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Lymphoma Causes Are Now Better Understood
According to a report this week in Nature, the
cellular mutation and repair processes of the immune system provide
information on the development of lymphatic cancer.
David Schatz, senior author of the study and immunobiologist at Yale
School of Medicine, reports that "the implications of these findings
are considerable." Widespread mutations and an increased risk of cancer
could be the results of "anything that compromises the function of
these DNA repair processes."
Lymphatic cancer, or lymphoma, is a type of cancer that originates when
a type of white blood cell (lymphocyte) becomes abnormal or mutated.
One piece of the lymphatic system is infection-fighting lymphocytes
called B cells. The researchers focused on the somatic hypermutation
(SHM) process, which introduces random mutations in B cells' antibody
genes to make them more effective in fighting infection.
There are two steps in the SHM process:
A mutation initiator - or activation-induced deaminase
(AID) - causes genetic mutations.
DNA repair enzymes spot the changes and begin making
"sloppy" repairs, leading to even more mutations.
When these two steps combine, they present a major risk to genomic
stability - the ability of DNA to perform its duties of replication,
recombination, and repair without mutation. The same DNA repair enzymes
are able to see mutations in many other types of genes present in the B
cells, but they fix the genes in a very precise manner.
Previously, researchers believed that genomic instability was not
likely since the first step of the SHM process only happened in
antibody genes. However, Schatz and colleagues discovered that AID acts
on many other genes in B cells, including genes linked to lymphatic and
other types of cancer.
Schatz indicated that the research team was surprised when learning
that, "most of these non-antibody genes do not accumulate mutations
because the repair, for whatever reason, is precise, not sloppy." This
means that researchers who study lymphatic cancer must understand both
the original mutations and the repair process.
"If the precise, or high fidelity, repair processes break down, this
would unleash the full mutagenic potential of the initial mutation,
resulting in changes in many important genes," Schatz reports. "We
hypothesize that exactly this sort of breakdown of the repair processes
occurs in the early stages of the development of B cell tumors."
Nature: doi:10.1038
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Here to View Journal Website
Written by: Peter M Crosta
Copyright: Start Sanatate
Not to be reproduced without permission of Start Sanatate
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