Posted at regular intervals along our body like checkpoints on the border between hostile countries, our lymph nodes form a critical barricade against infection.
These checkpoints are manned by lymph cells (aka lymphocytes) that come in two varieties: T-cells and B-cells. But sometimes instead of being the protectors, these cells go rogue and become cancers called lymphomas in which mutant lymphocytes multiply out of control and overcrowd the lymph nodes and bone marrow – which causes the enlarged lymph nodes, fatigue, and low blood counts we associate with the disease.
Like all cancers, lymphoma occurs when genetic errors cause cells to behave erratically, just as a corrupted computer code causes problems.
In lymphoma, these mutations occur three main ways:
- Risky genetic revision by lymphocytes. Lymphocytes have to be able to manufacture cells capable of recognizing infinite variation in potential invaders, otherwise our immune systems couldn’t adapt. They accomplish this the same way English makes an infinity of words from only twenty-six letters: by combining different combinations of letters. Similarly, lymphocytes produce an infinite variety of “sniffer receptors” from a finite number of genes. The variety comes from lymphocytes’ ability to copy, revise, and recombine these genes in endless combinations. But it also means that, with all that gene-revising going on, a few cells have accidents that turn cancerous.
- Viral hijacking. Viruses insert their genes into host cells, and this sometimes triggers cancer transformation – though this is a much less common cause of lymphoma than the first one above. Several viruses can do this, including the Epsetin-Barr virus and the HIV virus.
- Inherited mutations. Some people are born with mutations that take them part of the way to developing a cancer. This is well-known in colon and breast cancers, but BRCA1 and BRCA2 mutations also predispose to lymphoma development.
