Articles tagged with Oncogenes
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Researchers found that cancer's powerful genetic on switches, called super-enhancers, drive intense gene activity, causing DNA breaks and stress. This can lead to accumulation of mutations over time, fueling cancer's evolution.
Researchers have discovered a complex regulatory circuit involving SRSF1, AURKA, and MYC that promotes aggressive pancreatic cancer progression. The circuit, which involves alternative splicing, can be targeted with an antisense oligonucleotide to reduce tumor cells' viability and trigger apoptosis.
A new study from Texas A&M University reveals that circadian disruptions change the structure of mammary glands, weaken immune defenses, and fuel aggressive breast cancer. Disabling an immune checkpoint molecule called LILRB4 helps restore the immune system's ability to fight back.
The Alliance for Clinical Trials in Oncology will host a public webinar showcasing key findings from the 2025 ASCO Annual Meeting. Researchers will discuss latest information on colorectal, squamous cell, and renal cell cancers.
The Molecular Analysis for Precision Oncology Congress 2025 (MAP) brings together leading experts to explore the latest cancer research advances. Key topics include AI-integrated diagnostics and therapy, as well as immunotherapy and emerging developments in aging and cellular senescence.
Cancer cells with abundant circular DNA elements (ecDNA) carrying oncogenes like MYCN are resistant to chemotherapy. Combining standard chemotherapy with a secondary therapy targeting these senescent cells leads to improved outcomes in mouse models of neuroblastoma and medulloblastoma.
A team from The Hebrew University of Jerusalem has developed innovative druglike molecules capable of degrading HuR, a key RNA-binding protein that stabilizes oncogenes and fuels cancer progression. These molecular degraders improve anticancer properties by up to 3-4 orders of magnitude compared to traditional HuR-binding molecules.
Researchers have identified FAM111B as a promising candidate for glioma treatment. The study found that FAM111B overexpression enhances glioma malignancy through the PI3K/AKT pathway, providing a novel avenue for therapeutic intervention.
A rare form of childhood brain cancer called Diffuse Midline Glioma (DMG) hijacks gene control machinery to fuel its growth. A specific gene-silencing complex, CBX4/PCGF4-cPRC1, is essential for tumour growth and could be a promising drug target.
Researchers from the University of Southampton engineered a new type of super-strong antibody that triggers a stronger response from the immune system compared to naturally produced antibodies. The study confirms that making subtle increases in rigidity stimulates immune activity, creating a powerful immune response against disease.
Scientists at St. Jude Children's Research Hospital discovered FOXR2 activation in multiple pediatric CNS tumor types, including high-grade gliomas and pineoblastomas, with significantly different clinical outcomes. The study highlights the importance of combining molecular findings with other diagnostic approaches to improve treatment...
Researchers found that pancreatic cancer cells gain a survival edge by carrying copies of critical cancer genes on circular pieces of DNA outside chromosomes. The discovery highlights the importance of targeting extrachromosomal DNA in treating the disease.
Researchers at MUSC Hollings Cancer Center have developed a new model for ovarian cancer that suggests serous uterine cancer may originate in the fallopian tubes, rather than the uterus. The model has already shown promising results in replicating high-grade serous ovarian and uterine cancers.
Researchers at UCSF develop a method to target GTPases, enzymes involved in Parkinson's and many other diseases, by using drugs targeting the K-Ras oncogene. This approach reveals new drug binding sites that could not be predicted by computational tools.
Researchers have found that natural killer cells instinctively recognize and attack the XPO1 protein, which drives cancer growth. By targeting this protein, scientists may be able to activate more killer cells to destroy cancer cells. The study suggests that this approach could lead to personalized cancer treatment with less side effects.
Researchers at the University of Bologna have identified a specific location and genomic context where DNA breaks occur due to topoisomerase I inhibition. This discovery could lead to new cancer treatments by inducing DNA damage and genomic instability in cancer cells.
A new study has shown that a drug developed for pancreatic cancer is effective in treating the most aggressive form of medulloblastoma, a childhood brain tumor. The drug, Minnelide, reduced tumor growth and increased the efficacy of chemotherapy, offering hope for improved survival rates for children with this disease.
Researchers highlight difficulties in targeting metastatic tumors and propose two- and three-drug combinations to achieve effective tumor control. They also emphasize the need for simultaneous blocking of primary driving oncogene, evolving resistance mechanism, and secondary survival pathway.
Researchers have found that some tumors release a protein with a virus-like structure, triggering an out-of-control immune reaction that can damage brain cells. The immune system targets this protein as if it were a foreign invader, leading to rapid-onset memory loss and cognitive deficits.
