Articles tagged with Oncogenes
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.
The study identified three ways in which the FOXA1 gene mutates to trigger prostate cancer: FAST, FURIOUS, and LOUD. Class 1 mutations cause rapid DNA traversal, class 2 mutations prevent normal FOXA1 from binding, and class 3 mutations create duplications of oncogenes. These alterations have different clinical implications for patients.
A new CRISPR/Cas9 system allows for precise gene knock-in in live cancer mouse models, improving efficiency and control over gene insertion. The system was used to model intrahepatic cholangiocarcinoma, a type of liver cancer, and successfully induced tumor formation in mice.
Researchers have discovered that PLK1 acts as a tumor suppressor in some breast tumors, halting development and changing prognosis. This finding was made by researchers from CNIO and DKFZ.
Glioblastoma tumors exhibit cell-to-cell differences that contribute to therapy resistance. Extrachromosomal DNA is found to play a key role in oncogene amplification, driving cancer progression and evolution. Researchers are developing novel combination therapies targeting ecDNA elements to improve treatment outcomes.
Researchers at Uppsala University identified a new mechanism that could explain the tumor-promoting role of EZH2 in multiple myeloma. Inhibiting EZH2 reduces the survival of tumor cells by downregulating oncogenes and upregulating microRNAs with potential tumor suppressor functions.
Researchers identified a new subtype of cervical cancer with distinct genomic pathways, potentially benefiting from alternative treatments. The study found significant differences in tumor characteristics between HPV-active and -inactive subtypes.
Researchers identified unique genetic signatures in four human breast cancer cell types, which can be used to tailor therapies using combinations of targeted drugs. The study found that targeting multiple driving oncogenes with lower doses reduces side effects and increases effectiveness.
A novel nanotechnology-based approach detects c-myc mRNA biomarkers for early-stage colon cancer diagnosis. The technique uses peptide nucleic acid/silver nanoparticles to induce a reversible color change.
Researchers discovered that disruptions in chromosomal looping structures can activate oncogenes fueling aggressive tumor growth. These findings reveal the powerful influence of genome structure on human health and disease, offering new insights into cancer diagnostics and treatment protocols.
A recent study published in Oncogene reveals that alterations in an intermediate molecule called RNA can lead to protein mutations without DNA damage. This discovery highlights the importance of RNA editing enzyme ADAR1 in regulating gene expression and contributing to tumor growth.
Researchers identified a connection between DNMT3A gene mutations and the activation of oncogene MEIS1, which induces acute myeloid leukemia. The study found that this subtype of leukemia may be sensitive to drugs targeting both genes.
Researchers at the University of California, San Diego School of Medicine found that combining ROR1 and TCL1 oncogenes in mice accelerates and worsens blood cancer. The study suggests ROR1 could be an important therapeutic target for patients with CLL, a common form of blood cancer affecting over 15,000 new cases annually.
A new study at Harvard Medical School proposes that aneuploidy is a driver of cancer development rather than just a result. Researchers analyzed genome sequence data from over 8,200 pairs of cancerous and normal tissue samples to identify patterns in tumor evolution.
Researchers have discovered a new oncogene, NTRK1, that drives a subset of lung cancers. A novel targeted treatment approach has been proposed, with preclinical studies showing effective silencing of mutated NTRK1 genes using specific compounds.
Researchers identified a novel mechanism by which the activity of Src is limited by the cell's skeleton, resulting in the development of tumors. The cytoskeleton network, comprising actin proteins and actin-Capping Proteins, plays a crucial role in regulating protein activity.
Researchers argue that changing tissue landscape promotes higher cancer rates in the elderly, rather than accumulating oncogenic mutations. Healthy cells in young bodies outcompete cells with cancerous mutations when conditions change.
A study has identified an antitumor molecule originating from a cancer-causing gene that inhibits pro-cancer action of the oncogene. The finding could lead to discovering other oncogenes and anti-oncogenes, contributing to tumor development.
Researchers at Dana-Farber Cancer Institute discovered that advanced pancreatic cancers in mice cannot survive without the mutant Kras oncogene, which rewires key metabolic pathways. The study suggests that targeting these altered metabolic pathways might be a potential approach to treat the deadly cancer.
