Articles tagged with Leukemia
MUSC researchers discovered blocking an energy pathway for T-cells after hematopoietic stem cell transplant reduces graft-versus-host disease, while maintaining ability to kill leukemia cells. The study uses a lysosomal acid lipase-deficient mouse model, showing promising results with FDA-approved inhibitor orlistat.
Researchers have identified a new and evolutionarily conserved pathway responsible for silencing genes in mammalian cells. BAHCC1 protein is involved in the Polycomb pathway, which generates a chemical tag to silence genes, and its high expression is linked to leukemia, challenging current understanding of gene silencing.
Researchers have developed a new type of precise therapeutic vaccine against leukemia utilizing self-healing polylactic acid microcapsules. The vaccine co-encapsulates a new epitope peptide and PD-1 antibody, demonstrating superior performance over commercialized adjuvants in various models.
Researchers at Temple University Health System discovered a mechanism behind drug resistance in leukemia cells and found that combining PARP inhibition with TGFBR kinase blockade can overcome resistance. This breakthrough could lead to a new treatment strategy for leukemia patients.
Researchers identified a second path to defeating chronic myelogenous leukemia by disrupting the Gdpd3 gene, which regulates quiescence of CML stem cells. This approach reduces leukemia relapse rates even when BCR-ABL1 oncogene is not disrupted.
Scientists have identified new genes that are overexpressed in endothelial cells of people with Down syndrome, increasing their risk for leukemia. The study suggests these genes could be therapeutic targets for developing novel treatments and prevention strategies.
A study published in Nature found that blood cell mutations linked to leukemias become inevitable as people age, especially in the Japanese population. The research identified genetic variations associated with increased risk of these mutations, which can be detected through a simple blood test.
UConn researchers use patented nanoparticle with common chemotherapy drug doxorubicin to target leukemia stem cells, reducing treatment-resistant relapses. The nanoparticle enables slow release of the drug to bone marrow, improving survival rates and inhibiting cancerous stem cells.
Scientists create super-powered natural killer cells by deleting an inhibitory gene, resulting in improved anti-tumor activity and persistence. The modified cells also exhibit enhanced metabolic reprogramming and energy utilization, leading to more effective cancer treatment.
The E1912 trial showed that the ibrutinib-rituximab combination provided better leukemia control, prolonged life, and had fewer side effects compared to standard care in untreated patients with chronic lymphocytic leukemia. The FDA approval is based on data from the phase 3 trial developed by the ECOG-ACRIN Cancer Research Group.
Scientists have engineered T-cells to target multiple sites on leukemia cells, offering a more effective treatment for resistant acute lymphoblastic leukemia. The new CAR-T therapy, TriCAR T-cells, targeting CD-19/20/22, demonstrate improved efficacy compared to single-antigen therapies.
Researchers found that structural changes in protein bundles called chromosomes affect access to genes in T cell acute lymphoblastic leukemia. The new work shows that altering the 3D architecture of chromosomes can trigger cancer growth and spread, making targeted therapy a promising approach.
Researchers at Nemours have identified new genetic structural variants in childhood leukemia that can help assess minimal residual disease during chemotherapy. This breakthrough could lead to more precise diagnosis and targeted therapies for kids with cancer, improving treatment outcomes.
Researchers identified subpopulations of leukemia cells present at diagnosis that have distinct characteristics, leading to relapse in children and adults. These findings provide new avenues for overcoming resistance and improving treatment approaches.
The CD19 CAR NK-cell therapy achieved a 73% response rate in patients with relapsed or refractory non-Hodgkin's lymphoma (NHL) and chronic lymphocytic leukemia (CLL), with no major toxicities reported. The treatment was administered in an outpatient setting, and responses were evident within one month following infusion.
Chronic lymphocytic leukemia (CLL) patients respond differently to ibrutinib treatment due to individual genetic and epigenetic profiles. The study reveals a shared genetic program in CLL cells responding to ibrutinib, but with patient-specific execution, leading to varying disease progression rates.
A collaborative clinical trial has led to changes in the treatment of leukemia driven by the Philadelphia chromosome, a high-risk subtype associated with poor outcomes. Dasatinib was found to provide greater benefit than the standard of care, resulting in improved event-free survival rates.
Researchers have identified a promising drug candidate OT-82 that demonstrates remarkable efficacy in preclinical models. It targets the NAMPT enzyme responsible for NAD production, showing potential as a novel treatment option for refractory blood cancers.
The E1912 follow-up analysis shows that ibrutinib-based therapy lived longer and with sustained benefit in previously untreated CLL patients. The majority of patients were well-tolerated, with only 14% stopping due to side effects.
Researchers at the University of Zurich have identified a new target for treating incurable leukemia in children by analyzing the molecular causes of the disease. They found that an abnormal protein activates genes at the wrong time, triggering the formation of malignant white blood cells and causing leukemia.
