Articles tagged with Myeloid Leukemia
Anna Wojcicki, a University of Minnesota medical student, has been selected for the 2019 ASH Minority Medical Student Award Program to conduct translational research at Stanford University. She aims to develop new therapies for Acute Myeloid Leukemia by repurposing old drugs.
Researchers found that mature AML cells can become immature again, challenging traditional therapeutic strategies. This discovery highlights the need to eradicate all tumour cells, regardless of maturation state.
A study at UT MD Anderson Cancer Center identified a new therapeutic target in cancer cells, caseinolytic protease P (ClpP), which breaks down proteins within mitochondria. New anti-cancer agents called imipridones activate ClpP and cause cancer cell death via mitochondrial proteolysis.
Researchers identified vulnerabilities in AML cells with IDH mutation, allowing for a therapeutic strategy. A combination of drugs already used for another type of leukemia proved effective against this subset of AML in both human and mouse models.
Researchers find a long-overlooked molecular machine in the cell nucleus, the spliceosome, that produces mutant gene/protein fueling cancerous cells. Targeting this protein with existing and developing drugs may offer new treatment options for aggressive leukemia.
Acute myelogenous leukemia patients have only a one in four chance of survival after five years. Researchers created a protein atlas to identify and classify protein signatures at AML diagnosis. The online atlas helps recommend better treatment and personalized medicine for patients.
Researchers combined CRISPR with drug discovery to understand how AML treatment works and which weaknesses can be exploited. The study revealed that LSD1-GFI1B relationship is critical for AML survival, enabling more targeted treatments.
Researchers at the University of Pennsylvania have developed a targeted drug gilteritinib that helps patients with relapsed or refractory acute myeloid leukemia live longer. The trial showed significant survival benefits and well-tolerated side effects, offering a new treatment option for high-risk patients.
A phase III clinical trial found gilteritinib superior to standard chemotherapy in improving overall survival for patients with relapsed or refractory AML harboring a FLT3 mutation. Gilteritinib's relatively low toxicity enables outpatient management, shifting the treatment paradigm.
Researchers identified six age-related subgroups of acute erythroid leukemia with distinct mutations and patterns of gene expression. These findings suggest that genomic alterations can predict treatment outcomes, offering new insights into the diagnosis and treatment of this aggressive cancer.
Researchers at Oregon State University have patented a method for synthesizing cephalotaxine and homoharringtonine (HHT), previously only available from an Asian tree. This development paves the way for more readily available and affordable leukemia treatments.
Researchers found that EZH2 delays AML development but facilitates tumor growth once established. Inhibiting EZH2 prolongs animal survival, prevents AML cell growth, and has therapeutic potential for treating the blood cancer. The study highlights a dual role of EZH2 in AML.
A research team has assembled a detailed atlas of bone marrow cells from AML patients, revealing six stages of white blood cell development and a role for differentiated tumor cells in suppressing immune responses. The study may lead to personalized therapies targeting specific AML cell types.
A team of researchers has created a detailed 'atlas' of cell states for acute myeloid leukemia (AML), a type of aggressive cancer. The atlas, generated using single-cell genomics and machine learning, identifies distinct cell types and their genetic characteristics, shedding light on the disease's heterogeneity.
Researchers identified a critical vulnerability in AML patients with CEBPA mutations, where functional inhibition of the MLL1 complex leads to cell death. Targeting this complex could potentially release a block in normal blood cell maturation and restore healthy blood cells.
Researchers at Purdue University have developed a series of drug compounds that have shown promise in treating acute myeloid leukemia (AML), a type of blood cancer that is often lethal. The new compounds work on both common and drug-resistant forms of AML, including those with problematic mutations.
Scientists discover compound inhibiting SRPK1, a key gene controlling RNA splicing, effectively kills MLL-rearranged AML cells. The research offers a potential new approach to treating acute myeloid leukaemia with minimal harm to healthy blood cells.
Dr. Nazha presents results of a personalized prediction model that surpassed current prediction models for Myelodysplastic Syndromes (MDS), predicting patient mortality and transformation risk with high accuracy.
A new combination of venetoclax with standard drugs azacitidine or decitabine has been granted accelerated approval for treating elderly patients with acute myeloid leukemia. The trial showed a 67% overall response rate, with improved efficacy and tolerability compared to traditional hypomethylating agents.
A new combination treatment of venetoclax and azacitidine has shown a 91 percent response rate in older adults with newly diagnosed acute myeloid leukemia (AML). The treatment has been associated with no more side effects than the use of azacitidine alone, and patients with IDH mutations have experienced long-lasting responses.
A triple therapy combining two immune checkpoint inhibitors with standard-of-care chemotherapy has shown a complete response rate of 43% and projected one-year overall survival of 58%. The treatment approach showed promising results, but more study is needed to confirm its effectiveness.
