Cancer prevention is not a merely passive process: everyone can reduce their risk of tumor development by cancer driver interception, that is, by interrupting carcinogenesis at any point before the development of an invasive disease by acting on its driving factors. Let’s discover what cancer drivers are and how to intercept them well before a cancer diagnosis.
People struggle with treating or even curing cancer. This is understandable; however, cancer will never be controlled without prevention.
In the common imaginary, this means avoiding risk factors (e.g. tobacco smoke) to prevent the development of the disease (e.g. lung cancer), and entering into screening programs enabling the early detection of cancer.
However, early detection can prevent cancer deaths but not cancer onset. Also, primary prevention (that is, the interventions aimed at reducing generic external risk factors such as alcohol, unhealthy diet, radiation, and, as stated, smoke) is often perceived as a passive method requiring deprivation (of smoke, of alcohol, of some foods, and so on).
What is more, people are more and more seeking health information that could address cancer worries. That means that preventing cancer deaths (that is, the target of early detection) is not always the principal focus of people, who sometimes simply feel spontaneously compelled to take action rather than inaction against this disease.
Cancer driver interception is the answer to this need and the beforementioned “however”.
Cancer development can last decades
Cancer arises from a process of transformation of normal cells into cancer cells lasting years or decades; during this stage (the so-called prodromal phase) people are apparently healthy and totally asymptomatic, but several factors are actively driving this transformation process. Some of these factors are actionable; that is, it is possible to act on them to counteract cancer risk.
Cancer driver interception consists in interrupting carcinogenesis at any point before the development of an invasive cancer by acting on these driving factors.
What is more, once intercepted, actionable cancer drivers can be monitored, giving people a feedback not only on the progression of the cancer prodromal phase, but also on the effectiveness of the strategies (such as cancer chemoprevention, that is the use of drugs, vitamins or other agents to reduce the risk of cancer development) put in place to counteract their presence.
Interrupting carcinogenesis: a way paved by cardiovascular interception
Such an approach is well implemented against cardiovascular diseases (CVDs). In fact, CVDs can be intercepted by drugs that reduce CVD risk (such as antihypertensive or cholesterol-reducing drugs).
This idea of cardiovascular interception has been widely accepted. The use of antihypertensive agents in high-risk patients with severe hypertension or with class III/IV heart failure, the use of statins in patients with prior myocardial infarction and very high low-density lipoprotein (LDL) cholesterol, and the use of aspirin in patients with prior MI or stroke are the first success stories in the field. Once effective therapies in advanced disease, now all these strategies are CVD prevention standards.
In a similar way, cancer development can be intercepted by risk-reducing agents. The use of preventive substances that are active against lung cancer that develops in former smokers is a case in point of how cancer can be prevented by this new, active approach, before the advanced disease presents in the clinic.
However, up to now the idea of cancer interception has been a hard sell, even among educated people prone to trying active prevention for their personal health. Troubles with adherence to risk reduction-based approaches (e.g. the use of effective breast cancer risk-reducing agents) are around the corner.
One proposed hindrance is the risk of toxic effects, such as adverse cardiovascular events produced by nonsteroidal anti-inflammatory drugs (NSAIDs, for example celecoxib) when utilized to intercept colorectal neoplasia. However, low-baseline CVD risk or C-reactive protein levels (a well-established marker of inflammation) eliminate this risk, highlighting, at the same time, the importance of a more personalized cancer interception.
Interestingly, the use of antihypertensive drugs to reduce CVD is also associated with toxicity risk. The general acceptance of this risk highlights the need to fill the gap between education on CVD risk reduction and education on cancer risk reduction.
Another proposed reason behind the resistance to the idea of cancer interception is that whereas CVD risk reduction treats well-known measurable conditions (such as hypertension and high cholesterol level) that can be followed to assess treatment effectiveness, actionable cancer drivers and prodromal conditions are less known by the general population.
Actually, there is at least one good example of an actionable measurable condition for cancer too: colorectal adenomas preceding colorectal cancer. Their number can be reduced by aspirin, which has been shown to lower the incidence and mortality from colorectal cancer. Also, surgical control of colorectal adenomas can reduce cancer risk and mortality.
In summary, thanks to cancer driver interception, people can undergo periodic tests to evaluate cancer risk and monitor the efficiency of treatment aimed at reducing it – just as in the case of people undergoing regular cholesterol test to evaluate cholesterol-reducing therapy efficiency.
The need for cancer interception
Cancer is a leading cause of death. In 2020, it was responsible for nearly 10 million deaths worldwide. Lung, colorectal, liver, stomach, and breast cancer accounted for half of these losses, and, unfortunately, new diagnoses were common. The new cases were 2.26 million for breast cancer, 2.21 million for lung cancer, 1.93 million for colorectal cancer, 1.41 million for prostate cancer, 1.20 million for skin cancer (non-melanoma), and 1.09 million for stomach cancer.
