Cancer driver interception enables carcinogenesis interruption at any point before the development of an invasive disease. Among the strategies through which you can implement it is taking action against low-grade chronic inflammation. In fact, this actionable cancer driver can be intercepted well before cancer development by CYTOBALANCE, Bioscience Institute test allowing for periodic monitoring of blood inflammatory molecules in apparently healthy people.
Inflammation is not only the response of the organism to tissue injury and infection. It can also be induced by tissue stress and malfunctioning while in the absence of infections or overt tissue damage.
In particular, low-grade chronic inflammation is triggered by sentinel immune cells that monitor for tissue stress and malfunctioning. It has also been associated with a number of lifestyle factors (such as smoking, unhealthy diets, sleep deprivation, and low levels of physical activity) and new correlations are constantly emerging.
Among the health issues associated with low-grade chronic inflammation is cancer. Years of research led to the conclusion that immunity serves both as a tumor suppressor and as an initiator or promoter of the disease, and that chronic inflammation is among the factors responsible for these associations.
Moreover, chronic inflammation causes genome instability. Therefore, when working on cancer driver interception, evidence of genomic instability provokes the need to analyze the presence of inflammation as both a possible cause of the observed instability and a cancer-promoting factor.
The link between inflammation and cancer
The hypothesis of a link between inflammation and cancer is supported by several evidence.
First, more than 20% of all cancers are initiated or exacerbated by inflammation, and inflammatory molecules (the so-called pro-inflammatory cytokines) have been implicated in inflammation-associated tumors by epidemiological, genetic, and pharmacological studies.
For example, epatocellular carcinoma, gastric cancer, and colon cancer have all been associated with chronic inflammation. Gastritis, the inflammation of the lining of the stomach, correlates with gastric cancer, whereas colitis, the inflammation of the colon, associates with colorectal cancer.
Second, the use of anti-inflammatory drugs (in particular, non-steroidal anti-inflammatory drugs, NSAIDs) correlates with a 30-60% reduction in colon cancer incidence.
Also, non-infectious causes of chronic inflammation, such as hormonal changes, cigarette smoke and other toxicants (for example, adhesives, air fresheners, cleaning products, and glue) increase cancer risk. It is estimated that almost 20% of smokers with inflammation of their bronchial tubes’ mucous membranes (a bronchitis) can develop cancer.
Moreover, specific variants of genes encoding for cytokines (for example, tumor necrosis factor – TNF – and interleukin-1 – IL-1) and other inflammatory genes, and mutations in genes playing important roles in innate immunity have been associated with cancer. For example, the aberrant activation of NF-kB or STAT3, which are involved in inflammation control, is found in over 50% of all cancer; this activation renders both premalignant and fully transformed cells resistant to programmed cell death, and accelerates their rate of proliferation, increasing tumor growth.
In general, among cancer-associated causes of inflammation are:
- tobacco smoke
- toxic molecules
- changes in hormone levels
- mutations or drugs affecting mitochondrial DNA copy number
- immune mechanisms controlling proinflammatory factor response
- increased programmed cell death associated with chronic viral infections (e.g. Cytomegalovirus infection)
The role of inflammation in cancer
Inflammation plays a crucial role in several aspects of tumor development, including cellular transformation, cell survival, cell proliferation, invasion, metastasis formation, and angiogenesis. It can act both via chronic conditions associated with smoldering, non-resolving inflammation (such as obesity) and genetic events that orchestrate the generation of cancer-related inflammation.
In fact, inflammation can contribute to cancer initiation by promoting mutations in genes involved in cell division, survival, senescence, or genome instability (e.g. genes involved in error correction after DNA replication), chromosome instability, or DNA double strand breaks. It can also promote cancer development through cellular and extracellular signals making cells resistant to growth-inhibitory signals, apoptosis, or anticancer immunity.
What is more, the production of reactive oxygen and nitrogen species (ROS and RNS) is a key event in inflammation-related carcinogenesis. These highly reactive molecules damage DNA promoting cancer development (e.g. cholangiocarcinoma related to liver fluke infection), can induce irreversible and irreparable protein changes, and can contribute to the generation of reactive lipids that can further interact with and damage DNA and proteins. All these lesions result in molecule disfunction, damaging tissues, and activating stem cells for tissue regeneration.
Moreover, ROS and RNS damage stem cells too, resulting in mutation accumulation and, eventually, cancer stem cell generation. Damage to cancer stem cells’ DNA is associated with more aggressive cancer.
Another pivotal event is DNA methylation – the addition of a chemical group (methyl) to specific DNA sequences. ROS and RNS induce global DNA hypomethylation, resulting in genomic instability; at the same time, inflammatory cytokines can enhance the methylation of tumor suppressor genes – thus downregulating their expression, an event that can represent the first step of carcinogenesis.
Finally, chronic inflammation is associated with immune suppression. This means that ongoing inflammatory responses can suppress anticancer immune responses. In fact, tumor-associated immune cells can produce immunosuppressive cytokines such as Interleukin-10 (IL-10) and transforming growth factor (TGF-β) and other molecules that negatively influence immune responses against cancer cells.
How to intercept inflammation to prevent cancer
«The current approach to primary cancer prevention is often perceived as a passive method requiring deprivation: of smoke, of alcohol, of some food. But we can switch the focus from the generic reduction of external risk factors to actionable cancer driver interception. Low-grade chronic inflammation monitoring enables this change of perspective», Giuseppe Mucci, CEO of Bioscience Institute, explains. «The process of transformation of normal cells into cancer cells lasts years or decades; this is the window of time during which cancer driver interception is possible. Low-grade chronic inflammation is among the primary factors that drive the transformation process, and we can measure it and act on it».
Inflammation is present when the concentration or the activity of elements involved in innate responses, such as pro-inflammatory cytokines, is increased. CYTOBALANCE by Bioscience Institute is the inflammation monitoring program that makes finding out and correcting the increase of these molecules possible. Through the periodic monitoring of blood cytokine levels in apparently healthy people, CYTOBALANCE allows for cancer driver interception, inflammation monitoring and taking action against the disease well before its development.
The test analyzes the blood levels of 12 cytokines (IFN-α, IFN-γ, lL-2, IL-4, IL-5, IL-6, IL-9, IL-10, IL-12, IL-17A, TNF-α, and GM-CSF). Also, C-Reactive Protein (CRP, a well-known marker of inflammation whose testing is recognized as an easy and inexpensive tool to identify high cancer risk and people that may benefit from interventions like prophylactic therapy with anti- inflammatory drugs) is measured.
If at least one of the tested levels exceeds the attention threshold, lifestyle-based strategies are suggested to reduce inflammatory mediator levels. Maintaining inflammatory mediator levels below inflammation-associated thresholds is expected to reduce cancer risk.
For more information about CYTOBALANCE, please visit Bioscience Institute’s website or contact us at firstname.lastname@example.org. Our biologist will answer your questions with no commitment on your part.
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