Articles tagged with Myeloid Leukemia
St. Jude Children's Research Hospital scientists have found that survival of a deadly acute myeloid leukemia depends on production of heme, a molecular 'battery.' Researchers discovered that blocking heme synthesis kills leukemic cells, offering a potential new treatment strategy for AML.
Researchers identified a protein called galectin-9 that prevents the immune system from killing cancerous blood cells. This discovery paves the way for new biomarkers and potential targets for AML immune therapy.
Stem-cell researchers have identified two distinct populations of leukemia stem cells that can lead to relapse in AML. The study, published in Nature, provides new insights into the cell types fated to relapse and may help accelerate the development of targeted therapies.
A study found that only 9% of patients with Acute Myeloid Leukemia (AML) received the recommended seven genetic tests, highlighting a significant gap in adherence to guidelines. The CONNECT registry data also showed varying rates of compliance among different patient groups, including age and insurance status.
Researchers have identified BCAT1 as a key protein in aggressive leukemia cells that can produce branched-chain amino acids for cell growth. By blocking this protein, they were able to promote differentiation and make the disease less aggressive, suggesting BCAT1 as an ideal therapeutic target.
Researchers at UT Health San Antonio have discovered epigenetic changes that contribute to one-fifth of acute myeloid leukemia cases and a large majority of low-grade gliomas. These changes may be targeted by an existing drug, improving survival rates for patients.
The RICMAC trial found that dose-reduced conditioning followed by allogeneic stem cell transplantation improved overall and relapse-free survival for patients with myelodysplastic syndrome. Engraftment rates were comparable between the two groups, with higher non-relapse mortality after standard conditioning.
Researchers found reduced proliferation capacity and increased rates of cell death in MSCs from patients with acute myeloid leukemia at diagnosis. These alterations may play a role in the development of leukemia, according to the study published in Stem Cells and Development.
A recent analysis of data from a critical epidemiological study found no association between formaldehyde exposure and acute myeloid leukemia. The study's findings contradict previous studies that reported associations between formaldehyde exposure and certain types of leukemia.
Researchers at Fred Hutchinson Cancer Center are developing T-cell therapies for a type of acute myeloid leukemia. They aim to create targeted immunotherapy that recognizes and kills cancer-specific proteins within the cell.
Researchers at Ohio State University Wexner Medical Center correlated gene mutations with acute myeloid leukemia (AML) subgroups, identifying key mutational features and potentially important genetic differences among the subgroups. The study's findings may help guide mutation testing and treatment decisions in AML patients.
A recent study at MD Anderson Cancer Center found that a protein called ENL plays a key role in acute myeloid leukemia (AML), a fast-growing cancer of bone marrow and blood cells. Depletion of ENL led to anti-leukemic effects, suggesting BET inhibitor drugs as a potential treatment for AML.
Researchers at Rockefeller University Press discovered that tumor suppressor protein RUNX1 can promote AML in some cases, particularly when combined with mutant FLT3. Targeting RUNX1 may be an effective treatment for certain AML patients, potentially offering a promising therapeutic strategy.
Researchers developed a computer machine-learning model that accurately predicts which AML patients will go into remission following treatment. The model was trained using bone marrow data and medical histories of AML patients, achieving 100% accurate predictions for remission and 90% accurate predictions for relapse.
A study led by NYU Langone researchers identified CD99, a protein-sugar molecule, as a potential therapeutic target for blood stem cell cancers like acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS). Antibodies against CD99 can selectively kill cancer stem cells while sparing normal blood stem cells.
The European LeukemiaNet has released updated guidelines for the diagnosis and treatment of acute myeloid leukemia (AML) in adults, including revised genetic categories and a proposed response category based on minimal residual disease status. These recommendations aim to improve patient outcomes and harmonize clinical trials.
A study published in Nature Genetics has shown that a knowledge bank of patient data can be used to predict the best treatment option for people with acute myeloid leukaemia (AML). The tool takes into account individual genetic features, treatment schedule, and outcome, enabling therapeutic choices to become personalised. This approach...
Researchers from Goethe University Frankfurt discovered a novel biomarker, SAMHD1, that enables accurate prediction of therapy responders and non-responders in acute myeloid leukaemia (AML) patients. This biomarker can guide cytarabine-based chemotherapies to only those patients likely to respond, sparing others from toxic side effects.
A personalized cancer vaccine significantly improved outcomes for patients with acute myeloid leukemia (AML) in a clinical trial, showing protection from relapse in most patients and minimal side effects. The vaccine stimulated powerful immune responses against AML cells, using the body's own defense systems to fight cancer.
A new 17-gene signature derived from leukemia stem cells can predict AML patients' response to standard treatment, enabling clinicians to tailor treatment and improve patient care. The LSC17 score has been shown to accurately identify high-risk patients who are less likely to be cured by standard therapy.