A team of researchers developed new strategies to exploit CRISPR technology to target the mutant form of protein NPM1, which is associated with acute myeloid leukemia. By blocking the export of mutant NPM1 from the nucleus, they were able to inhibit leukemic cell growth and induce differentiation or death in cancerous cells.
A recent study found that cancer stem cells rely on amino acids for energy, rather than glucose, and this difference makes them susceptible to targeting without harming healthy cells. Researchers have already shown promise with this approach in clinical trials against acute myeloid leukemia, with potential applications to other cancers.
Scientists at the University of Birmingham have identified critical mutations that feed through to genes controlling cell identity and behavior in acute myeloid leukaemia, paving the way for personalized treatment. The research could lead to a different drug being given to treat each form of AML, increasing survival rates for blood can...
A Phase II study found a combination of azacitidine and nivolumab therapy resulted in a 33% overall response rate and 22% complete remission rate for patients with relapsed/refractory acute myeloid leukemia. The drug combination was particularly effective in patients who had not previously received hypomethylating agents, with an overa...
Researchers at The University of Hong Kong developed first-in-class YEATS inhibitors that target a novel therapeutic target for acute myeloid leukemia treatment. The inhibitors successfully suppressed cancer-promoting gene expression and demonstrated enhanced effects when combined with existing anti-leukemia drugs.
Researchers found that relapsed leukemia cells have reduced expression of genes involved in immune recognition, making them invisible to the immune system. Interferon gamma has been shown to turn back on these hidden immune markers, suggesting a potential therapeutic approach for AML patients who relapse after transplantation.
Researchers developed a targeted strategy to treat chemotherapy-resistant AML by targeting the MTF2-MDM2 axis, resulting in complete remission in all mouse models treated with the new combination. The findings hold promise for treating AML patients who would otherwise die from their disease.
A study led by OHSU has published the largest cancer dataset of its kind, involving hundreds of patient samples and revealing new insights into acute myeloid leukemia (AML). The dataset may help researchers and physicians solve specific questions about AML treatment options.
Researchers have released a massive dataset detailing molecular makeup of tumor cells from over 500 AML patients, enabling rapid advancement in clinical trials. The dataset includes how individual patients' cells responded to various drugs, providing insights into targeted therapies for specific subsets of AML cells.
Researchers have discovered a new combination treatment targeting pre-leukemia stem cells by inhibiting protein synthesis and oxidative phosphorylation pathways. The treatment, involving FDA-approved drugs omacetaxine and venetoclax, has shown promising results in killing cancerous cells while leaving healthy stem cells unharmed.
Researchers found that cortisol enables AML cells to evade the immune system by inducing latrophilin 1 expression. This allows cancer cells to suppress anti-cancer immune mechanisms, leading to disease progression.
Researchers at University of Illinois Chicago discovered that a mutation in the NPM1 gene helps improve sensitivity to chemotherapy in patients. The study found that patients with this mutation tend to respond better to chemotherapy and have higher rates of remission.
A study by St. Jude Children's Research Hospital and UCSF identified germline mutations in the genes SAMD9 or SAMD9L as responsible for a rare bone marrow disorder, myelodysplasia and leukemia syndrome with monosomy 7. The research found that some children with these mutations can spontaneously recover normal bone marrow function witho...
A team of international researchers has mapped the family trees of cancer cells in AML to understand its response to enasidenib and how it can be combined with other anti-cancer drugs. The study provides clues about how AML cells become resistant to therapy and may help design future therapy trials.
Researchers at Cincinnati Children's Hospital Medical Center have found a potential therapeutic target for acute myeloid leukemia (AML), a deadly blood cancer with a dismal survival rate. By targeting the F-box protein Skp2, they were able to kill AML cells and induce healthy white blood cell regeneration in preclinical tests.
A team of leukemia scientists has discovered how to predict healthy individuals at risk of developing acute myeloid leukemia (AML) by identifying genetic mutations in their blood. By analyzing data from a large population health study, the researchers found that people with early mutations are more likely to develop AML.
Scientists have discovered genetic mutations in healthy people's blood that can reveal their high risk of developing acute myeloid leukemia (AML) years before they develop the disease. The study found that blood tests can identify these changes, which could lead to earlier detection and monitoring of people at risk.
A phase 1 trial of ivosidenib against IDH1+ acute myeloid leukemia (AML) achieved an overall response rate of 41.9% and median progression-free survival of 8.2 months. Twenty-four percent of patients reached a complete response.
A Phase I trial shows ivosidenib, a protein inhibitor drug, is safe and effective for treating acute myeloid leukemia (AML) patients with IDH1 mutations. The study achieved an overall response rate of 41.6% and complete remission rates of 21.6%, with improved survival rates at 18 months compared to historical controls.
