Featured Research

from universities, journals, and other organizations

Paradoxical Gene Suppresses Tumors Yet Makes Them Grow

Date:
September 25, 1998
Source:
University Of North Carolina Medical Center
Summary:
Scientists at the University of North Carolina at Chapel Hill have found that a gene discovered earlier in the decade has paradoxical properties -- it helps bring about tumor cell death yet is also necessary for their growth. The new study highlights an important molecular mechanism in the evolution of tumors and could lead to new anti-cancer drugs targeted to a specific gene.

CHAPEL HILL,NC -- Scientists at the University of North Carolina at Chapel Hill have found that a gene discovered earlier in the decade has paradoxical properties -- it helps bring about tumor cell death yet is also necessary for their growth. The new study highlights an important molecular mechanism in the evolution of tumors and could lead to new anti-cancer drugs targeted to a specific gene.

A report published in the Sept. 24 issue of Molecular Cell focuses on the gene E2F1, a cell cycle regulating molecule first identified in 1992. On the molecular chain of events leading to tumor formation and growth, E2F1 exerts its action "upstream" of the tumor suppressor gene known to researchers as p53, according to the new study.

Study senior author Dr. Terry Van Dyke, professor of biochemistry and biophysics at UNC-CH School of Medicine, says E2F1 apparently prompts p53 to defend against developing tumors: apoptosis ? programmed cell death. The study examined mice that had been genetically engineered in Van Dyke?s laboratory to develop a type of cancerous brain tumor that occurs rarely in people. Some of these "transgenic" mice were selectively bred not to have E2F1.

"We found that cell death was diminished by 80 percent in the tumors of animals without E2F1," Van Dyke says.

But the researcher and her colleagues also discovered that without E2F1 the growth of brain tumors slowed considerably, even though the rate of tumor cell death had dropped sharply.

"This was surprising. Although p53 cell death drops because E2F1 is not there to induce it, tumor growth does not accelerate," Van Dyke says. "And the reason the growth rate is not accelerated, we discovered, is that E2F1 is required also for proliferation of the tumor cells."

Thus E2F1 is a kind of molecular paradox. Not only does it help suppress tumors, its presence is also needed for tumor growth. Moreover, unlike p53, which is absent in about half of cancers, E2F1is not deleted from cells, normal or cancerous.

As a result, Van Dyke says E2F1 may be "an appropriate target" for drug therapy specifically aimed at inhibiting tumor growth by shutting down the gene. "E2F1, at least in the mouse, is dispensable for all normal cell cycles. The mouse is fine without it," the Carolina researcher says. "E2F1-deficient mice develop normally and live long lives."

The study authors say it will be important to determine if E2F1 is required for tumor cell proliferation in diverse tumor types. Van Dyke, a member of the UNC Center for Molecular Biology and Biochemistry and of the Lineberger Comprehensive Cancer Center, says her Carolina laboratory is extending studies to other tumors, including glioma, a more common brain tumor. Her laboratory already has created a transgenic animal model for lymphoma. In development are animal models for cancers of the breast and prostate and for glioblastoma, also a brain tumor.

"Cancer is not one disease but many," she adds. "We really have to understand the individual events that could happen in a given type of tumor that could lead to changes in the cell that eventually lead to cancer."

Along with Dr. Van Dyke, UNC-CH co-authors of the report are Dr. Huichin Pan and Dr. Chaoying Yin. Other collaborators include Drs. Nicholas J. Dyson, Ed Harlow, and Lili Yamasaki of Massachusetts General Hospital Cancer Center, Charlestown, Mass.


Story Source:

The above story is based on materials provided by University Of North Carolina Medical Center. Note: Materials may be edited for content and length.


Cite This Page:

University Of North Carolina Medical Center. "Paradoxical Gene Suppresses Tumors Yet Makes Them Grow." ScienceDaily. ScienceDaily, 25 September 1998. <www.sciencedaily.com/releases/1998/09/980925025118.htm>.
University Of North Carolina Medical Center. (1998, September 25). Paradoxical Gene Suppresses Tumors Yet Makes Them Grow. ScienceDaily. Retrieved September 2, 2014 from www.sciencedaily.com/releases/1998/09/980925025118.htm
University Of North Carolina Medical Center. "Paradoxical Gene Suppresses Tumors Yet Makes Them Grow." ScienceDaily. www.sciencedaily.com/releases/1998/09/980925025118.htm (accessed September 2, 2014).

Share This




More Health & Medicine News

Tuesday, September 2, 2014

Featured Research

from universities, journals, and other organizations


Featured Videos

from AP, Reuters, AFP, and other news services

Snack Attack: Study Says Action Movies Make You Snack More

Snack Attack: Study Says Action Movies Make You Snack More

Newsy (Sep. 2, 2014) You're more likely to gain weight while watching action flicks than you are watching other types of programming, says a new study published in JAMA. Video provided by Newsy
Powered by NewsLook.com
U.N. Says Ebola Travel Restrictions Will Cause Food Shortage

U.N. Says Ebola Travel Restrictions Will Cause Food Shortage

Newsy (Sep. 2, 2014) The U.N. says the problem is two-fold — quarantine zones and travel restrictions are limiting the movement of both people and food. Video provided by Newsy
Powered by NewsLook.com
Doctors Fear They're Losing Battle Against Ebola

Doctors Fear They're Losing Battle Against Ebola

AP (Sep. 2, 2014) As a third American missionary is confirmed to have contracted Ebola in Liberia, doctors on the ground in West Africa fear they're losing the battle against the outbreak. (Sept. 2) Video provided by AP
Powered by NewsLook.com
Tech Giants Bet on 3D Headsets for Gaming, Healthcare

Tech Giants Bet on 3D Headsets for Gaming, Healthcare

AFP (Sep. 2, 2014) When Facebook acquired the virtual reality hardware developer Oculus VR in March for $2 billion, CEO Mark Zuckerberg hailed the firm's technology as "a new communication platform." Duration: 02:24 Video provided by AFP
Powered by NewsLook.com

Search ScienceDaily

Number of stories in archives: 140,361

Find with keyword(s):
Enter a keyword or phrase to search ScienceDaily for related topics and research stories.

Save/Print:
Share:

Breaking News:
from the past week

In Other News

... from NewsDaily.com

Science News

Health News

Environment News

Technology News



Save/Print:
Share:

Free Subscriptions


Get the latest science news with ScienceDaily's free email newsletters, updated daily and weekly. Or view hourly updated newsfeeds in your RSS reader:

Get Social & Mobile


Keep up to date with the latest news from ScienceDaily via social networks and mobile apps:

Have Feedback?


Tell us what you think of ScienceDaily -- we welcome both positive and negative comments. Have any problems using the site? Questions?
Mobile: iPhone Android Web
Follow: Facebook Twitter Google+
Subscribe: RSS Feeds Email Newsletters
Latest Headlines Health & Medicine Mind & Brain Space & Time Matter & Energy Computers & Math Plants & Animals Earth & Climate Fossils & Ruins