Articles tagged with Leukemia
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Researchers at UT Southwestern Medical Center found that vitamin C regulates stem cell function and suppresses leukemia development. The study used mice with limited ascorbate production to mimic human levels and discovered a link between ascorbate, DNA modifications, and Tet2 enzyme activity.
A team of researchers has discovered that a DNA-cutting enzyme plays a broad role in driving abnormal genetic rearrangements, including translocations that cause cancer. The study identified specific sites of DNA damage along the entire genome of human leukemia cells.
Researchers have identified the KMT2A gene translocations as a common underlying cause of infant and treatment-related leukemias. The Penn/CHOP team has also found that topoisomerase II cleavage clusters in specific regions of the genome, which may play a role in DNA damage repair and cancer development.
Researchers developed an anti-PD-1 antibody that blocks PD-1/PD-L1 interaction, reinvigorating antivirus immune response and decreasing BLV counts. The new treatment could be effective against various intractable infectious diseases in cows.
Researchers discovered a protein signature that predicts leukemia, which could lead to novel treatments. The activation of STAT5 causes competition among proteins, leading to acute lymphoblastic leukemia.
A study published in Leukemia reveals an epigenetic lesion that correlates with the activation of a powerful oncogene capable of malignizing lymphocytes, leading to acute T-cell leukemia. The research suggests that targeting this gene may offer new treatment options for patients with this aggressive type of cancer.
A study using human stem cells found that deep space radiation may increase the risk of leukemia in humans. The research team identified a dietary supplement as a potential protector against these effects.
The OHSU Knight Cancer Institute research team discovered a previously unreported flaw in the standard leukemia assay, which can lead to non-functional mutations appearing functional. They recommend an additional sequencing step to improve the assay's accuracy and reproducibility.
Researchers identified L-asparaginase in yeast that efficiently kills leukemia cells with low toxicity to healthy cells. The enzyme depletes asparagine, a crucial amino acid for cancer cell survival, leading to apoptosis and inducing programmed cell death.
Researchers at Northwestern University have discovered a genetic driver of mixed lineage leukemia, a rare and deadly form of childhood leukemia. They identified a targeted molecular therapy that halts the proliferation of leukemic cells by stabilizing the wild-type MLL protein, which drives cancer.
Researchers identified gene mutations associated with steroid resistance in pediatric T-cell acute lymphoblastic leukemia, leading to poor clinical outcomes. A new therapeutic approach targeting individual signaling proteins restored steroid sensitivity in leukemic cells from patients.
The technology platform, Phenotypic Personalized Medicine, uses visual representations to identify optimal drug and dose combinations for patients with acute lymphoblastic leukemia. This approach reduces side effects while maintaining or enhancing efficacy, offering a game-changer for cancer treatment.
A recent study identifies inherited genetic mutations in the IKZF1 gene as a major risk factor for pediatric ALL. The variants affect protein Ikaros, crucial for white blood cell development, and reduce cancer cells' sensitivity to chemotherapy drug dasatinib.
A University of Liverpool study found that reducing the dose of leukemia drug tyrosine kinase inhibitors (TKI) can safely reduce side effects in patients with chronic myeloid leukemia. Patients who achieved stable molecular remission levels showed no evidence of leukaemia rebound after cutting their TKI dose, with some reporting signif...
A study by The University of Texas MD Anderson Cancer Center found pre-leukemic mutations can predict the development of therapy-related myeloid neoplasms (t-MNs), a leukemia with poor prognosis. Patients with these mutations are at higher risk, and detecting them earlier could help prevent or treat t-MNs.
Researchers from Penn Medicine present early results from studies of CAR T cell therapy for multiple myeloma and relapsed/refractory acute lymphoblastic leukemia, showing high efficacy and safety profiles. The findings build on the team's work in CAR T cell therapies dating back to 2010.
Researchers have created a mouse model that replicates the human genetic flaw causing infant leukemia, making it easier to study. The model mimics the disease found in humans both phenotypically and molecularly, with all mice developing Pro-B ALL identical to patient cases within 22 weeks.
Researchers at CHLA are developing a new treatment approach for patients with relapsed acute lymphoblastic leukemia (ALL) by targeting the molecule integrin alpha4, which shelters leukemia cells from chemotherapy. The goal is to develop a novel inhibitor of this molecule for clinical use.
Researchers have discovered a new high-risk subtype of acute lymphoblastic leukemia (ALL) characterized by chromosomal rearrangements involving the MEF2D gene. A possible targeted therapy, panobinostat, has been shown to stop proliferation of human leukemic cells with this rearrangement.
Researchers find that specific DNA mutations in bone cells can cause nearby blood stem cells to develop leukemia. A new class of drugs has been identified to dampen this 'neighbor cell effect', offering hope for improved treatment options for Noonan syndrome patients.
