Featured Research

from universities, journals, and other organizations

Protein common in cancers jumps anti-tumor mechanisms

Date:
March 17, 2014
Source:
Stony Brook Medicine
Summary:
A cellular protein, STAT3, which is overactive in a majority of cancers, interferes with an antitumor mechanism in cells and therefore promotes the growth of cancer, an international research team has discovered. The researchers made their discovery by using the Epstein-Barr virus (EBV) as a tool to probe fundamental cancer development-related questions. EBV, which causes infectious mononucleosis, is carried by approximately 95 percent of the world's population, is implicated in several types of lymphoma and other cancers, and was the first virus identified to cause cancer in humans.

A Stony Brook University-led international team of infectious disease researchers have discovered how a cellular protein, called STAT3, which is overactive in a majority of human cancers, interferes with an antitumor mechanism in cells and therefore promotes the growth of cancer. The findings, to be published this week in the Proceedings of the National Academy of Sciences (PNAS) add to the understanding of cancer development and provide a basis for potentially new targeted methods to prevent and treat cancer.

In the paper, titled "STAT3 interrupts ATR-Chk1 signaling to allow oncovirus-mediated cell proliferation," lead author Sumita Bhaduri-McIntosh, MD, PhD, and colleagues made their discovery by using the Epstein-Barr virus (EBV) as a tool to probe fundamental cancer development-related questions. EBV, which causes infectious mononucleosis, is carried by approximately 95 percent of the world's population, is implicated in several types of lymphoma and other cancers, and was the first virus identified to cause cancer in humans.

"Our findings add to the short list of known mechanisms by which a key cellular anti-tumor barrier is breached by STAT3 prior to cancer development," said Dr. Bhaduri-McIntosh, an Assistant Professor in the Departments of Pediatrics and Molecular Genetics and Microbiology at Stony Brook University School of Medicine and pediatric infectious diseases specialist at Stony Brook Children's Hospital. "Because STAT3 interferes with this innate anti-tumor mechanism in cells, the opposite occurs when blood cells are infected in the lab with the cancer-causing virus EBV, and the cells continue to divide -- a necessary step in cancer development."

More specifically, Dr. Bhaduri-McIntosh explained that STAT3 damages a cancer-suppressing cellular activity called the DNA damage response (DDR). Normally this response pauses cell division allowing for repair of damaged DNA. This new study shows that EBV not only causes DNA damage when it infects and replicates in cells, but it also very quickly turns up a cellular protein, STAT3, which starts a chain reaction leading to a loss of this pause in cell division thereby promoting cell proliferation. This in combination with other pro-proliferative effects of the virus can lead to cancer.

Previous research has identified both STAT3 and another protein Chk1 as potential targets for cancer therapeutics. The authors write that their research results add fresh insight to anticancer drug development because they "provide a mechanistic link between the two, further lending support to these approaches."

Dr. Bhaduri-McIntosh emphasized that because STAT3 is involved in most cancers, their findings could potentially impact the prevention or treatment of several types of cancer -- something that her lab is investigating. In addition to uncovering more about EBV-mediated cancers, the research is simultaneously helping the team to better understand EBV infections.


Story Source:

The above story is based on materials provided by Stony Brook Medicine. Note: Materials may be edited for content and length.


Journal Reference:

  1. Siva Koganti, Joyce Hui-Yuen, Shane Mcallister, Benjamin Gardner, Friedrich Grasser, Umaimainthan Palendira, Stuart G. Tangye, Alexandra F. Freeman, and Sumita Bhaduri-Mcintosh. STAT3 interrupts ATR-Chk1 signaling to allow oncovirus-mediated cell proliferation. PNAS, March 2014 DOI: 10.1073/pnas.1400683111

Cite This Page:

Stony Brook Medicine. "Protein common in cancers jumps anti-tumor mechanisms." ScienceDaily. ScienceDaily, 17 March 2014. <www.sciencedaily.com/releases/2014/03/140317155203.htm>.
Stony Brook Medicine. (2014, March 17). Protein common in cancers jumps anti-tumor mechanisms. ScienceDaily. Retrieved September 1, 2014 from www.sciencedaily.com/releases/2014/03/140317155203.htm
Stony Brook Medicine. "Protein common in cancers jumps anti-tumor mechanisms." ScienceDaily. www.sciencedaily.com/releases/2014/03/140317155203.htm (accessed September 1, 2014).

Share This




More Health & Medicine News

Monday, September 1, 2014

Featured Research

from universities, journals, and other organizations


Featured Videos

from AP, Reuters, AFP, and other news services

We've Got Mites Living In Our Faces And So Do You

We've Got Mites Living In Our Faces And So Do You

Newsy (Aug. 30, 2014) A new study suggests 100 percent of adult humans (those over 18 years of age) have Demodex mites living in their faces. Video provided by Newsy
Powered by NewsLook.com
Liberia Continues Fight Against Ebola

Liberia Continues Fight Against Ebola

AFP (Aug. 30, 2014) Authorities in Liberia try to stem the spread of the Ebola epidemic by raising awareness and setting up sanitation units for people to wash their hands. Duration: 00:41 Video provided by AFP
Powered by NewsLook.com
California Passes 'yes-Means-Yes' Campus Sexual Assault Bill

California Passes 'yes-Means-Yes' Campus Sexual Assault Bill

Reuters - US Online Video (Aug. 30, 2014) California lawmakers pass a bill requiring universities to adopt "affirmative consent" language in their definitions of consensual sex, part of a nationwide drive to curb sexual assault on campuses. Linda So reports. Video provided by Reuters
Powered by NewsLook.com
New Drug Could Reduce Cardiovascular Deaths

New Drug Could Reduce Cardiovascular Deaths

Newsy (Aug. 30, 2014) The new drug from Novartis could reduce cardiovascular deaths by 20 percent compared to other similar drugs. Video provided by Newsy
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