A new study found exposure to CT scans is associated with higher risks of developing thyroid cancer and leukemia. The risk is stronger in patients who have received multiple scans, particularly younger adults and females.
A clinical trial at St. Jude Children's Research Hospital found that adding chemotherapy doses in the cerebrospinal fluid improved CNS control without increasing toxicity for high-risk patients. The study reduced CNS relapse rates from 5.7% to 1.8%, making it the lowest among reported studies.
A months-old infant with rare childhood leukemia was treated with sorafenib, a targeted therapy approved for adults with inoperable liver cancer. The patient's unique genetic mutation led to a significant response to the treatment, highlighting the importance of identifying genetic mutations in cancer treatment.
Researchers have identified a potential combination targeted therapy for a deadly type of leukemia found in some infants, which was linked to high levels of the BCL6 protein and poor outcomes. The therapy involves 'turning off' the BCL6 protein using ABT-199, promising a lifesaving treatment option for babies and young children.
Researchers sequenced biopsies from pediatric patients with acute lymphoblastic leukemia and found that they harbored T cells specific to many neoepitopes. The patients' T cells responded to a significant proportion of these neoepitopes, forming hierarchies in their responses.
A study by Maxime Caru found that childhood ALL survivors have significantly worse cardiorespiratory fitness than healthy Canadians, with a 22% reduction. The research also identified specific trainability genes linked to the decline in cardiorespiratory fitness among female survivors.
Researchers have discovered a new treatment approach for T-cell acute lymphoblastic leukemia (T-ALL) that targets the Notch signaling pathway with greater safety and efficacy than previous treatments. The findings, published in Science Translational Medicine, show promise for translating this therapy to patients.
Researchers found that the combination of ibrutinib and venetoclax was highly effective in achieving complete remission with undetectable minimal residual disease in high-risk CLL patients. The study also showed that this combination therapy had no new toxic effects compared to individual agents.
Scientists at Johns Hopkins University have unraveled how the DNA machinery fits together, revealing a paradigm shift in understanding genetic illness. The discovery of how nucleosomes change shape to bind with an enzyme could unveil new treatment opportunities for childhood leukemia.
Researchers have shed light on how leukemia cells become resistant to drugs and describe a potential solution using two drugs in combination. The study identifies the genes responsible for resistance, revealing that cancer cells overcome the lack of asparagine by breaking down proteins.
Scientists identify CXCL12-expressing mesenchymal stromal cell niches as a strategy to target and eliminate treatment-resistant leukemic stem cells in chronic myelogenous leukemia. The study reveals that these niche interactions control quiescence of leukemic stem cells.
Researchers at Tel Aviv University developed a novel biosensor that can isolate and target leukemic stem cells, the most malignant of all leukemic cells. The sensor uses genetic encoding to identify and characterize these cells, which have high regenerative potential and escape targeted therapies.
Scientists at CeMM Research Center have developed a method to identify promising drug combinations for chronic lymphocytic leukemia. By combining epigenetic analysis and high-throughput imaging, researchers can predict which drugs are likely to work together effectively, reducing trial-and-error approaches.
A new study from Instituto Gulbenkian de Ciencia shows that leukemia can emerge as a consequence of prolonged precursor cells in the thymus. This blood cancer affects mostly children and is associated with a high risk of developing T-cell acute lymphoblastic leukemia.
Researchers discovered that STAT5B facilitates leukemogenesis in B-cell acute lymphocytic leukemia. They found that the absence of STAT5B increases interferon response and suppresses transformation. This understanding may enable precision medicine strategies to treat disease.
A new study led by St. Jude Children's Research Hospital found that high-risk leukemia patients did not experience improved long-term survival with bone marrow transplantation. Treatment guided by measuring minimal residual disease was associated with better outcomes, with 58% of patients becoming long-term survivors.
St. Jude Children's Research Hospital scientists identify 23 subtypes of B-cell acute lymphoblastic leukemia (B-ALL), including eight new subtypes, with distinct genomic and clinical features. The study's findings may lead to the development of precision medicines and customized treatments for high-risk patients.
Acute lymphoblastic leukemia (ALL) researchers find bone marrow stromal cells harbor leukemia cells, shielding them from chemotherapy. Yong-Mi Kim seeks integrin molecules to block treatment evasion.
Researchers at Nova Southeastern University have identified a genetic marker, NER gene expression levels, to predict early relapse in pediatric acute lymphoblastic leukemia (ALL) patients. This finding has the potential to guide targeted treatment and improve patient outcomes.
A Syracuse University physicist has developed tiny sensors that can detect and analyze protein-protein interactions in blood serum, which could lead to improved cancer detection. The technology, known as nanobiosensors, uses a nanopore to measure changes in electric current when proteins are present.