Researchers have determined that combining CX-4945 and JQ1 can efficiently kill T-cell acute lymphoblastic leukemia cells while sparing normal blood cells. The findings provide new hope for the treatment of refractory/relapsed T-cell leukemia, a form of cancer with a high mortality rate.
Researchers at Dana-Farber Cancer Institute have found that CML stem cells die in response to inhibition of the protein Ezh2, suggesting a potential cure for some patients. Adding Ezh2-targeting agents to standard treatment could dramatically shorten the treatment period and achieve a cure.
A recent study has shed light on the pathogenesis of DNA breakpoints associated with leukemia, revealing a mechanism that explains up to 90% of DNA damages in the most common type of childhood leukemia. The study identified a new high-risk subtype of leukemia characterized by abnormal expression of enzymes causing DNA damage.
Researchers discovered leukemia stem cells in fatty tissue of obese patients were more resistant to chemotherapy, using fatty acids as their energy source and actively signaling fat for lipolysis. This adaptation could help explain poorer outcomes in obese patients, potentially shedding light on new strategies to target cancer stem cells.
A randomized Phase III study found nearly 81% of patients in the inotuzumab ozogamicin group achieved complete remission, compared to 31-41% with standard therapies. The drug enabled 41% of patients to proceed with stem cell transplants, increasing their chances of a curative treatment.
HTLV-1, a retrovirus that co-exists with humans, infects 30 million people worldwide. Persistent infection is attributed to CTCF, which controls viral DNA integration into human DNA. This discovery may lead to new prevention and treatment strategies for refractory leukemia.
Leukemia cells exhibit stiffer mechanical signatures compared to healthy cells. The study suggests that these mechanical data can be used to grade the loss of cell mechanical functions depending on leukemia progression. This approach may aid in cancer diagnosis and provide insights into disease evolution
Researchers at the University of Zurich have discovered a new way to kill off resistant leukemia cells via necroptosis, a cell death program that can bypass traditional apoptosis. SMAC mimetics, which activate necroptosis, showed promise in killing leukemia cells in 33% of patient samples tested.
Researchers at St. Jude Children's Research Hospital discovered that combining tyrosine kinase inhibitors with an FAK inhibitor synergizes to decrease tumor growth in mouse models of BCR-ABL1+ B-progenitor ALL. This combination approach is a promising treatment strategy for this subset of ALL.
Chronic lymphocytic leukemia (CLL) researchers have improved their models of the disease by understanding how cancer cells differentiate into antibody-secreting plasma cells in mice. Patient-derived T cells play a crucial role in this process, and therapies promoting differentiation may offer new treatment options for CLL.
A study found that IGF2BP3 promotes B cell proliferation in B-cell acute lymphoblastic leukemia by regulating oncogenes like MYC. The RNA binding protein is reactivated in some cancer cells, making it an attractive target for cancer-fighting drugs.
Researchers found that IGF2BP3 regulates various RNA messages contributing to the development of MLL-rearranged leukemia. The protein binds to and stabilizes hundreds of leukemia-promoting messages, leading to cancer cell growth.
Researchers at The Ottawa Hospital and University of Ottawa identified a compound called GSK-J4 that can kill a severe form of childhood leukemia. By targeting the TAL-1 gene, the compound stops cancer cell growth, showing promise for personalized treatment.
A particular enzyme called DLST in the TCA cycle supports the growth and survival of T-cell leukemia cells. Inhibiting this enzyme's activity can effectively kill these tumor cells.
Researchers have identified the EZH2 gene as a driver of aggressive pediatric leukemia subtype ETP-ALL, characterized by stem-like cells and increased growth signaling. The study provides potential therapeutic targets, including the existing drug ruxolitinib, for this previously challenging disease.
Researchers at St. Jude Children's Research Hospital have discovered a unique mechanism underlying Ph-like ALL, a particularly aggressive form of acute lymphoblastic leukemia. The findings reveal that chromosomal rearrangements lead to the activation of a truncated EPOR gene, driving white blood cells to proliferate out of control.
A new study from Children's Hospital Los Angeles found that leukemia therapy leads to a significant drop in bone mineral density during the first month of treatment, affecting the lower spine and legs. This earlier onset than previously thought highlights the need for new approaches to mitigate bone toxicity in cancer patients.
A new study proposes that genetic drift contributes to the development of leukemia in young children. The researchers used a computational model describing blood stem cell population dynamics and found that drift plays a significant role in early-life leukemia formation. In contrast, selection drives leukemia development in older adults.
A study by UC San Diego researchers found that populations living at high latitudes with limited sunlight exposure are at a higher risk of developing leukemia due to low vitamin D levels. This epidemic of vitamin D deficiency in winter populations contributes significantly to the burden of leukemia worldwide.
