Acute Myeloid Leukemia (AML) is a rapidly progressing cancer of the blood characterized by the uncontrolled proliferation of immature blast cells in the bone marrow. The Leukemia and Lymphoma Society estimates that over 13,000 new cases of AML were diagnosed and approximately 9,000 deaths from AML occurred in the U.S. during 2007. AML is generally a disease of older adults, and the median age of a patient diagnosed with AML is about 67 years. A majority of elderly patients are not considered candidates for standard induction therapy or decline therapy, resulting in an acute need for new treatment options.
Researchers have developed a new method to distinguish between cancerous and healthy stem cells and progenitor cells from samples of patients with acute myeloid leukemia (AML), a disease driven by malignant blood stem cells that have historically been difficult to identify.
Acute myeloid leukemia (AML) is an aggressive blood cancer that causes uncontrolled accumulation of white blood cells. Because of the poor outcomes of this disease, researchers across the globe have been on the hunt for new ways to treat AML, while preserving normal blood development.
Johns Hopkins Medicine scientists say their 20-year study of more than 200 people with premature aging syndromes caused by abnormally short telomeres, or shortened repetitive DNA sequences at the ends of chromosomes, may upend long-held scientific dogma and settle conflicting studies about how and whether short telomeres contribute to cancer risk.
A team of researchers has discovered a potential therapeutic that can synergize with existing drugs to more effectively kill certain leukemia cells.
Pediatric acute myeloid leukemia or pAML is a childhood blood cancer, one that has proved confounding to clinicians and researchers, with a high relapse rate and relatively few identified genetic mutations (compared to the adult version) that might explain its cause.
Researchers at University of California San Diego School of Medicine, Sanford Stem Cell Institute and Moores Cancer Center report that a late-stage, pre-clinical small molecule inhibitor, called rebecsinib, reverses malignant hyper-editing by an inflammation-induced protein isoform, known as ADAR1 p150.
Acute myeloid leukemia (AML) is an aggressive form of cancer that originates in the bone marrow, rapidly spreads to the blood and can quickly cause death if not treated promptly.
The DDX41 gene encodes the nuclear enzyme DEAD-box-type RNA helicase. Hematopoietic malignancies are caused by DDX41 mutations. However, the mechanism behind the development of this malignancy remains unknown.
A groundbreaking study from the Icahn School of Medicine at Mount Sinai found that astronauts are more likely to experience mutations that could be connected to spaceflight and increase their lifetime risk of acquiring cancer and heart disease.
Researchers from Barts Cancer Institute at Queen Mary University of London have identified a way to reverse resistance to a group of cancer drugs, known as kinase inhibitors, in leukemia cells.
A complex network of three-dimensional structures assembles to read, copy and produce the genetic materials required for cellular function, for cells to thrive.
Researchers from The University of Texas MD Anderson Cancer Center discovered that treatment resistance in patients with myelodysplastic syndromes (MDS) is caused by two distinct classes of stem cells and identified possible therapeutic approaches that target these cells.
A group of researchers from UNIGE in Switzerland and Inserm in France has discovered a previously unknown process that could lead to the creation of novel medicines.
There are many different ways in which the genetic material DNA can be damaged, resulting in the development of diseases such as cancer. Certain forms of DNA damage are associated with so-called R-loops.
Acute myeloid leukemia (AML) is an aggressive cancer of white blood cells with few effective targeted therapies available to treat it.
In the late 1980s, scientists developed a revolutionary approach to treating acute myeloid leukemia (AML), a type of blood cancer. Called differentiation therapy, it amounted to a bona fide cure for many patients.
University of Delaware biochemist Jeff Mugridge is trying to figure out how so-called mRNA eraser enzymes work in our cells, why those erasers can sometimes misbehave and lead to cancer, and how science can pave the way for possible solutions to this problem.
Inositol is a sugar required for cells to survive. Most cells either get it from the bloodstream or make it themselves. Since there is plenty of inositol available, some cancer cells decide to stop making it.
Researchers elucidate why certain drugs, in clinical trials, for treating a kind of acute myeloid leukemia often fail and revealed a means to restore their efficacy.
The chemotherapy drug decitabine is commonly used to treat patients with blood cancers, but its response rate is somewhat low. Researchers have now identified why this is the case, opening the door to more personalized cancer therapies for those with these types of cancers, and perhaps further afield.