Epigenetic changes and cancer continue to tie together. A new example arises from CEBPA. It’s a gene. The purpose of CEBPA is to cause production of a protein needed in the transcription process by which DNA is duplicated, allowing life.
Without CEBPA, the leukemic disease known as AML may arise. CEBPA mutations also are tied to other cancers, including lung cancers. Smoking appears to disrupt CEBPA. Cigarette smoke includes benzene. In fact, some researchers refer to and seek to quantify the number of smoking-induced AMLs.
To date, much attention has been focused on mutations in the CEBPA gene. The mutations exist in different forms, with two most common forms. Families with CEBPA mutations and AML are thus a subgroup that is well known to cancer researchers.
Now, however, ScienceDaily brings news of a paper published in Nature this week indicates that AML may arise in persons without CEBPA mutations. But, according to the paper, CEBPA problems still are part of the disease process. How so, if the gene is not mutated? According to the new paper, the CEBPA gene can be turned off by epigenetic changes. That is, the gene is NOT mutated but rather its function is turned off. How? By chemical changes known as methylation. They block the normal action of the gene. That’s epigenetics – the gene is not damaged but it’s function is changed by an external chemical process.
Studies of the sort above raise questions for toxic tort lawyers. For example, how many different circumstances cause methylation? Is there a fingerprint for the cause of methylation? And, are the epigenetic changes passed on to children, thereby perhaps creating multigenerational cancers or other disease? Said another way, could someone show that a family’s pattern of CEBPA mutations was caused by a particular external source?