Scientists at University of California, San Diego discover protein Wnt5a stimulates CLL cell growth via ROR1 and ROR2 proteins. Experimental monoclonal antibody cirmtuzumab inhibits growth and spread of cancer cells.
Researchers have developed a new diagnostic method for a deadly fungal lung infection in leukemia patients, offering improved early detection and treatment options. The breakthrough uses distinct test results to identify the infectious mold, potentially refining diagnostics and improving survival rates.
Patients who discontinued ibrutinib or idelalisib due to side effects experienced durable responses after switching to another kinase inhibitor, with a 50% objective response rate and 11.9-month median progression-free survival.
A study found that breast cancer survivors with therapy-related leukemia often have inherited cancer susceptibility and gene mutations. Researchers suggest a long-term follow-up study to understand the impact of these genes on leukemia risk, enabling personalized conversations about treatment benefits and risks.
A multi-center study found ibrutinib to be more effective than chlorambucil in treating CLL, with a 97.8% overall survival rate after two years compared to 85.3%. Ibrutinib also improves hemoglobin and platelet levels.
Researchers identified CD19 splicing alterations as a cause of resistance to CAR T-cell therapy in pediatric patients. The study found that alternative splicing led to the production of a modified version of the CD19 protein, which was functional but could not be recognized by the immune system.
Scientists engineered stem cells with PTPN11 mutations to recreate JMML, clarifying early events in its development and providing new targets for drug design. This 'leukemia in a dish' model can help improve treatment options for patients with this rare blood cancer.
A research group in Japan and Korea found that certain dipeptide species support CML stem cell activity. Pharmacological inhibition of nutrient uptake decreased CML stem cell activity in vivo, suggesting a potential therapeutic target for CML therapy. This discovery may provide concrete benefits to patients with CML.
A team of international scientists decoded the molecular characteristics of a fatal subtype of leukemia in children, paving the way for new therapeutic approaches. The study identified genetic aberrations and altered gene expression programs that lead to tumorigenesis, providing potential druggable targets.
Scientists have decoded the genome and transcriptome of an incurable subtype of acute lymphoblastic leukemia, revealing a novel program associated with leukemic cells. The study identifies key genes that trigger a reprogramming of the leukemia cells, leading to promising drug tests, including Venetoclax.
A Dartmouth team has successfully synthesized molecules that induce rapid apoptosis in leukemia cells, paving the way for further study of their biological mechanism of action. The findings hold promise for developing novel therapeutic strategies against cancer and other diseases linked to abnormal cell death.
The Damon Runyon Cancer Research Foundation has established a new award to increase the number of physician-scientists in cancer research. The grant provides $100,000 per year for three years and up to $100,000 of medical school debt repayment. Two awardees will investigate novel approaches to fighting cancer.
A small pilot study found an experimental treatment approach can send deadly leukemia into remission in patients who have failed standard therapy. The combination of immunotherapy and gene manipulation buys critical time for patients to receive a potentially life-saving stem cell transplant.
Research suggests that breastfeeding for at least six months can significantly reduce the risk of childhood leukemia. The study analyzed data from 18 studies and found a 19% lower risk compared to no breastfeeding or shorter breastfeeding periods. Breast milk's immunological components may play a key role in this association.
A UCSF-led team discovered that the Haemophilus influenzae Type b vaccine protects against acute lymphoblastic leukemia by preventing the conversion of 'pre-leukemia' blood cells into full-blown cancer. Chronic infections push these cells into malignancy.
Researchers at Children's Hospital Los Angeles found that minimal residual disease alone is not predictive of risk or outcome in children with T-cell leukemia. Despite having few remaining leukemia cells, patients achieved complete remission and had excellent outcomes without intensifying therapy.
A new gene involved in blood-forming stem cells has been discovered by U-M researchers, providing insights into the body's ability to create and maintain a healthy blood supply. The Ash1l gene plays a critical role in regulating hematopoietic stem cell maintenance and self-renewal potential.
Dr. Owen Witte, a pioneer in human leukemias and immune disorders, received the AACR G.H.A. Clowes Memorial Award for his groundbreaking work on tyrosine kinases as drug targets. His discoveries have led to multiple approved targeted therapies, transforming patient outcomes.
Researchers at the University of Michigan Medical School found that patients with chronic myelomonocytic leukemia (CMML) who responded to decitabine treatment had a distinct DNA methylation pattern. This signature can be used to predict patient response to treatment, enabling more effective treatment planning.
Researchers at Michigan Medicine have developed a new compound that shows promise in treating acute leukemia and may also play a role in prostate cancer. The MLL-menin interaction is a key driver of the disease, and blocking this interaction has shown potential in laboratory studies.
Researchers identified a panel of genetic markers that predicted which tumor samples would likely respond to treatment for chronic myelomonocytic leukemia, a cancer affecting older adults with limited treatment options.