Conference
DO MORE CHILDREN MEAN MORE CANCERS? CALL FOR A NEW VISION OF MEDICINE ABLE TO CHANGE THE WORLD WE LIVE IN
Abstract
In the most famous Italian encyclopedic dictionary published by Treccani in 1955, the term "tumor" was explained by a definition of "occupational disease suffered by workers of the chemical industry", thus referring to a very specific cause. This clear reference to a clear cancer etiology as linked to chemicals gradually disappeared in the following decades in all the medical literature, opening the door to generic explanations based on a vague “multifactorial” pathogenesis. Today, cancer is generally associated with the aging of the population as a consequence of the random (or "stochastic" as they say) accumulation of oxidative “genetic damage”. The increase in cases is also attributed by many professionals to the continuous improvement of our diagnostic capabilities: that is, we are able to diagnose more tumors than in the past. However, this explanation risks “muddying the waters” as it does not clarify why the highest and most rapid increases in cancer incidence, in terms of average annual changes, are observed in younger age groups, including children, who do not they are exposed to traditional risk factors such as cigarette smoking ("children don't smoke"), professional factors or prolonged adoption of so-called "unhealthy lifestyles".
Annual new cases of paediatric cancers are estimated to increase to 13.7 million globally from 2020 to 2050, resulting in 9.3 million deaths among children living in low-income countries. But there's more: over the last 20 years, cancer has become the leading cause of disease-related death across all paediatric age groups in Europe. The ACCIS (Automated Childhood Cancer Information System) project conducted by the International Agency for Research on Cancer (IARC) on 63 huge cancer registries in 19 European countries has highlighted an annual increase of up to 1.5% in all paediatric cancers: +2% in the first year of life, with the most significant increases for lymphomas, sarcomas, germ cell tumors and the nervous system. These neoplasms are more frequent and documented in areas with high environmental contamination, in which air pollution seems to have a particular impact.
In this context, it is not reasonable to minimize this phenomenon when evaluating the incidence of paediatric cancers at a national level, simply pointing out that the observed increases are consistent with current international "trends", which are known to be continuously rising. We cannot resign ourselves to the axiom that regions with a higher number of children must also experience a higher incidence of pediatric cancers. When did we start thinking that having more children had to mean having more cancers? The response of the medical community cannot be limited to counting the number of deaths and incident cases (where this is done), with the risk of providing (as often happens) these data after many years, so that they may be less useful for health policy makers.
The increased incidence of cancer in the first year of life has been potentially linked to transplacental (maternal-fetal) exposure to pro-carcinogenic agents or to the transgenerational transmission of epigenetic alterations already present in gametes as a consequence of parental exposure to different environmental contaminants in the "first thousand days of life" as well as during the fertile years of the adult: this is a change of perspective compared to the etiological paradigm of the theory of carcinogenesis. In fact, in children we cannot hypothesize - unlike adults and the elderly - a progressive accumulation of random (stochastic) DNA mutations, as the classically accepted pathogenetic model presupposes (the above mentioned "Somatic Mutation Theory", SMT ). Recognizing the most appropriate etiological theory for carcinogenesis would allow us to implement adequate primary prevention measures, such as removing individual exposure to chemical and environmental carcinogens (IARC 1 and 2). Actually, even in medicine and public health, “thought always precedes action”.
Annual new cases of paediatric cancers are estimated to increase to 13.7 million globally from 2020 to 2050, resulting in 9.3 million deaths among children living in low-income countries. But there's more: over the last 20 years, cancer has become the leading cause of disease-related death across all paediatric age groups in Europe. The ACCIS (Automated Childhood Cancer Information System) project conducted by the International Agency for Research on Cancer (IARC) on 63 huge cancer registries in 19 European countries has highlighted an annual increase of up to 1.5% in all paediatric cancers: +2% in the first year of life, with the most significant increases for lymphomas, sarcomas, germ cell tumors and the nervous system. These neoplasms are more frequent and documented in areas with high environmental contamination, in which air pollution seems to have a particular impact.
In this context, it is not reasonable to minimize this phenomenon when evaluating the incidence of paediatric cancers at a national level, simply pointing out that the observed increases are consistent with current international "trends", which are known to be continuously rising. We cannot resign ourselves to the axiom that regions with a higher number of children must also experience a higher incidence of pediatric cancers. When did we start thinking that having more children had to mean having more cancers? The response of the medical community cannot be limited to counting the number of deaths and incident cases (where this is done), with the risk of providing (as often happens) these data after many years, so that they may be less useful for health policy makers.
The increased incidence of cancer in the first year of life has been potentially linked to transplacental (maternal-fetal) exposure to pro-carcinogenic agents or to the transgenerational transmission of epigenetic alterations already present in gametes as a consequence of parental exposure to different environmental contaminants in the "first thousand days of life" as well as during the fertile years of the adult: this is a change of perspective compared to the etiological paradigm of the theory of carcinogenesis. In fact, in children we cannot hypothesize - unlike adults and the elderly - a progressive accumulation of random (stochastic) DNA mutations, as the classically accepted pathogenetic model presupposes (the above mentioned "Somatic Mutation Theory", SMT ). Recognizing the most appropriate etiological theory for carcinogenesis would allow us to implement adequate primary prevention measures, such as removing individual exposure to chemical and environmental carcinogens (IARC 1 and 2). Actually, even in medicine and public health, “thought always precedes action”.
Keywords
Epigenetics
Epidemiology
Prevention
Cancer
