Researchers have identified two key genes that contribute to the aggressive spread of neuroblastomas. The study found that high levels of LMO1 expression promote metastasis in MYCN-induced neuroblastoma by dysregulating extracellular matrix genes, paving the way for new therapies.
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Researchers developed nanoparticles loaded with curcumin, a common spice compound, to target and destroy treatment-resistant neuroblastoma tumor cells. The study showed promising results in killing cancer cells while producing minimal toxicity in healthy cells.
Research at the University of Chicago Medical Center identified genetic variations that pre-dispose children to severe forms of neuroblastoma, paving the way for more targeted treatments. Children with MYCN-amplified tumors have a lower survival rate, but understanding their genetic predispositions could lead to more effective therapies.
Researchers found that combining a kinase inhibitor and an oncolytic herpes virus results in significantly increased antitumor efficacy against MPNST and neuroblastoma. The study suggests that this combination could lead to improved treatment options for patients with these rare cancers.
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A team at Children's Hospital Los Angeles received a three-year grant to investigate chemoimmunotherapy in children with neuroblastoma. Recent pilot data showed promising results, leading to changes in standard care for treatment-resistant patients.
A common nerve protein, neuropeptide Y (NPY), is elevated in the blood of patients with aggressive neuroblastoma, associated with poor survival rates and disease relapse. NPY's release from tumors into the bloodstream may also serve as a marker for metastatic disease.
Researchers discovered a nuclear protein, EYA1, that contributes to neuroblastoma's aggression. The protein migrates to the nucleus in more aggressive forms of the disease, and its structure can be altered by inhibiting an enzyme called PRMT1.
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A study led by Boston Children's Hospital researchers finds that the loss of let-7 microRNA family is central to neuroblastoma development. The study suggests strategies focused on restoring let-7 could provide a fresh, low-toxicity approach to treating this childhood cancer.
A new combination of immunotherapy and chemotherapy has shown a remarkable 53% response rate in pediatric neuroblastoma patients, with some tumors shrinking or disappearing completely. Researchers plan to expand the study to include more children, offering hope for a potential cure.
A Phase II clinical trial has shown an 80% success rate in shrinking tumors in newly diagnosed, high-risk neuroblastoma patients treated with a new monoclonal antibody. The experimental agent was found to have reduced treatment-limiting pain compared to other anti-GD2 monoclonal antibodies.
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Researchers at VCU Massey Cancer Center have developed a combination therapy that targets the MYCN and BCL2 proteins to kill neuroblastoma cells. The therapy, which uses investigational drugs ABT-199 and MLN8237, shows promising results in laboratory experiments and advanced mouse models.
A new study published in Developmental Cell suggests that the KIF1Bβ gene plays a key role in determining whether neural crest cells live or die. The research team found that loss of KIF1B-β is associated with poor prognosis and reduced survival in neuroblastoma patients.
Researchers at the Children's Hospital of Philadelphia have identified a powerful new drug with unparalleled strength against forms of neuroblastoma that resist crizotinib. The study found that PF-06463922 showed more profound inhibition of ALK than crizotinib, leading to rapid and sustained regression in animal models.
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A new $1.5 million grant will support an innovative approach to treating relapsed or refractory neuroblastoma through a dynamic clinical trial design allowing for quick incorporation of new treatments based on genetic changes in individual patients' tumors.
Researchers at Children's Hospital of Philadelphia identified a crucial change in a single DNA base that both predisposes children to aggressive neuroblastoma and drives disease progression. This discovery may lead to novel therapies for the complex and deadly disease.
Australian scientists identified a critical molecular feedback loop in neuroblastoma that accelerates cancer development. Experimental drug CBL0137 has the potential to interrupt this loop and halt tumour progression, showing promising results in laboratory models.
Researchers at Children's Hospital of Philadelphia identified a signaling network involving three cancer-causing genes that drive high-risk neuroblastoma. The study found that variants in the LIN28B gene generate abnormal signals that regulate RAN and AURKA proteins, leading to uncontrolled cell growth.
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Researchers develop new targeted delivery method using silk sponge to reduce chemotherapy's toxic effects on children with neuroblastoma. The approach slows tumor growth and reduces systemic toxicity, offering a promising alternative to traditional chemotherapy.
Researchers have discovered that neuroblastoma cells produce a molecule called 'arginase' that breaks down arginine, an essential energy source for immune cells. This creates an immunosuppressive microenvironment that impairs the body's ability to fight the disease.
