Myeloid Leukemia is an aggressive (fast-growing) disease in which too many myeloblasts (immature white blood cells that are not lymphoblasts) are found in the bone marrow and blood. Also called acute myeloblastic leukemia, acute myelogenous leukemia, acute nonlymphocytic leukemia, AML, and ANLL.
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.
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.
Metabolic reprogramming, accepted as a hallmark of cancer, might indicate a vulnerability to be used by targeted cancer therapy.
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.
According to recent research at the University of Guelph, a compound found in avocados may one day lead to improved leukemia treatment.
According to a new study, targeting a pathway that is critical for the survival of some cases of acute myeloid leukemia could open up a new therapeutic route for patients.
The abundant presence of an enzyme known as low molecular weight protein tyrosine phosphatase (LMWPTP) in tumor cells has long been considered an indicator of cancer aggressiveness and metastatic potential.
Knocking out a protein known to stifle T cell activation on CAR T cells using the CRISPR/Cas9 technology enhanced the engineered T cells' ability to eliminate blood cancers, according to new preclinical data from researchers in the Perelman School of Medicine at the University of Pennsylvania and Penn's Abramson Cancer Center.
Scientists have discovered that sodium bicarbonate - also known as baking soda or bicarbonate of soda - can reprogram T cells in leukemia patients to resist the immune-suppressing effects of cancer cells, which can drive leukemia relapse after stem cell transplants.
Scientists have shown that cancer rebuilds the architecture of human chromosomes, which allows the disease to take hold and spread.
A combination regimen of venetoclax and azacitidine was safe and improved overall survival (OS) over azacitidine alone in certain patients with acute myeloid leukemia (AML), according to the Phase III VIALE-A trial led by The University of Texas MD Anderson Cancer Center.