Researchers developed a new approach to treat Acute Myeloid Leukemia (AML) with CAR T cells by removing CD33 from healthy blood-forming stem cells using CRISPR/Cas9. This makes the cancer-specific antigen unique to leukemia cells, allowing CAR T cells to attack without harming normal bone marrow.
Researchers have identified SETD2 as a critical effector protein in MLL-fusion proteins, driving oncogenesis in AML. This finding paves the way for a more effective therapy using a combination of compounds.
A study published in the Journal of Experimental Medicine found that a signaling protein called interleukin-1 receptor accessory protein (IL1RAP) plays a critical role in driving the development and progression of acute myeloid leukemia. IL1RAP amplifies multiple key pathways, making it a promising target for treatment.
Researchers found that the Y-chromosome gene UTY acts as a tumour suppressor, protecting male mice from developing AML. The study also reveals that loss of UTX leads to increased cancer risk in both humans and mice, highlighting potential new treatment avenues for AML.
Acute myeloid leukemia (AML) has a poor five-year survival rate of less than 20%. Researchers at the National University of Singapore identified a novel molecular pathway involving circadian clock gene SHARP1, which causes AML growth. Removing or reducing SHARP1 levels can stop leukemic cell growth.
A clinical trial is underway to test an experimental peptide drug, ALRN-6924, which has shown promise against acute myeloid leukemia (AML) by tripling the median survival rate in animal models. The drug targets p53 and MDMX/MDM2 proteins, blocking tumor growth in both mature and immature AML cells.
Scientists at Cold Spring Harbor Laboratory have discovered a way to rein in an overactive protein that drives some aggressive leukemias. The team's CRISPR-based system identifies two enzymes, LKB1 and salt-inducible kinase, as critical for the survival of certain AML cells.
A study published in Leukemia found that starting mixed phenotype acute leukemia (MPAL) treatment with a less-toxic regimen is linked to better remission rates and long-term survival. Patients treated initially with ALL therapy were three to five times more likely to achieve complete remission than those receiving AML therapy.
Researchers have developed a novel compound targeting STAT5, which selectively disrupts its activation and gene transcription, impairing AML cell proliferation. The compound showed efficacy in patient-derived AML cell lines and freshly isolated patient samples, indicating its potential as a new treatment option for leukemia.
Researchers at Cold Spring Harbor Laboratory have developed a method to selectively disable the MYB protein, which enables cancer cells to proliferate. In tests in mice, this approach resulted in an 80% reduction in size of aggressive leukemia without harming normal cells.
A multi-national phase Ib study has demonstrated a complete response in up to 50 percent of patients with relapsed or refractory acute myeloid leukemia (AML) treated with venetoclax and idasanutlin. The combination therapy shows promise as an effective treatment option for patients with limited treatment options.
The QXDx BCR-ABL %IS Kit uses Droplet Digital PCR technology to detect deep molecular response values with high reproducibility and precision. This allows for more confident disease management decisions in patients with chronic myeloid leukemia.
UC San Diego researchers receive nearly $8 million to develop and test stem cell-based treatments for acute myeloid leukemia (AML). The funding will support testing of novel therapeutic approaches targeting cancer stem cells in AML, which is responsible for a high relapse rate in the disease.
Researchers have identified the METTL3 gene as a promising new drug target for acute myeloid leukemia (AML), a potentially lethal disease. Inhibiting this gene destroys AML cells while leaving healthy blood cells unaffected.
Researchers have discovered a cocktail of drugs that effectively eliminate acute myeloid leukemia (AML) by targeting key pathways. By simultaneously blocking two important pathways, the team was able to achieve complete elimination of AML in most cases tested.
A study found that patients with acute myeloid leukemia (AML) overestimate the risk of dying from treatment and the likelihood of a cure, while physicians believe it is very unlikely. The gaps in perception are most striking for patients receiving non-intensive therapy.
Scientists at Albert Einstein College of Medicine have discovered a compound that directly makes cancer cells commit suicide while sparing healthy cells. The new treatment approach, BTSA1, works by triggering apoptosis in cancer cells through the BAX protein, leaving healthy cells unscathed.
A genetic fault in the CDKN2A gene has been linked to reduced effectiveness of leukemia treatment, highlighting the need for personalized treatment approaches. The study, which treated 259 people with AML or MDS, found that those with the mutation survived for 4.5 months on average, compared to 11 months for those without it.
Researchers have developed a new leukemia therapy that combines inhibitors with immune therapies to eliminate cancer cells, showing promising results in preclinical trials. The combination of treatments worked better than using one active substance alone.
Researchers at the Francis Crick Institute found that acute myeloid leukemia causes bone marrow to 'leak' blood, preventing chemotherapy from working. Drugs that reversed this leakiness boosted chemotherapy's effect in mice and human tissue.