Tumours of the elderly, such as breast cancer and colon cancer, accumulate thousands of DNA mutations. These genetic defects contribute to cancer-specific properties including uncontrolled growth, invasion in neighbouring tissues, and evasion from the immune system.
Similar properties are also found in Childhood Cancers, although those tumours carry much fewer genetic defects, making it difficult to explain their clinical heterogeneity.
This is particularly true for Ewing Sarcoma, an aggressive bone cancer in children and adolescents.
A single genetic defect – the EWS-ETS fusion – is present in all tumours, initiating cancer development and defining Ewing sarcoma as a disease, but the tumours carry very few DNA mutations that could explain the observed differences in the disease course of Ewing sarcoma patients.
Tackling this question, a team of scientists from Austria, France, Germany and Spain led by Eleni Tomazou from the St. Anna Children’s Cancer Research Institute in Vienna profiled many Ewing Tumours. They found that the disease’s clinical diversity is reflected by widespread epigenetic heterogeneity.
In the science of genetics, epigenetics is the study of changes in organisms caused by modification of gene expression rather than alteration of the genetic code itself.
Attention has, over time, moved further from the DNA’s code and more toward the way that DNA is packaged and the proteins that interact with it. These so-called epigenetic factors can be inherited, are reversible, and hugely influential.
Every cell in the human body (except for a few) contains exactly the same DNA, but not every part of the DNA is active at the same time. A liver cell, for instance, will have different portions of DNA “switched on” to a skin cell or muscle cell.
Epigenetic mechanisms are responsible for ensuring the correct DNA information is expressed in each specific cell type.