrophils, lymphocytes, and macrophages, and inflammatory markers such as cytokines, chemokines, and tumor growth factors, which are central to tumor progression. These inflammatory markers are usually hijacked by cancer cells, and instead of mounting an effective defense, they support tumor growth and enable the cancer to evade immune surveillance. Tumor-associated inflammation, largely driven by innate immune cells, together with complex tumor-microenvironment interactions, plays a key role in cancer plasticity, cancer progression, and the development of anticancer drug resistance.

Common Conditions That Cause Chronic Inflammation and Raise Cancer Risk

The key difference between acute and chronic inflammation lies in their duration and underlying triggers. Acute inflammation is a rapid response aimed at restoring homeostasis after injury. In contrast, chronic inflammation can persist even without an obvious injury or harmful stimulus, and often fails to resolve when it should. The exact reasons for this prolonged activity are not yet fully understood. Unfortunately, chronic inflammation is often mediated by some chronic infections, and other factors, such as:

• Chronic inflammatory diseases;
• Hepatitis B and C;
• Pancreatitis;
• Autoimmune disorders;
• Obesity;
• Environmental factors;

In summary, these chronic conditions are known cancer risk factors and can become devastating by transforming normal cells into cancer through several pathways, such as cell proliferation, cell mutation, and DNA damage. Managing the underlying disease or conditions alongside utilizing risk-reduction strategies can help mitigate these cancerous risks..

The Role of Inflammatory Cytokines and Immune Cells in Cancer Progression

Cytokines are signaling proteins produced by many cell types. While some of them are pro-inflammatory cytokines, others are not. They were initially thought to modulate immune response and inflammation, but an increasing number of studies are pointing to the roles of some of them in the induction and progression of cancer.

The cancer-related cytokines promote or enhance cancer development in a coordinated manner. This cytokine network of inflammatory molecules, which includes interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha), transforming growth factor beta (TGF-beta), and Chemokines (CK), induces or promotes cancer in the following ways:

• Interleukins: Are usually produced by many cell types; some (IL-6) can act as a pro-oncogenic agent. It does so by working in synergy with the Signal Transducer and Activation of Transcription (STAT) family to promote tumorigenesis. However, other interleukins are not pro-oncogenic.
• Tumor necrosis factor: This cytokine impacts cancer development by contributing to epithelial-mesenchymal transition (EMT), boosting the cell proliferation rate, and accelerating angiogenesis.
• Transforming growth factor beta: TGF-B is produced by many cells (platelets, macrophages, T cells, fibroblasts, and tumor cells) and can act as a tumor suppressor early and a pro-tumor factor at later stages..
• Chemokines: The relationship between chemokines and cancer is seen in immune cell recruitment and tumor cell proliferation. Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine with chemokine-like functions that can promote tumour angiogenesis, tumor progression, and metastasis. These processes not only sustain tumor growth but also contribute to complications such as cancer-associated thrombosis.

On the other hand, immune cells associated with cancer development and their mechanisms of action include:

• Tumor-associated macrophages: Fosters immunosuppression, angiogenesis, and tumor progression through the release of inflammatory cytokines, production of VEGF, EGF, and secretion of TGF-beta and IL-10
• Myeloid-derived suppressor cells (MDSCs): Create a suppressive immune environment that protects tumors by inhibiting T cell activation through nitric oxide, ROS, and TGF-beta. It also produces IL-6, which promotes tumor proliferation and survival.
• Th17 cells: Depending on the tumor context, TH17can drive chronic inflammation, angiogenesis, and may suppress anti-tumor responses by induction of IL-6 production, and activation of STAT3, while reducing tumor-infiltrating lymphocytes such as CD8+ cytotoxic T cells.
• Neutrophils: Neutrophil recruitment into the tumor microenvironment is mediated by chemokines, cytokines, lipids, and growth factors. They contribute to tumor progression by releasing proteases, ROS, and pro-angiogenic factors that promote invasion and metastasis.

Overall, the interplay between inflammatory cytokines and immune cells creates a tumor-friendly microenvironment that supports cancer initiation, progression, and metastasis. By driving chronic inflammation, suppressing anti-tumor immunity, and fostering angiogenesis, these factors highlight the critical link between the immune system and cancer development and underscore the importance of targeting them in cancer therapy.

Anti-Inflammatory Foods and Nutrients That May Lower Cancer Risk

No singular food or nutrient can prevent cancer, but research suggests that a combination of a variety of foods rich in vegetables, fruits, whole grains, beans, limiting red meat, and adding other plant foods may help lower cancer risks. Based on this, the American Institute for Cancer Research recommends the following foods: apples, turmeric, blueberries, cruciferous vegetables, carrots, brussels sprouts, cauliflower, cherries, coffee, cranberries, flaxseed, grapefruit, garlic, etc.

These foods contain phytochemical nutrients, some of which have been found to have anti-inflammatory and anti-cancer properties. These nutrients include: Anthocyanins, indole-3-carbinol, allicin, diallyl sulfide, curcumin, and sulforaphane.

Adopting a healthy dietary pattern, such as the Mediterranean diet, and “eating the rainbow” by seeking nourishment rich in fruits, vegetables, whole grains, legumes, nuts, and seeds, can provide a steady supply of these protective nutrients. While no single food can prevent cancer, incorporating a variety of anti-inflammatory, nutrient-dense foods into your meals may exert chemopreventive activities, helping to lower cancer risk and support overall health.

Can Reducing Inflammation Help Prevent Cancer? What Research Says

While there is currently no established cure or guaranteed way to prevent cancer by targeting inflammation, scientists at the National Cancer Institute (NCI) are optimistic that the inhibition of this pathway can provide a new therapeutic application in cancer treatment, as early studies have yielded promising results.