A new treatment for children with neuroblastoma has shown promise in a phase I study, with minimal side effects and long-term survival of three patients. The drug DFMO targets an important cancer stem cell pathway to 'turn cells off,' potentially preventing relapse.
A study by Children's Hospital of Philadelphia researchers found that cancer-driving mutations in neuroblastoma can be targeted with existing MEK inhibitors, offering hope for improved treatments. The study identified specific mutations on the RAS-MAPK pathway that are sensitive to these drugs.
Researchers at Georgetown University Medical Center found that maternal stress can increase the risk of fetal neuroblastoma in mice. The study showed that even non-stressed handling of the animals led to a faster development of cancer, suggesting that prenatal stress may exacerbate genetic mutations that promote tumor growth.
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A common nerve protein, neuropeptide Y (NPY), is elevated in the blood of patients with aggressive neuroblastomas, associated with adverse prognostic factors and worse survival rates. NPY may serve as a potential prognostic marker and therapeutic target for this pediatric cancer.
A new study found that high-risk neuroblastoma cells use an efficient but erroneous DNA repair pathway, giving them a survival advantage. This alternative repair mechanism may be the target of new therapies to improve treatment options for children with neuroblastoma.
Researchers have defined riskier mutations in neuroblastoma, a childhood cancer, which could help match patients with optimal treatment using ALK inhibitors. The study, published in Cancer Cell, analyzed DNA from nearly 1,600 patients and discovered ALK mutations in 8% of tumors.
A pre-clinical study finds that a specially crafted compound can disrupt the production of MYCN protein, causing tumors to shrink with little or no harm to normal cells. The approach uses an alternative mechanism to target the defective transcriptional mechanisms involved in cancer growth.
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Researchers successfully silenced chemokine receptor 4 in SH-SY5Y cells, inhibiting neuroblastoma cell invasion. This approach may provide a new therapeutic strategy for blocking neuroblastoma metastasis.
Researchers at Duke University Medical Center have identified a new strategy for treating neuroblastoma using a modified version of heparin. The study found that the derivative suppressed and shrunk neuroblastoma tumors in mice without causing severe bleeding.
The INBRACED initiative has awarded a $400,000 grant to launch an international phase I clinical trial for children with relapsed or refractory neuroblastoma. The vaccine targets the GD2 and GD3 antigens and has shown promising results in children with neuroblastoma in the US.
Dr. Garrett Brodeur's work has significantly advanced our understanding of neuroblastoma, a childhood cancer. His research has led to the development of more effective and less toxic treatments for children.
A Phase I study of an experimental antibody produced at St. Jude Children's Research Hospital found tumors shrank or disappeared in some patients with advanced neuroblastoma, and disease progression was temporarily halted in 15 children.
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Researchers have developed a new laboratory screening technique to find novel treatments for pediatric neuroblastoma. MicroRNAs play an important role in regulating cell development and differentiation, revealing promising targets for new therapies.
A new clinical trial combines NK cell therapy with an immunocytokine to target children with relapsed/refractory neuroblastoma, promising a less toxic treatment option. Researchers at the University of Wisconsin-Madison will use haploidentical natural killer cells infused with hu14.18-IL2 to destroy cancer cells.
A new study from Children's Hospital of Philadelphia reports proton therapy as an effective, organ-sparing treatment option for children with high-risk neuroblastoma. Protons precisely target tumors while minimizing radiation exposure to healthy tissue.
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Researchers have developed two monoclonal antibodies that boost the immune system to fight neuroblastoma, a form of childhood cancer. The study found that 40-60% of tumors treated with the antibodies regressed in laboratory models, leading to long-term survival.
Researchers found that neuroblastoma cells with low levels of HDAC10 enzyme are more resistant to chemotherapy, and blocking this enzyme using autophagy prevents cancer cell survival. The study suggests a new approach for treating aggressive neuroblastoma tumors.
Researchers at Karolinska Institutet have discovered a promising strategy for defeating neuroblastoma by targeting the MYCN protein. The approach involves inhibiting the MYC gene, which leads to the accumulation of fat droplets in cancer cells and ultimately causes cell death or development into harmless neurons.
Researchers have identified a new compound class that promotes neuroblastoma cell differentiation, which can stop tumor cells from dividing and growing. This breakthrough could lead to the development of novel treatments for high-risk childhood cancer.
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A genetic biomarker, MYCN amplification, has been identified as a potential target for a new class of anti-cancer drugs in neuroblastoma patients. The study found that tumors with excess copies of the gene were highly sensitive to BET bromodomain inhibitors, leading to impaired cell growth and induction of cell death.