Researchers report a case of a patient with EGFR L858R mutant non-small cell lung cancer (NSCLC) who experienced durable disease improvement after empirical treatment with osimertinib. The 'Lazarus effect' refers to the phenomenon where cancer appears to recur after seeming to be in remission.
A new study by Tulane University has identified a previously unknown molecular pathway that could halt lung cancer growth. The research found that protein RBM10 can suppress lung cancer by targeting the function of c-Myc, a protein that drives cancer cell growth and proliferation.
CNIO researchers have discovered a previously unknown mechanism of action for the first oncogene, c-Src. The study reveals that c-Src can autonomously activate itself through autophosphorylation, leading to cancer formation. This finding has significant implications for the development of new drugs targeting this enzyme.
A team of Chinese and UK researchers has identified superoxide dismutase 1 (SOD1) as a potential target for reversing drug resistance in ovarian cancer. By using nanoparticles to deliver siRNA that reduces SOD1 levels, the study showed reduced growth and decreased resistance to cisplatin in female mice.
Researchers used base editors to introduce specific combinations of activating and inactivating mutations into healthy organoids, creating realistic models for various types of cancer. This allows for further investigation into the development and treatment of cancer, with potential applications including testing new drugs.
Researchers at NUS developed a mathematical formula to predict the fraction of cells with a unique oncogenic combination linked to low survival rates in DLBCL patients. This combination involves high MYC and BCL2 positivity, but negative BCL6 expression, suggesting BCL6 plays a protective role.
Australian researchers have discovered a link between circular RNAs and DNA mutations that cause cancer. The study found that specific circular RNAs can bind to DNA, leading to mutations and cancer development. This discovery opens the door for using these molecules as new therapeutic targets and markers of disease.
Researchers investigated the roles of STAT3α and STAT3β in aggressive breast cancer and found that differential silencing of these isoforms leads to changes in STAT3 activation. This study emphasizes the importance of distinguishing between STAT3 isoforms for accurate cancer diagnosis and therapy.
Researchers at St Jude Children's Research Hospital have developed a tool to comprehensively characterize oncogenic fusions in pediatric cancer cells. The tool has the potential to cure certain tumors by targeting these fusion genes with CRISPR-Cas9, selectively killing cancer cells while leaving healthy ones intact.
Researchers studied how tumors adapt to Sotorasib and found that gene amplification and transcriptional programs lead to resistance. This knowledge can help develop targeted treatments for patients with KRAS mutations, potentially increasing survival rates.
Cancer develops when genome doubling leads to chromatin disorganization, promoting oncogene activation and genomic instability. Researchers found that WGD causes sub-compartment repositioning and loss of chromatin segregation.
Researchers from Northwestern University discuss the multifaceted tumorigenic functions of EZH2, including its role in regulating translation and coactivating transcription. This new understanding may provide novel insights into advancing EZH2-targeting strategies for prostate cancer patients.
Researchers identify the minimum contribution of TACC3 for FGFR3-TACC3 fusion protein activation, revealing a novel target for treating FGFR translocation-driven cancers. The study shows that clinically identified FGFR3-TACC3 fusion proteins differ in biological activity depending on specific breakpoints.
The study reveals that SETD1A overexpression is associated with poorer disease-free survival in pancreatic cancer patients. Artificially cultured cells showed increased cell growth and migration when SETD1A levels were overexpressed, while knocking down SETD1A expression led to decreased RUVBL1 gene expression.
Researchers at the Salk Institute have identified mechanisms that activate oncogenes in cancer cells, providing insights into predicting and treating the disease. The study found that structural variants in DNA can impact gene expression, leading to cancer, but most variants have no effect.
Researchers have discovered that targeting a specific mutation in fibrolamellar tumors can reduce tumor growth in mice, offering a promising approach to treating this nearly incurable cancer. The findings highlight the potential for novel therapies against an intractable disease.
The TRIDENT-1 trial suggests that repotrectinib could be effective for treating ROS1 positive non-small cell lung cancer (NSCLC) in patients who have received other targeted treatments and those who have not. The drug showed promising results, with an objective response rate of 79% in patients not previously treated with a ROS TKI.
Researchers have developed a drug compound that stops cancer cell growth in mice with little effect on normal healthy cells, making it potentially nontoxic for patients. The therapy targets the epidermal growth factor receptor gene, which is overexpressed in about half of all triple-negative breast cancer cases.
Researchers have developed a model of how human embryos are formed, revealing that genes are switched on almost immediately after fertilization. This discovery may also shed light on the origins of cancer, which is often diagnosed at an advanced stage.
Researchers at the University of Helsinki have identified target genes of the MYC oncogene responsible for its growth-promoting effects. By modifying these genomic binding sites, they slowed down cell growth. This finding has significant implications for developing new cancer treatments.