A Phase IB/II study found that combining nivolumab with azacitidine improved response rates (34%) and overall survival (9.3 months) in patients with acute myeloid leukemia, compared to a historic response rate of 12-15% with azacitidine alone.
High-risk acute myeloid leukemia (AML) patients can live longer with quicker identification and transplantation. Researchers found that rapidly identifying genetic mutations and matching donors increased two-year survival rates from 22% to 45%. The streamlined approach could establish a new standard of care for these patients.
Patients with acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) who were initially ineligible for clinical trials due to existing medical conditions responded well to treatment with azacitidine (AZA) and vorinostat. Sixty-day survival rates were 83% and 79% respectively, with low-grade gastrointestinal side effects reported.
CPX-351 significantly improved 100-day mortality rates and overall survival in older untreated secondary AML patients receiving hematopoietic cell transplants. The treatment also demonstrated better median overall survival compared to standard 7+3 cytarabine and daunorubicin therapy.
Researchers found that AML patients with TP53 mutations respond to milder chemotherapy drug decitabine, achieving remission and median survival over a year. The study suggests using targeted therapy for younger patients carrying the mutation.
The American Society of Hematology has partnered with several organizations to create a specialized curriculum for acute myeloid leukemia (AML) care. The program aims to address knowledge gaps in the entire multidisciplinary team involved in AML management, including accurate diagnosis, risk stratification, and treatment options.
A novel therapeutic target and treatment strategy for acute myeloid leukemia (AML) have been discovered, using a small molecule drug to block fructose utilization. This approach shows dramatic therapeutic benefit for AML treatment, improving patient outcomes.
Researchers discovered CD98 promotes AML, a type of aggressive cancer, and inhibiting it with the anti-CD98 antibody IGN523 blocks AML growth in patient-derived cells and mouse models.
Researchers at MUSC Hollings Cancer Center discover a mechanism conferring resistance to AML drugs and develop a ceramide-based therapeutic that reactivates mitophagy, killing drug-resistant cancer cells. The treatment has clinical appeal due to its specificity towards cancer cells.
Researchers used CRISPR to identify genes essential for AML cell survival, including the novel KAT2A gene. Inhibition of KAT2A destroys AML cells while sparing healthy blood cells in laboratory and mouse studies, offering new potential treatment options.
Researchers found that combining FLT3 inhibition with drugs inducing oxidative stress improves efficacy against acute myeloid leukemia (AML). This approach, which targets genes involved in antioxidant response, shows promise for combination therapy.
Researchers at Massachusetts General Hospital have identified a promising new approach to treating acute myeloid leukemia by inhibiting the enzyme DHODH, which promotes blood cell differentiation. This inhibition prompts the differentiation of leukemic cells, reducing their number and ability to propagate cancer.
Researchers discovered a combination of two inhibitor drugs that can stop CML completely and significantly lower treatment costs. The study, published in Science Translational Medicine, found encouraging response and cure rates for both chronic phase and blast crisis, offering new hope for patients.
Researchers developed an assay to identify chemotherapy-resistant cells in acute myeloid leukemia (AML) tumors. The least sensitive cells can predict a patient's response to chemotherapy, improving therapeutic outcomes.
Researchers discovered that supplementing an epigenetic cancer drug with vitamin C enhances its ability to impede cancer cell growth and trigger cellular self-destruction. The therapy combines azacitidine with vitamin C, addressing a common deficiency in cancer patients. If successful, the approach may improve the existing therapy for ...
A team of researchers from TUM has identified a molecular signaling pathway for programmed cell death that is suppressed in leukemia cells. This discovery offers new insights into the mechanisms underlying cancer progression and may lead to targeted treatment options.
JAX researchers found a precise way to identify the kind of cell that leads to a given case of leukemia through whole-genome profiling of open chromatin. This approach may provide insight into tumor subtypes and possibly diagnostic and therapeutic benefits.
A study found that adults with acute leukemia had a significantly higher risk of death if they lived in certain North Carolina regions with limited healthcare resources. Researchers analyzed data from 2003 to 2009 and found that patients in these areas were more likely to die, even after controlling for other factors.
Researchers at UNC Lineberger Comprehensive Cancer Center have discovered how a faulty genetic instruction drives the development of acute myeloid leukemia (AML) in adults. A mutation in the DNMT3A gene gives normal cells faulty instructions, leading to immature blood cells that can become cancerous.
Researchers identified a lymphatic endothelium origin for angiomyolipoma and lymphangioleiomyomatosis, two related tumors with previously unknown cellular origins. The study suggests a potential novel origin for LAM mechanistically dependent upon TSC inactivation as well.
Scientists identified 11 major groups of AML, each with unique genetic changes driving the disease. The study's findings improve diagnosis and treatment for young AML patients by predicting survival rates based on genetic complexity.