Scientists at Cold Spring Harbor Laboratory have identified ZFP64 as the single key to the cascade of events leading to mixed lineage leukemia (MLL), an aggressive blood cancer. Shutting down this protein may be a cure for MLL, which predominantly occurs in infants and is difficult to treat.
A study published in Cell Stem Cell found that the PPM1D gene confers a survival advantage to blood cells exposed to chemotherapy, potentially favoring the development of secondary leukemia. The research suggests that the presence of this gene and other mutations should be considered when choosing chemotherapies.
A low-fat diet has been shown to increase the survival rate of obese children with acute lymphoblastic leukemia by five times compared to a high-fat diet. This dietary intervention could potentially help kill cancer cells and improve treatment outcomes.
Researchers in Barcelona have received an ERC Synergy grant to study chronic lymphocytic leukemia at unprecedented resolution using single-cell analysis. The BCLL@las project aims to generate comprehensive information from thousands of individual cells, leading to novel insights into the origin and evolution of cancer.
Leukemia undercuts normal cells' ability to consume glucose, leading to a diabetic-like condition that favors cancer growth. Researchers have identified key strategies, including manipulating insulin production and gut bacteria, which can be targeted with low-tech therapies like serotonin supplementation.
Loyola will produce a more purified CAR-T cell product potentially reducing toxicities and costs. The Leukemia Research Foundation is supporting the research with a $250,000 grant.
A new study of 96 patients with chronic lymphocytic leukemia (CLL) found that those experiencing stress have higher levels of cancerous cells and cytokines in their blood. The researchers also discovered a link between stress and disease severity, even after controlling for other factors.
Scientists have introduced a microfluidic chip for manipulation and nucleic-acid analysis of individual cells. The technique uses dielectrophoresis to trap and analyze cells efficiently, overcoming conventional methods' limitations. This innovation paves the way for personalized medicine and improved diagnostics.
A team of researchers has discovered a protein called LEDGF/p75 that contributes to the regulation of gene expression in mixed lineage leukemia. The study found that this interaction is strongly modulated by phosphorylation from an enzyme called casein kinase 2, providing a new therapeutic route against the cancer.
A large cohort study found CLL patients have a 600% higher risk of melanoma compared to the general population. Close monitoring for early detection is crucial in managing this skin cancer with targeted therapies.
A study reveals that blocking heat shock transcription factor 1 (HSF1) signaling in T cell acute lymphoblastic leukemia (T-ALL) could represent a new approach in treating the aggressive disease. The discovery identifies a subset of T-ALL patients most likely to benefit from a new therapy.
Children with leukemia experience frequent vertebral fractures during chemotherapy, often persisting into adulthood. Vertebral deformities are more common in older children and those with severe collapse.
Researchers found that bacterial signals play a crucial role in developing pre-leukemic myeloproliferation, a precursor condition to leukemia, in mice with TET2 mutations. The study suggests that targeted treatments could reverse the disease by blocking aberrant IL-6 signals.
Researchers at Boston University School of Medicine identified ubiquitin-fusion degradation 1 (UFD1) as a key protein in aggressive T-cell leukemia. Reducing UFD1 levels by 50% inhibited leukemia development without impacting healthy tissues.
Researchers discovered genetic defects typical in ANKL, a shared genetic background with NK- and T-cell malignancies, and novel gene amplifications in the JAK-STAT signaling pathway. Potential drug candidates were found, including JAK inhibitors that could improve treatment for various NK-cell malignancies
Researchers identified a fourth gene, IKZF1, associated with childhood leukemia predisposition, expanding cancer screening options. Germline variants in IKZF1 increase the risk of developing B-cell acute lymphoblastic leukemia (ALL), a common pediatric cancer.
Researchers at Friedrich-Alexander-Universität Erlangen-Nürnberg have identified a new molecular cause of aggressive infant leukemia in children. The study found that changes in genes in white blood cells disrupt cell growth control, leading to the production of abnormal proteins that facilitate leukaemia.
Research from St. Jude Children's Research Hospital found that leukemia itself may increase the risk of long-term neurocognitive problems, even before treatment starts. Elevated biomarkers in cerebrospinal fluid indicate injury to brain cells, suggesting a complex interaction among genetics, treatment intensity, and other factors.
Two genes, JAK3/STAT5 and HOXA9, have been found to cooperate in triggering leukemia development. This cooperation leads to more rapid and aggressive disease progression. The discovery provides a basis for targeted therapies, not only for acute lymphoblastic leukemia but also for other leukemias.
A new technique using mass cytometry predicts relapse in acute lymphoblastic leukemia patients with 85% accuracy, identifying a subset of malignant cells that predispose to relapse. The method could lead to more precise treatment and targeted therapies for high-risk patients.