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s a postdoc at the Broad Institute of MIT and Harvard in
2008, cancer biologist Ravid Straussman worked on a collab-
orative effort to screen normal cells for their influence on can-
cer cells’ responses to various anticancer therapies. The project
turned up hundreds of examples of stromal cells—best known for
forming the connective tissues that support organs—somehow con-
ferring drug resistance on their cancerous neighbors in vitro.^1 One
of these cases caught Straussman’s attention: human pancreatic and
colorectal cancer cell lines could evade the chemotherapeutic drug
gemcitabine when cultured with dermal fibroblasts.
In the lab, the cancer cells “continue to proliferate under
therapy,” Straussman explains. “This was really fascinating tome because I didn’t understand... how stromal cells can pro-
tect cancer cells from chemotherapy.”
He spent the next year and a half trying to figure out what was
going on. He ruled out several hypotheses, including that the stro-
mal cells were secreting a protective protein or exosome. “We had
tons of ideas that turned out to be not true,” Straussman says. Then,
he discovered that the fibroblasts he and his colleagues had been using
contained bacteria called Mycoplasma, a common contaminant of tis-
sue and cell cultures. “I was devastated at the time,” he recalls—in pre-
sentations, he has used a photo of a wrecked sedan to depict his reac-
tion to the discovery. “I spent a year and a half, probably, tracing this,
and this is a complete artifact.” He almost trashed the whole project.