Researchers at the University of Chicago have developed a novel immunotherapy approach that activates the STING pathway, which has shown promising results in treating acute myeloid leukemia (AML) in animal models.
Researchers discovered a new way to kill rapidly multiplying cancer cells using necroptosis, an alternative form of cell death. This approach may lead to more effective treatments for patients with acute myeloid leukaemia (AML) who have resisted traditional therapies.
A novel therapeutic approach has been discovered using a breast cancer drug to treat acute myeloid leukemia (AML) patients with FLT3 mutations. The compound blocks the production of the FLT3 gene and subsequently downregulates its activity, leading to the death of cancer cells.
Acute myeloid leukemia researchers have identified a microRNA pathway that could lead to new targets for treatment. The study found that miR-22 is down-regulated in AML, leading to the development of cancer-causing genes and pathways. This discovery offers hope for developing effective therapies against this deadly disease.
A pediatric oncologist at The Children's Hospital of Philadelphia has received a $1 million grant to develop new treatments for acute myeloid leukemia (AML) through immunotherapy. The goal is to identify specific proteins on AML cells that can be targeted by the immune system.
Researchers have developed a novel mouse model of acute myeloid leukemia, offering a new tool for understanding the disease and identifying potential therapeutic targets. The model has revealed insights into the genetic mechanisms underlying AML, including the role of Dnmt3a mutations.
Researchers have identified a novel tyrosine kinase inhibitor that targets both resistant tumors and FLT3-independent AML. The compound, MRX-2843, exhibits antitumor effects in culture and preclinical models, improving survival rates even in cases of tumors resistant to existing treatments.
A University of Colorado study reveals a weak link between MN1 and aggressive AML, suggesting EPZ-5676 as a potential tool to break this link. The drug inhibits chromatin regulators Mll1 and Dot1l, which are essential for MN1's leukemia-causing effects.
Researchers at the Walter and Eliza Hall Institute have discovered a new combination of birinapant and p38 inhibitors that shows promise as a treatment for acute myeloid leukaemia (AML). The combination has been shown to be more effective than either agent alone, with fewer toxic side effects.
Melbourne researchers discovered a protein called Hhex that puts the brakes on leukemia cell growth and division. Targeting this protein could lead to new therapies for acute myeloid leukemia (AML), an aggressive blood cancer with poor prognosis.
Researchers at McMaster University have discovered a clear and compartmentalized sequence of events leading to the development of acute myeloid leukemia (AML) from myelodysplastic syndromes (MDS). The study provides an early and accurate prediction tool for this aggressive cancer.
Researchers have identified four potential treatment opportunities for acute myeloid leukemia, including compounds targeting metabolism, internal communications, and protein transport. These findings represent significant progress in seeking out new ways to approach an intractable cancer.
Midostaurin has been shown to improve the five-year survival rate of patients with high-risk acute myeloid leukemia (AML) who carry the FLT-3 gene mutation. The clinical trial found that midostaurin added to standard chemotherapy reduced the risk of death by 23% compared to placebo, resulting in a 50.9% five-year survival rate.
A clinical trial showed midostaurin, a multi-kinase inhibitor, improved the five-year survival rate of patients with high-risk acute myeloid leukemia (AML) who carry the FLT-3 gene mutation. The treatment resulted in a 50.9% survival rate compared to 43.9% for those without the mutation.
Researchers from Montefiore-Einstein Center for Cancer Care presented findings on genetic risk factors, preleukemic states, and novel treatments for acute myeloid leukemia. They identified a genetic risk factor for avascular necrosis associated with treatment of ALL in children and demonstrated that moderate PU.1 inhibition can drive m...
The Beat AML collaboration has identified over 10 cell signaling pathways and mutations that may contribute to disease progression in acute myeloid leukemia. Researchers have also found promising therapeutic approaches, including disrupting the cancer cell microenvironment and targeting key inflammatory pathways.
Researchers have identified a novel approach to targeting protein homeostasis in cancer, using p97 inhibitor CB-5083. Preclinical data show CB-5083 induces disease regression in acute myeloid leukemia and demonstrates antitumor activity in solid tumors.
Researchers from Sylvester Comprehensive Cancer Center are presenting their latest hematology research at the American Society of Hematology (ASH) Annual Meeting. Highlights include the discovery of a potent inhibitor of Lysine demethylase Lsd-1, which augments pro-differentiation effects in acute myeloid leukemia (AML), and targeting ...
A team of researchers discovered how a new anti-leukemia drug, JQ1, works by inhibiting BRD4 and causing the NSD3-short protein to 'fly apart', disrupting cancer cell growth. The NSD3-short protein acts as an adaptor protein, coupling BRD4 to CHD8, and has four distinct functions necessary for AML cells to thrive.