thescientist | Fusobacterium nucleatum is a Gram-negative oral commensal
microbe, but it has the potential to become pathogenic, occasionally
causing periodontal disease. In October 2011, two separate teams
from Canada’s BC Cancer Agency and the Broad Institute in Cambridge
showed that the bacterium could also be found in the gut, where its
abundance was associated with colorectal cancer. Now, two new studies
present functional evidence to help explain how F. nucleatum spurs the development of cancer.
In papers published in Cell Host & Microbe today (August
13), teams led by Harvard Medical School’s Aleksandar Kostic and Case
Western Reserve University’s Mara Roxana Rubinstein used a mouse model
of intestinal tumorigenesis and human colon cancer cells, respectively,
to show that F. nucleatum induces proinflammatory and oncogenic activities that promote the growth of colorectal cancer.
“It is usually impossible to infer whether microbes are causative or
opportunistic colonizers without functional studies,” said Robert Holt, who led the BC Cancer Agency team that in 2011 reported an association between F. nucleatum
in the gut and colorectal cancer but was not involved in the present
studies. “Identifying an infectious origin for disease almost always
starts with observing an association between the presence of a microbe
and the presence of a particular pathology, but an understanding of
causality—or lack thereof—requires the gradual accumulation of
experimental and epidemiological evidence,” such as that reported today.
The Washington University School of Medicine’s Gautam Dantas
agreed that the new work helps distinguish cause from consequence. “Is
an observed altered microbiome state in a diseased individual the cause
of the disease, or a symptom?” Dantas, who was not involved in the
studies, wrote in an e-mail to The Scientist. The papers
published today “report on significant strides towards . . . identifying
the mechanisms by which a human commensal bacterium, Fusobacterium nucleatum, promotes colorectal cancer.”
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