Scientists at the institute believe that the tumor-microenvironment (TME) acts like a fortress for cancer cells, which sustains chronic inflammation that builds a protective barrier and prevents immune cells from infiltrating to destroy them. Within the field of tumor immunology, this inflammation-driven shield is recognized as a major challenge. Researchers propose that breaking down this cancer-related inflammatory barrier could open a new frontier in cancer therapy.

To demonstrate the potential of this approach, a small clinical trial involving 24 patients with localized advanced breast cancer and those with metastatic breast cancer was carried out using a standard chemotherapeutic agent and an anti-inflammatory drug called L-NMMA, which blocks the production of nitric oxide, a pro-inflammatory molecule.

Results showed that the tumors in approximately half of the patients shrank, when historically only about one-third of the patients would have responded to chemotherapy alone. Furthermore, three patients with localized advanced breast cancer in the trial had all their cancer signs disappear after treatment.

Another molecule of interest is STAT3, which possesses inflammatory properties implicated in cancer development. Researchers are exploring strategies to block this pathway as a potential therapeutic approach in cancer treatment.

Studies in animal models already show that STAT3 inhibitors may reduce tumor growth while also enhancing the immune system’s ability to clear the remaining tumor cells. (antitumor immunity) While still in the early days, growing evidence in animal studies provides hope that cancer may be prevented by reducing inflammation.

Anti-Inflammatory Medications and Their Potential Role in Cancer Prevention

Because chronic inflammation can promote tumor development, targeting key inflammatory pathways and molecules- such as COX-2, – may offer an effective strategy for both cancer prevention and treatment. The data mainly shows prevention evidence strongest with NSAIDs/aspirin.

A class of drugs currently being investigated for their potential role in this is Nonsteroidal anti-inflammatory drugs (NSAIDs). Examples include Diclofenac, Ibuprofen, Celecoxib, Aspirin, Meloxicam, and Piroxicam.

Studies have found COX enzymes to be overexpressed in various cancers, such as pancreatic, prostate, cervical, breast, lung, and particularly, colon cancer. The overexpression, in turn, was found to stimulate angiogenesis, which is a key step in invasion and metastasis. Since NSAIDs are COX inhibitors, they may be a good candidate for anticancer therapy and prevention. Furthermore, the products of COX activities, such as prostaglandins, are also involved in tumorigenesis.

Several studies of both human and laboratory experiments suggest that NSAIDs have the potential to play a key role in cancer prevention and treatment.

Final Thoughts: Practical Steps to Control Inflammation and Reduce Cancer Risk

Inflammation can be caused by both intrinsic and extrinsic factors. While we have little control over some of the intrinsic factors, we have some by applying the following practical steps to reduce our cancer risk through inflammation by:

• Reducing exposure to environmental toxins such as asbestos.
• Quitting smoking.
• Reducing excessive alcohol intake.
• Practicing safe sex, since chronic inflammation can be caused by cancer-related microorganisms.
• Maintaining an appropriate body mass index (BMI) is important since obesity is a chronic inflammatory condition.
• Eating less processed foods and more whole foods and vegetables.
• Exercising moderately.

These lifestyle-related inflammation control measures can help reduce the burden of chronic inflammation, lower your overall risk of cancer, and promote better long-term health and wellness. As researchers continue to explore cancer biomarkers, they provide vital tools for early detection and monitoring. This helps us better understand and disrupt links between cancer and immunity.

Since chronic inflammation can be triggered or worsened by toxins and oxidative stress, keeping your body’s detox organs—particularly the liver and kidneys—healthy is crucial. These organs help filter out harmful compounds, reduce systemic inflammation, and maintain the internal balance your immune system depends on. Supporting them naturally can further protect against the long-term cellular damage that sets the stage for disease.

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Frequently Asked Questions

What is the number one food that kills inflammation?

There isn’t a single number one food that kills inflammation, but foods rich in omega-3 fatty acids, garlic, leafy greens, berries, and olive oil are among the most powerful anti-inflammatory options.

What are the 5 signs of inflammation?

The five common signs of inflammation are redness, heat, swelling, pain, and loss of function in the affected area.

What is the fastest way to flush inflammation?

The fastest way to reduce inflammation is to combine short-term and long-term relief strategies. Short-term strategies include staying hydrated, resting, applying cold compresses, or taking anti-inflammatory medications when advised. Long-term strategies include eating an anti-inflammatory diet, exercising regularly, managing stress, and getting quality sleep.

What drink kills inflammation?

Drinks like green tea, turmeric tea, tart cherry juice, and keeping hydrated with water can help reduce inflammation and/or support overall health.

What foods trigger inflammation?

Foods that trigger inflammation include processed meats, high fructose corn syrup, fake sugar, fried foods, refined carbohydrates, sugary drinks, excessive alcohol, and foods high in trans fats or added sugars.

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From inflammation to cancer

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Chronic Inflammation 

Chronic Inflammation’s Transformation to Cancer: A Nanotherapeutic Paradigm

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The recruitment of neutrophils into the tumor microenvironment is regulated by multiple mediators

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AICR’s Foods that Fight Cancer

7 foods to fight cancer, heart disease, and enhance health

Targeting Inflammation Emerges as a Strategy for Treating Cancer

Anti-Inflammatory Drugs as Anticancer Agents

Role of Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) in Cancer Prevention and Cancer Promotion

Colorectal cancer prevention: Is an ounce of prevention worth a pound of cure?

The effect of celecoxib, a cyclooxygenase-2 inhibitor, in familial adenomatous polyposis

Targeting Inflammation in Cancer Prevention and Therapy