Opening the door to the cause of myeloid leukemia: Finding the targets of common mutation
2015-07-23
(Press-News.org) Researchers at the University of Birmingham have made a breakthrough in understanding how mutated genes in leukaemia reprogram blood stem cells and send them spiralling out of control.
The findings help to explain the early development of leukaemia, representing the essential first step to developing new treatments for patients based on these findings.
A study, published in Cell Reports by Professors Peter Cockerill and Constanze Bonifer, investigated the role of one specific mutation in the FLT3 gene found in acute myeloid leukaemia (AML).
AML is diagnosed in around 2,400 people in the UK each year. While younger patients have a better prognosis, overall survival rates are very poor and new treatments are needed.
FLT3 is a protein that normally makes sure that blood stem cells produce just the right number of blood cells every day. When it gets mutated it sends the wrong signals and keeps the stem cells expanding out of control, swamping the body with abnormal blood cells.
Professor Peter Cockerill, of the University of Birmingham, explained: "We found that the mutated FLT3 protein always sends the same signals to the same set of genes in all AML patients that have this mutation. By finding out which signals and genes are the targets, we now have new targets that will allow us to attack this pathway."
The team found that the mutated FLT3 protein used one specific signalling pathway inside the cell to activate over 1,000 different targets within the DNA, leading to the abnormal activation of over 100 genes in patients who have this mutation. Many of these genes were already known to contribute to cancer by sending growth signals.
The project was funded by Leukaemia and Lymphoma Research. Dr Matt Kaiser, Head of Research at Leukaemia & Lymphoma Research, said: "Unfortunately there have been no significant improvements in survival rates for acute myeloid leukaemia in the last two decades. These findings provide renewed hope for developing new treatments for this aggressive type of leukaemia."
INFORMATION:
ELSE PRESS RELEASES FROM THIS DATE:
2015-07-23
Researchers add a new twist to the more than century old biological principles of Mendelian inheritance - describing a small group of cells in pregnant mothers that promote genetic fitness and multi-generational reproductive health.
Scientists at Cincinnati Children's Hospital Medical Center report their findings online July 23 in Cell. The study suggests a scientific basis for developing new therapies to promote reproductive health and prevent pregnancy complications like prematurity and stillbirth, according to Sing Sing Way, MD, PhD, senior author and pediatrician ...
2015-07-23
When does aging really begin? Two Northwestern University scientists now have a molecular clue. In a study of the transparent roundworm C. elegans, they found that adult cells abruptly begin their downhill slide when an animal reaches reproductive maturity.
A genetic switch starts the aging process by turning off cell stress responses that protect the cell by keeping important proteins folded and functional. The switch is thrown by germline stem cells in early adulthood, after the animal starts to reproduce, ensuring its line will live on.
While the studies were conducted ...
2015-07-23
Highly-social zebra finches learn foraging skills from their parents. However, new research has found that when juvenile finches are exposed to elevated stress hormones just after hatching, they will later switch strategies and learn only from unrelated adult birds - ignoring their parents' way of doing things and instead gaining foraging skills from the wider network of other adult finches.
Researchers say that spikes in stress during early development may act as a cue that their parents are doing something wrong, triggering the young birds to switch their social learning ...
2015-07-23
If you find yourself downing that extra piece of chocolate fudge cake even though you're not hungry, it might be the absence of a hormone in your brain that's causing you to overeat purely for pleasure.
In a new Rutgers Robert Wood Johnson Medical School study published in Cell Reports, researchers found that when the hormone glucagon like peptide-1 (GLP-1) was reduced in the central nervous system of laboratory mice, they overate and consumed more high fat food.
"The mice in which the GLP-1 deficiency was induced ate beyond the need for calories and showed an increase ...
2015-07-23
A new study by researchers at University of California, San Diego School of Medicine reveals a protein's critical - and previously unknown -- role in the development and progression of acute myeloid leukemia (AML), a fast-growing and extremely difficult-to-treat blood cancer.
The finding offers a novel target for better treating AML, and possibly other cancers, by cutting off the ability of tumors to access nearby cellular players that feed its growth. The study was published July 23 in Cell Stem Cell.
"The work really focuses on trying to understand the dependence ...
2015-07-23
Alexandria, VA - EARTH Magazine takes you to Le Mans, France, to cover how the World Endurance Competition (WEC) race series is transforming automotive efficiency in both high-performance racing and the commercial automotive industries. EARTH's latest feature explores the science behind efficiency upgrades used by three major racing competitors: Porsche, Audi and Toyota.
Using physics and cutting-edge materials results in a "fascinating case study of how unbridled competition can produce unique, innovative and extraordinary solutions to engineering barriers once thought ...
2015-07-23
CHAPEL HILL, NC (July 23, 2015) - For years, a crisis has been brewing in molecular biology. The problem is that antibodies--research tools used to identify key proteins at work in a cell--aren't always what they seem. Unreliable antibodies have led to numerous instances of false findings, failed experiments, and wasted money and samples.
Enter the Histone Antibody Specificity Database, a newly launched online portal that lets scientists find the right antibodies for their research with a much higher degree of confidence than ever before. Rather than relying on the claims ...
2015-07-23
It's well known that being socially connected promotes a person's overall and psychological health. A new study from the University of Rochester now shows that the quantity of social interactions a person has at 20--and the quality of social relationships that person has at age 30--can benefit her well-being later in life.
People with poor social connections have been shown to be at an increased risk for early mortality. "In fact," said lead author Cheryl Carmichael, who conducted the research as a PhD candidate in psychology at the University of Rochester, "having ...
2015-07-23
Astronomers using the Karl G. Jansky Very Large Array (VLA) have discovered jets of material ejected by still-forming young brown dwarfs. The discovery is the first direct evidence that brown dwarfs, intermediate in mass between stars and planets, are produced by a scaled-down version of the same process that produces stars.
The astronomers studied a sample of still-forming brown dwarfs in a star-forming region some 450 light-years from Earth in the constellation Taurus, and found that four of them have the type of jets emitted by more-massive stars during their formation. ...
2015-07-23
Chemotherapy for patients with end-stage cancer was associated with worse quality of life near death for patients with a good ability to still perform many life functions, according to an article published online by JAMA Oncology.
Physicians have voiced concerns about the benefits of chemotherapy for patients with cancer who are nearing death. An American Society of Clinical Oncology (ASCO) expert panel has called chemotherapy use among patients for whom there was no evidence of clinical value the most widespread, wasteful and unnecessary practice in oncology.
Holly ...
LAST 30 PRESS RELEASES:
[Press-News.org] Opening the door to the cause of myeloid leukemia: Finding the targets of common mutation
