In the beginning

What developmental biology can teach about cancer

Melissa Marino, Ph.D.
Published: February, 2007

Light microscopic image of a 9.5-day-old mouse embryo.
Courtesy of Richard Behringer, Ph.D., University of Texas M. D. Anderson Cancer Center. Published in Manipulating the Mouse Embryo, 3rd Edition. Copyright 2003, Cold Spring Harbor Laboratory Press.
It could be nature’s cruelest joke—the molecules that give us shape at the beginning of our life also can lead to the end of it.

The genes and proteins that help sculpt a single cell, the fertilized egg, into a complex multicellular organism are also responsible for the birth of many cancers.

This link between embryogenesis and tumorigenesis has been suspected for more than a century, but only within the last 20 years have the striking molecular similarities between these two monumental events come into focus.

“These developmental molecules that cell biologists know and love—our favorite proteins that operate in the early embryo—are the same molecules that seem to go haywire in cancer,” says Jason Jessen, Ph.D., assistant professor of Medicine and Cancer Biology at Vanderbilt University Medical Center.

The rapid and exponential cell division, differentiation and cell movements that characterize embryonic development bear a close resemblance to those involved in tumor initiation and metastasis.

“It does make sense because in the developing embryo, so many things are happening: cell migration, cell specification, cells interacting with each other,” Jessen says. “So, if those proteins get activated in an adult cell, it’s no wonder it can have dire consequences.”

Definitive links between the two processes have been a long time coming, mostly because of the academic divide between the separate cultures of developmental biology and cancer research. Now that divide is beginning to close.

One of the first links between cancer and embryogenesis was made in the early 1980s.

Roel Nusse, Ph.D., and Harold Varmus, M.D., identified a cancer-causing “oncogene,” which they called int-1, in a mouse model of breast cancer. When int-1 is activated or turned on by the “integration” (thus its name) of a mouse mammary tumor virus into its DNA, a tumor forms.

Around the same time, Christiane Nusslein-Volhard, Ph.D., and Eric Weischaus, Ph.D., who were studying development of the fruit fly, Drosophila, found that a gene they called wingless was involved in setting up the polarity of the embryo. When the protein encoded by the gene is defective, the fly fails to develop proper body segment boundaries—and wings.

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