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Childhood leukemia is the most common childhood cancer, accounting for 29% of cancers in children aged 0–14 in 2018. [1] There are multiple forms of leukemia that occur in children, the most common being acute lymphoblastic leukemia (ALL) followed by acute myeloid leukemia (AML). [ 2 ]
[1] Cancer is a genetic disease where changes to genes can cause cells to grow and divide out of control. Each cancer can have a unique combination of genetic mutations, and even cells within the same tumour may have different genetic changes. In clinical settings, it has commonly been observed that the same types and doses of treatment can ...
Cancer in children is rare in the UK, with an average of 1,800 diagnoses every year but contributing to less than 1% of all cancer-related deaths. [70] Age is not a confounding factor in mortality from the disease in the UK. From 2014 to 2016, approximately 230 children died from cancer, with brain/CNS cancers being the most commonly fatal type.
The variable traits must be heritable. When a cancer cell divides, both daughter cells inherit the genetic and epigenetic abnormalities of the parent cell, and may also acquire new genetic and epigenetic abnormalities in the process of cellular reproduction. That variation must affect survival or reproduction .
Human somatic variations are somatic mutations (mutations that occur in somatic cells) both at early stages of development and in adult cells. These variations can lead either to pathogenic phenotypes or not, even if their function in healthy conditions is not completely clear yet.
The central role of DNA damage and epigenetic defects in DNA repair genes in carcinogenesis. DNA damage is considered to be the primary cause of cancer. [17] More than 60,000 new naturally-occurring instances of DNA damage arise, on average, per human cell, per day, due to endogenous cellular processes (see article DNA damage (naturally occurring)).
Under this model, cancer arises as the result of a single, isolated event, rather than the slow accumulation of multiple mutations. [4] The exact function of some tumor suppressor genes is not currently known (e.g. MEN1, WT1), [5] but based on these genes following the Knudson "two-hit" hypothesis, they are strongly presumed to be suppressor genes.
The hallmarks of cancer were originally six biological capabilities acquired during the multistep development of human tumors and have since been increased to eight capabilities and two enabling capabilities. The idea was coined by Douglas Hanahan and Robert Weinberg in their paper "The Hallmarks of Cancer" published January 2000 in Cell. [1]