Articles tagged with Leukemia
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.
A global clinical trial of CAR T-cell therapy tisagenlecleucel found that 61% of children and young adults achieved complete remission after treatment, with durable responses lasting months or years. Most side effects were short-lived and reversible, with overall survival rates exceeding 90% at six months.
Researchers found that germline variations in the tumor suppressor gene TP53 predispose children to develop leukemia and increase their chances of developing a second cancer. The variants are associated with reduced gene activity and were five times more frequent in pediatric ALL patients than those without the disease.
Patients with advanced leukemia who rely on blood transfusions face barriers to quality end-of-life care, including limited hospice services and higher hospital deaths. Research suggests that improving access to blood transfusions could increase hospice care use among these patients.
Research found that leukemia patients who rely on blood transfusions face difficulties enrolling in hospice care, leading to shorter hospice stays and delayed access to palliative care. The study suggests that adding support for transfusions to the Medicare hospice benefit could maximize its benefits.
Research at Lund University found that HLF gene's failure to shut down leads to inadequate lymphocyte development, resulting in a single type of immune defense. The study aimed to identify mechanisms for breaking down leukemia, an aggressive blood cancer with poor prognosis.
Barbara Savoldo, MD, PhD, received a three-year grant to support research into an investigational CAR T-cell treatment for acute lymphoblastic leukemia with a built-in safety switch. The goal is to adapt an 'off switch' to reduce potentially lethal side effects of immunotherapy treatments.
A study by St. Jude Children's Research Hospital found that young leukemia patients who received the flu vaccine were still susceptible to flu infections, highlighting the need for additional measures to protect vulnerable individuals. Researchers emphasize the importance of hand washing and other precautions.
Hui Feng's research aims to understand why T-ALL is so aggressive and resistant to treatment. The grant will support further studies on the role of a novel protein contributor to leukemia's aggressiveness and its potential targeting through available drugs.
A team of scientists has identified a protein called TOX that drives the initiation and growth of an aggressive form of leukemia. TOX is expressed in 95 percent of human T-ALL cases and required for cancer's growth and persistence, offering new targeted treatment approaches.
Scientists at UC San Diego uncover a previously unknown link between non-coding DNA regions and the formation of immune cells. The discovery reveals a precise mechanism for the pairing of promoter and enhancer elements, which brings them into close proximity to initiate immune cell development.
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.
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.
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 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.
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.
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 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.