Researchers at Genentech have identified a binding pocket on the Ras oncogene that provides an opening for therapeutic agents to attach. The discovery makes Ras, a gene mutated in 25% of human tumors, 'druggable' for cancer treatment.
Researchers reveal that MLL-AF9 hijacks Myb to enforce aberrant self-renewal in leukemia cells. Inhibiting Myb results in rapid and complete eradication of cancer, validating a new approach for targeting oncogene addiction in vivo.
Research findings challenge traditional views on cancer treatment, revealing Cop1's role in tumor suppression rather than promotion. The study suggests that inhibiting Cop1 could stimulate cell proliferation in cancer cells.
Researchers have identified a novel oncogene GNA11 associated with uveal melanoma in over 40% of tumor samples. This discovery offers new targets and treatments for the disease, which affects about 1,500 people in the US each year.
A team of scientists at Beth Israel Deaconess Medical Center discovered that the Rictor protein plays a key role in destroying a close cousin of the AKT oncogene, SGK1. This finding suggests that faulty regulation of Rictor may play a part in some forms of cancer and could offer new targets for treating the disease.
Researchers at Stanford University School of Medicine found that certain cancer therapies require the presence of a specific immune cell type, T helper cells, for optimal efficacy. The study showed that disabled oncogenes were more successful in eradicating tumors in mice with intact immune systems.
Researchers propose a new approach to combat cancer and autoimmune diseases by targeting the balance between NF-kB and p53 signaling pathways. This balance is believed to be a promising target for developing new drugs, with potential benefits including improved disease treatment outcomes.
Researchers deciphered a key pathway used by Myc oncogene, finding that disabling it can restore cellular senescence and prevent cancer growth. This discovery offers new potential for treating various types of cancer by targeting the oncogene's dependence on Miz1.
Peter K. Vogt's groundbreaking discovery of src, the first cancer-causing gene, has profoundly changed biology and medicine. His research has yielded several important targets in cancer therapy.
Researchers from the University of Innsbruck have identified a primitive cancer gene in a fresh water polyp, revealing similar biochemical functions to those found in humans. This discovery sheds light on the evolution of cancer and its relationship to stem cells.
Researchers at the University of Innsbruck have discovered that BASP1 inhibits uncontrolled cell growth and proliferation caused by the Myc gene, which is a key factor in tumor development.
Researchers at Cold Spring Harbor Laboratory discovered that DNA damage response pathways mediate oncogene-induced senescence. The study suggests that targeting these pathways could lead to novel approaches for preventing cancer formation.
Researchers found that melanocytes use a mechanism called premature senescence to prevent cancer-causing mutations from triggering melanoma. This process involves the endoplasmic reticulum, which senses oncogene activity and triggers a response that stops cell division and prevents tumor growth.
Researchers at Georgia Institute of Technology have discovered the rules governing gene amplification events, including the role of palindromic sequences and hairpin-capped double strand breaks. This finding has potential applications in cancer prevention and treatment by identifying strategies to restrict gene amplification.
Researchers identified a sequence within the 3' UTR of Her2 mRNA that overrides inhibitory effects of 5' uORF, increasing Her2 translation in breast cancer cells. This mechanism is crucial for understanding post-transcriptional control processes and identifying new molecular targets for cancer treatment.
Researchers have found that Cdk4 expression is essential for Ras-induced cancer development, making it a potential target for therapy. Dr. Hiroaki Kiyokawa and colleagues showed that Cdk4-deficient cells can enter a protective state of senescence when exposed to oncogenes like Ras.
The Ras oncogene's suppression of p53 could explain why some cancers are resistant to radiation therapy. The finding suggests that Ras may play an indirect role in many more cancers by regulating the tumor-suppressor gene, contributing to cancer development.
Researchers found that telomerase expression can activate the c-myc oncogene, a hallmark of cancer cells. This raises concerns about using telomerase in human tissue culture cells for therapeutic purposes.
Research at Emory University Health Sciences Center suggests that high blood pressure caused by sodium retention could be related to oncogenes involved in cancer. Understanding the complex communication and regulation of kidney cells may help better comprehend how kidney diseases begin and hypertension is controlled.