HOME ABOUT CONTACT AVAILABLE ISSUES SUBSCRIBE MEDIA & ADS
LATEST UPDATES » Vol 22, No 06, June 2018 – Cancer - Therapies and strategies for better patient outcomes       » Gardasil 9 supply running short in Hong Kong       » China helps Tajikistan tackle grassland degradation       » Immuno-oncology trials in China surge more than 50 per cent       » Yeast for industrial biotechnology       » Uncontrolled hypertension in rural communities      
BIOBOARD - UNITED STATES
Study reveals how a protein common in cancers jumps anti-tumor mechanisms

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 add to the understanding of cancer development and provide a basis for potentially new targeted methods to prevent and treat cancer.

In the study, 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.

Click here for the complete issue.

NEWS CRUNCH  
news Shire, Microsoft and EURORDIS form Global Commission to accelerate time to diagnosis for children with rare diseases
news EmTech Asia explores future of life, humanity and economy
news Biology of Ageing II - Impactful Interventions
PR NEWSWIRE  
Asia Pacific Biotech News
EDITORS' CHOICE  
COLUMNS  
Click here to receive APBN e-newsletters once a month!

APBN Editorial Calendar 2018
January:
Obesity / Outlook for 2018
February:
Searching for the fountain of youth
March:
Women in Science - Making a difference
April:
Digestive health in the 21st century - Trust your guts
May:
Dental health - The root to good health
June:
Cancer - Therapies and strategies for better patient outcomes
July:
Water management / Vaccination
August:
Regenerative medicine / Biotech start ups
September:
Digital healthcare / 3D printing
October:
Bones / Breast cancer
November:
Liver health / Top science research nations & institutions
December:
AIDS / Breakthrough of the year/Emerging trends
Editorial calendar is subjected to changes.
MAGAZINE TAGS
About Us
Events
Available issues
Editorial Board
Letters to Editor
Instructions to Authors
Advertise with Us
CONTACT
World Scientific Publishing Co. Pte. Ltd.
5 Toh Tuck Link, Singapore 596224
Tel: 65-6466-5775
Fax: 65-6467-7667
» For Editorial Enquiries:
   biotech_edit@wspc.com or Ms Lim Guan Yu
» For Subscriptions, Advertisements &
   Media Partnerships Enquiries:
   biotech_ad@wspc.com
Copyright© 2018 World Scientific Publishing Co Pte Ltd  •  Privacy Policy