Pediatric oncologist Garrett Brodeur will receive the Pediatric Oncology Award and deliver a lecture highlighting his work on predicting disease course in neuroblastoma. His research has led to better understanding of the cancer's biology and development of more effective treatments.
A new dendritic cell vaccine has been shown to induce complete remission in a six-year-old boy with recurrent neuroblastoma. The vaccine uses cancer-specific targets to stimulate the immune system and attack tumor cells.
A recent study published in Nature Genetics found that neuroblastoma tumors undergo rapid evolution, rendering traditional targeting strategies less effective. Researchers refocused on understanding the dynamic nature of these tumors and their response to medicine.
Researchers found ARID1A and ARID1B gene mutations in 8 patients, associated with worse survival outcomes. The discovery could lead to early identification of high-risk patients requiring additional treatments.
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Researchers have discovered two related genes, ARID1A and ARID1B, involved in the most aggressive form of childhood cancer neuroblastoma. These findings identify a novel pathway that scientists can now study to develop potential new therapies for children with tumors having these mutations.
A whole-genome scan can help identify large-scale chromosomal damage, enabling doctors to choose the most effective treatment option for children with neuroblastoma. The study recommends that all children diagnosed with neuroblastoma worldwide have a whole-genome scan as part of their treatment.
Researchers at Children's Hospital of Philadelphia have discovered two gene variants that increase the risk of neuroblastoma and promote its progression. These variants in HACE1 and LIN28B genes were found to exert opposite effects, with low expression of HACE1 and high expression of LIN28B correlating with worse patient survival.
Researchers have found a way to overcome drug resistance in childhood cancer by combining crizotinib with an mTOR inhibitor. This combination has shown promise in treating aggressive neuroblastoma tumors that are resistant to current treatments.
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A recent study discovered an association between the ATRX gene mutation and age at diagnosis in children with advanced-stage neuroblastoma. The research found that ATRX mutations were more common in adolescents and young adults, suggesting a potential molecular marker and therapeutic target for this age group.
Researchers identified a gene mutation associated with chronic neuroblastoma that typically affects adolescents and young adults. The discovery provides clues about the genetic basis of treatment outcome and age at diagnosis.
Researchers have identified common genetic variants associated with the development of high-risk neuroblastoma and poor treatment outcomes in patients of African ancestry. These variants may also affect patients of other ethnic backgrounds, highlighting the importance of personalized medicine.
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Researchers have found a new treatment option for children with relapsed or primary refractory high-risk neuroblastoma, using combined positron emission tomography and X-ray computed tomography to select patients for molecular radiotherapy. The therapy was well-tolerated and showed promise in improving symptoms and quality of life.
Childhood cancer researchers have identified checkpoint kinase 1 (CHK1) as a potential new treatment target for neuroblastoma. By blocking CHK1 activity, chemotherapy can be made more effective against the cancer cells.
Researchers at The Children's Hospital of Philadelphia have discovered a new gene, LMO1, as a significant contributor to neuroblastoma, the most common solid cancer of early childhood. Variants in this gene increase the risk of developing aggressive forms of neuroblastoma and mark the gene for continued disease progression.
A new study found that black children are more likely to have the high-risk form of neuroblastoma and show signs of resistance to modern treatment. The study also showed disparities in outcome according to race, with black patients having a lower survival rate than white patients.
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The addition of immunotherapy to standard therapy increases the percentage of children with high-risk neuroblastoma who are alive and free of disease progression after two years. The new regimen, which targets a substance on tumor cells called GD2, presents a clear paradigm shift in treating this cancer.
A new clinical trial found that 96% of patients with intermediate-risk neuroblastoma survived for three years after receiving reduced chemotherapy doses. The study, led by Katherine Matthay at UCSF Benioff Children's Hospital, aimed to minimize the toxic effects of cancer drugs on young children.
A new immunotherapy treatment has improved two-year survival rates for high-risk neuroblastoma patients by 20 percent compared to standard treatment. Researchers report a higher cure rate, but also more pain and toxic side effects.
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Recent advances in neuroblastoma research have led to a better understanding of the disease's genetic landscape, including common DNA variations on chromosome 6 and mutations in the ALK gene. Innovative therapies such as immunotherapy trials using monoclonal antibodies and cytokines are also being explored.
New research published in the FASEB Journal suggests that DHA and its derivatives can effectively kill neuroblastoma and other cancer cells. The study found that toxic byproducts of DHA were even more effective at killing cancer cells, providing a promising new avenue for anti-cancer treatment.