Cancer in children, also known as pediatric cancer, refers to malignancies that develop in individuals from birth through adolescence, typically up to 14 or 19 years of age. This group of diseases is notably rare compared to cancers in adults; approximately 15,000 children and adolescents are diagnosed annually in the United States.
The fundamental causes of childhood cancers often differ significantly from those seen in adults. While adult cancers frequently arise from prolonged exposure to environmental factors or lifestyle choices over many years, childhood cancers are generally linked to genetic changes that occur early in development, sometimes even before birth. Understanding these distinctions is important for comprehending the unique nature of cancer in younger populations and the ongoing research efforts dedicated to this field.
Distinct Nature of Childhood Cancers
Childhood cancers differ fundamentally from those primarily affecting adults. These pediatric cancers originate from processes related to growth and development. The mutations causing them frequently occur early in a child’s life, sometimes even before birth, indicating an internal, rather than external, primary driver.
The cell types involved in childhood cancers are unique, stemming from embryonic or rapidly dividing cells. For example, leukemias, which are cancers of blood-forming cells in the bone marrow, are the most common type of childhood cancer. Brain and spinal cord tumors are significant, alongside solid tumors such as neuroblastoma, which arises from immature nerve cells, and Wilms tumor, a kidney cancer. These cancers frequently exhibit rapid progression, as exemplified by acute leukemias that require immediate intervention.
The underlying genetic changes in pediatric cancers are distinct from those found in adult versions of similar cancers. This difference in origin means that prevention strategies effective for adult cancers do not apply to childhood cancers. Instead, the focus shifts to understanding the errors in cellular development and genetic predispositions that contribute to these unique forms of cancer in young individuals.
Genetic and Developmental Factors
Internal biological factors, genetic and developmental processes, play a role in the origins of childhood cancers. A proportion of pediatric cancers are linked to inherited genetic mutations. These are changes in DNA passed down from a parent, increasing a child’s susceptibility to developing cancer. However, inheriting such a mutation does not guarantee cancer will develop, only that the likelihood is higher.
Several specific genetic syndromes are associated with an increased risk of childhood cancer. Li-Fraumeni syndrome, caused by a mutation in the TP53 gene, increases the risk of various cancers, including sarcomas, brain tumors, and leukemia. Neurofibromatosis, an inherited condition, predisposes children to tumors of the nervous system. Children with Down syndrome have an increased incidence of some leukemias compared to the general population. Retinoblastoma, an eye cancer, is an example where an inherited faulty gene can be responsible for some cases.
Beyond inherited predispositions, many childhood cancers arise from de novo mutations. These are genetic changes that are not inherited but occur spontaneously in a child’s cells during development. These random errors can happen during the rapid process of cell division as a fetus develops or in early childhood. Unlike adult cancers, which accumulate numerous somatic mutations over time due to environmental exposures, childhood cancers tend to have a lower overall burden of these acquired mutations, yet the ones that do occur can be impactful.
The link between these mutations and cancer lies in errors during cellular growth and differentiation. During fetal development, cells undergo division and specialization to form tissues and organs. Mistakes in these processes, those affecting genes that regulate cell growth, cell repair, or programmed cell death, can lead to uncontrolled cell proliferation and cancer. These developmental abnormalities highlight why many childhood cancers are considered diseases of development, originating from the earliest stages of life when cells are rapidly multiplying and specializing.
Environmental and External Influences
While internal biological factors are drivers, external environmental influences contribute to childhood cancer development, though they account for a smaller proportion of cases compared to adults. The direct impact of environmental exposures on pediatric cancer incidence is complex and under investigation. Unlike adult cancers, which are linked to cumulative carcinogen exposure, childhood cancers are rarely attributed to such factors.
Ionizing radiation is one external factor with an established link to childhood cancer. Exposure to medical imaging procedures has been associated with an increased risk of some cancers, including leukemia and brain tumors. Children are more sensitive to radiation than adults, and exposure during childhood can elevate cancer risk later in life. Radiation therapy administered for a prior cancer can increase the risk of developing a secondary malignancy.
Chemical exposures have been investigated for their role. Associations have been reported between childhood cancers and exposure to pesticides. Chemicals like benzene, found in air pollution, are known carcinogens, though definitive links are challenging to establish for most children. Parental occupational exposures to specific substances before or during pregnancy have been explored as risk factors.
Some viral infections are recognized as contributing factors to childhood cancers. The Epstein-Barr virus (EBV) is associated with types of lymphoma in children. Other chronic infections, like HIV, can increase a child’s susceptibility. Understanding these environmental and infectious links is an area of research, as many suspected associations require further study to clarify their role in childhood cancer causes.
The Role of Chance and Unexplained Origins
For a proportion of childhood cancer cases, a definitive cause cannot be identified, despite research into genetic, developmental, and environmental factors. For many families, this can be a reality, as there is no clear explanation for why a child developed cancer. In these instances, the development of cancer appears to be largely a matter of chance.
This concept of chance refers to random errors that occur during normal cell division. Every time a cell divides, it must copy its genetic material. While cells possess mechanisms to ensure fidelity and repair errors, mistakes can still happen spontaneously. These random errors can lead to mutations in genes that control cell growth and behavior.
Over time, even a single mutation, or a series of such random mistakes, can accumulate and lead to a cell becoming cancerous. Since children, especially infants, have had little time for these genetic errors to accumulate from external exposures, the role of these spontaneous mistakes becomes more apparent. This understanding is important for parents to know that their actions or inactions during pregnancy or their child’s early life are rarely the cause of their child’s cancer.