A team of scientists has determined the structure of the RAF1 protein, a therapeutic target against cancers associated with KRAS oncogenes. The study reveals structural vulnerabilities in RAF1, making it possible to design drugs capable of destroying it.
Researchers at the University of São Paulo found that deactivating the light-sensitive protein melanopsin slows melanoma progression in animal experiments. The study, published in Communications Biology, suggests that melanopsin acts as an oncogene in melanoma, a type of skin cancer.
Researchers discover gene AVIL responsible for deadly brain tumor also causes two forms of childhood cancer, rhabdomyosarcoma. Blocking AVIL activity prevents formation of the disease in lab samples and mouse models.
Researchers used Guardant NGS to analyze nearly 17,000 lung cancer samples and found MET amplification in 1.2% of cases, with 20.8% having overlapping oncogenic drivers. The study suggests that high gene copy numbers and smaller amplified regions can be used to enrich for the true MET-sensitive population.
Researchers at Osaka University identified Src as a key molecule in the process of epithelial cells becoming invasive and cancerous. The study found that CDCP1 forms a molecular scaffold that activates Src, promoting cancer cell invasion.
Researchers at the University of Cincinnati are studying how lipids help fortify lung cancer cells and if targeting them can lead to better outcomes. The team discovered that lipids play a crucial role in cancer cell growth, membrane fortification, and energy production.
Researchers found that hypomethylating agents can activate the SALL4 oncogene in patients with myelodysplastic syndrome, resulting in poor survival outcomes. Early intervention targeting SALL4 pathways may improve treatment and patient outcomes.
Research found that hypomethylating agents (HMAs) activated the oncofetal protein SALL4 in up to 40% of patients with MDS, resulting in poor patient survival. This activation is linked to demethylation and upregulation of oncogenes, suggesting a need for additional combination therapy.
The NCCN Annual Conference focuses on the cancer patient journey, featuring state-of-the-art practice algorithms, updates to clinical guidelines, and new therapies. Leading experts present treatment recommendations for various cancer types, including breast, colorectal, and lung cancer.
A recent study found that mutant clones expand in the normal endometrium through a rhizome structure, which arises from a common ancestral clone. This expansion increases the risk of developing endometriosis and endometrial cancer. The study proposes a new model of clonal expansion in the normal endometrium.
A recent study published in Developmental Cell reveals that Kras mutation causes chromatin rearrangement, leading to stem-like cell regeneration and tumor onset. The team discovered a protein complex called AP-1 as the mediator of this process, which can be targeted with small-molecule drugs.
Researchers at Children's Hospital of Philadelphia define a 3-tiered molecular classification system for pediatric differentiated thyroid cancer, where fusion oncogenes are associated with more invasive disease and lower remission rates. The study contrasts findings from adults, who have a two-tiered system based on BRAF mutations.
Researchers discover a chromatin degrader that blocks cancer-causing genes, offering potential treatment for over 90% of prostate cancers. The study found that blocking the SWI/SNF complex slowed cancer cell growth and induced cell death, especially in tumors driven by FOXA1 or androgen receptor.
New study suggests inhibiting Shp2 in tumor cells may boost tumor growth and survival, complicating its use as a potential cancer therapy for HCC.
Researchers discovered a microRNA, miR-766-5p, that targets super-enhancers and reduces MYC expression in cancer cells, inhibiting growth rates. The study suggests this molecule could be used as an anti-cancer therapeutic to fight MYC-driven cancers.
Researchers developed a machine learning tool, BoostDM, that evaluates the potential contribution of mutations in genes to cancer development. The tool helps understand how tumors are caused at the molecular level and can facilitate medical decisions regarding therapy.
A study led by D. Ross Camidge found that MET amplification drives a rare subtype of non-small cell lung cancer, which responded to crizotinib therapy. The research also highlights the importance of MET amplification testing and therapies for this unique patient population.
Researchers at IMIM-Hospital del Mar and CIBERONC discover a low-toxicity treatment combining chemotherapy and BRAF inhibitors eradicates malignant melanoma by preventing DNA repair. The strategy offers a new therapeutic perspective for patients with BRAF oncogene mutations.
Researchers at Lund University discovered how E. coli bacteria target and degrade the MYC oncogene, a well-known contributor to many forms of cancer. This discovery has shown potent effects on tumor growth and increased survival in two different cancer models.
Researchers have identified AVIL as an oncogene that plays a critical role in the development of glioblastoma. Targeting this gene shows promise as an effective approach for treating the disease.
St. Jude Children's Research Hospital scientists have developed a computational tool called cis-X to identify alterations that drive tumor formation in the human genome. The method analyzes abnormal expression of tumor RNA and identifies novel pathogenic variants and oncogenes activated by such variants in regulatory noncoding DNA.