In a Dutch study presented at the European Cancer Congress
this week, researchers examined data from 999 colon cancer patients whose
medical records showed they had been regular users of aspirin and had survived
colon cancer. Specifically they were looking at differences in three proteins
among tissue samples taken from the patients. The proteins were HLA-1, COX-2
and PIK3CA.
HLA proteins are the “ID” badges
that tell the immune system which cells belong to the body and which are
foreign. COX-2 is an enzyme that is produced in inflammatory responses, and
PIK3CA is a gene that is mutated in many cancers.
They found a couple of interesting things. First people
whose colon tumors produced HLA-1 and who took low doses of aspirin had 47
percent better survival. On the other hand, aspirin use did not correlate with
survival in tumors showing high levels of either COX-2 or PI3KA. Just as
importantly, patients whose tumors did not produce
HLA-1 protein gained no added survival benefit from aspirin therapy.
They concluded that aspirin’s protective effect is related
to platelet action in colon cancer. Platelets are the blood cells that clump
together to form clots to prevent bleeding. Aspirin tends to interfere with that
clumping action. Researchers think HLA-1 positive colon cancer cells may use
platelets in some way to travel or metastasize to other parts of the body. It
may be that aspirin disrupts that ability of tumor cells to interact with
platelets and thereby reduces metastatic cancer.
In most cancers, once metastasis occurs the cancer becomes
incurable. The implication of this study, if proven correct, is that metastasis
may occur, in part, by way of the tumor’s ability to figuratively use “fake ID”
to elude the body’s immune system, and aspirin may be able to show us how to
block that and perhaps one day prevent cancers from traveling to distant parts
of the body.
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