In the last 40 years, while preventive risk reduction was contributing to the steady fall in heart disease death rates, cancer became the leading cause of death in many US states. In 1999, age-standardized heart disease mortality still was higher than that for cancer in all states, but in 2016 the situation was the opposite in 19 states.
«Age is among the most important cancer risk factors, and the world population is aging, reaching cancer-prone ages. Moreover, treatment improvement increased cancer patients’ lifespan, but survivors’ cancer risk is higher», Giuseppe Mucci, Bioscience Institute CEO, explains. The company, with several facilities worldwide, is a leader in the field of biomolecular tools to assess the real health status of asymptomatic individuals. «This increasing cancer burden can only be tempered by an approach in which efforts in disease treatment are paralleled by an increase in its interception. This second way is more cost-effective, counts less human costs, and will further reduce cancer burden on public health and wellbeing».
«Today», Mucci concludes «it is possible to switch the focus from early cancer detection and generic external risk factors reduction to actionable cancer driver interception. And we know that just like we can monitor hypertension, hypertriglyceridemia, obesity, and other risk factors that drive CVD development, cancer drivers are measurable too».
What are cancer drivers?
Among cancer drivers, genomic instability is the leading physiological condition that promotes carcinogenesis.
We all know that genes are strongly involved in determining cancer risk. They are responsible for the hereditary susceptibility to the development of the disease. Also, several cancer risk factors are associated with the build-up of mutations promoting the transformation of normal cells into cancer cells. Cells that accumulate such mutations are genetically unstable, and genomic instability is a feature of the cancer prodromal phase.
Other important cancer drivers (chronic inflammation, immune system imbalance, and an altered microbiota) provide an environment favorable to the transition from pre-malignancy to malignancy. They can both promote genomic instability or insist on it, resulting in the amplification of the risk of cancer.
Inflammatory cells may produce molecules, such as reactive oxygen species (ROS), that can lead to DNA damage and, as a consequence, to mutations. And immune cell imbalance can halt the ability of the body’s natural defenses to kill cancer cells.
Also, the human microbiota (that is, the microbial population living on the organism’s internal and external surfaces) can play a role; sometimes, carcinogenesis is linked to the presence of a single bacterial species, whereas in other cases microbiota imbalance (the so-called dysbiosis) are involved.
Actionable cancer driver interception and management: Bioscience Institute’s solution
Bioscience Institute proposes a program that enables actionable cancer driver interception and management starting from the monitoring of the factors promoting genomic instability, the primary driver of cancer development.
The first, crucial, step is the analysis of the sequence of genes involved in the maintenance of genomic stability, such as the ones encoding factors involved in DNA damage response. If mutated, such genes work as cancer driver factors and their presence should prompt the monitoring of genome instability.
The second step included in the program allows for the simultaneous monitoring of the secondary drivers of cancer: low-grade chronic inflammation, immune system imbalance, and dysbiosis.
For each driver condition, Bioscience Institute developed chemopreventive treatments through which the program completely translate the model of CVD active prevention on cancer driver interception, offering the possibility to act before the onset of cancer to counteract the disease well before early diagnosis, in healthy individuals, and to monitor the efficiency of the lifestyle and chemoprevention-based strategies put in place to halt its development.
For more information about Bioscence Institute’s cancer driver interception program, please visit Bioscience Institute’s website, or feel free to contact us at email@example.com. Our biologists will answer your questions without commitment on your part.
- Beane j et al. Genomic approaches to accelerate cancer interception. Lancet Oncol. 2017 Aug;18(8):e494-e502. doi: 10.1016/S1470-2045(17)30373-X
- Blackburn EH. Cancer Interception. Cancer Prev Res (Phila). 2011 Jun;4(6):787-92. doi: 10.1158/1940-6207
- Harding MC et al. Transitions From Heart Disease to Cancer as the Leading Cause of Death in US States, 1999-2016. Prev Chronic Dis. 2018 Dec 13;15:E158. doi: 10.5888/pcd15.180151
- Lin R et al. Chronic inflammation-associated genomic instability paves the way for human esophageal carcinogenesis. Oncotarget. 2016 Apr 26; 7(17): 24564– 24571. doi: 10.18632/oncotarget.8356
- Lippman SM. The dilemma and promise of cancer chemoprevention. Nat Clin Pract Oncol. 2006 Oct;3(10):523. doi: 10.1038/ncponc0609
- Meyskens FL Jr et al. Regulatory approval of cancer risk- reducing (chemopreventive) drugs: moving what we have learned into the clinic. Cancer Prev Res (Phila). 2011 Mar;4(3):311-23. doi: 10.1158/1940-6207.CAPR-09-0014
- Scherer LD et al. A bias for action in cancer screening? J Exp Psychol Appl . 2019 Jun;25(2):149-161. doi: 10.1037/xap0000177
- World Health Organization. Cancer. 3 March 2021. https:// www.who.int/news-room/fact-sheets/detail/cancer