Hutch News Stories

The Myc monopoly

Eisenman, Hockenbery labs find new roles for long-studied protein that ultimately may help researchers counter its cancerous effects
Dr. Fionnuala Morrish
Dr. Fionnuala Morrish, staff scientist in the Hockenbery lab, pipets serum into a culture of growing cells. She studies the role of the protein Myc in programmed cell death. Photo by Todd McNaught

In the software industry, a company that quashes competition in the Web-browser market risks a lawsuit for unfair business practices.

But no antitrust laws regulate the commerce within a human cell, wherein a few molecular tycoons monopolize the networks crucial for normal growth.

Chief among these cellular moguls is Myc, a protein best known for its role as a key driver of many types of tumors when produced in overabundance.

Now, more than 25 years after its discovery, scientists increasingly recognize that Myc's central role in cancer results from its CEO-like status in an astonishing variety of biological enterprises.

Ramped-up cell growth

New studies from the laboratories of Dr. Robert Eisenman, an investigator in the Basic Sciences Division, and Dr. David Hockenbery, of the Clinical Research and Human Biology divisions, identify Myc as central to development of the nervous system in mice, clarify Myc's role in a process known as programmed cell death and shed new light on how Myc ramps up cell growth.

The discoveries ultimately may help researchers devise strategies to counter the cancerous effects of Myc when its normal activities are disrupted.

Most intriguing to Eisenman, who has made Myc his livelihood for more than 20 years, is that these additions to Myc's already impressive repertoire of activities underscore the protein's profound connection to cancer.

"Myc comes up again and again in tumor pathways of many different cell types, ranging from colon carcinomas to neuroblastomas to lymphomas," he said.

"This says that it has a fundamental role to play in the control of normal and abnormal cell functions, and we are slowly beginning to see how that function is manifested. That's really exciting."

Hitchhiker genes

Scientists first identified Myc as a cancer-causing gene (called myelocytoma), in a virus that infects birds. Later studies revealed that Myc and other so-called viral oncogenes that cause tumors are actually normal cellular genes acquired by certain types of viruses during the course of infection. When such viruses infect a new cell, the hitchhiker genes may be expressed aberrantly, leading to cancer.

A family of related Myc proteins has since been discovered in organisms ranging from fruit flies to mice to humans. Though essential for life when produced at normal levels, excess Myc propels cells into overdrive.

Twenty years ago, Eisenman's lab showed that the Myc protein functions inside the nucleus of a cell, where genes are housed. Later, the lab found that Myc teams with two other proteins to switch on or off a network of genes that control cell division.

Increase in cell size

More recently, in collaboration with Dr. Bruce Edgar's lab, Eisenman's group demonstrated that Myc plays a role in cell growth, a process that is distinct from - but often confused with - cell division. True cell growth refers to an increase in cell size or mass.

Other studies, led by Dr. Gerard Evan, now at the University of California at San Francisco, revealed a role for Myc in a process known as programmed cell death. In this essential biological process, which is under study in Hockenbery's lab, cells deliberately engineer their own destruction, either because they are abnormal - due, for example, to overproduction of Myc - or because their elimination is required at a particular time during animal development.

Three center studies shed light on Myc's management strategy for these and other cell processes.

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