Articles tagged with Cancer Proliferation Genes
A new clinical trial will investigate whether adding the oral medication vorasidenib to standard chemotherapy improves progression-free survival for people with newly-diagnosed, grade 3 IDH-mutant astrocytoma. The study aims to recruit 400 individuals with this type of brain cancer and evaluate the safety and side-effect profile of the...
Researchers at MD Anderson have made significant discoveries in the treatment of rare bile duct cancers, with zanidatamab showing promising results. Additionally, a study identified RASH3D19 as a target to overcome treatment resistance in KRAS-mutant 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.
R-loops are essential regulatory elements in gene expression, DNA replication, and repair mechanisms. However, when dysregulated, they pose risks to genome integrity, threatening diseases such as cancer and neurodegeneration.
A new study finds that a specific genetic variation in the PTGS2 gene is associated with an increased risk of benign prostate hyperplasia (BPH) in Lebanese men. Men carrying the C version of this gene were more than twice as likely to have BPH compared to those without it.
A novel circular RNA, circTP63-N, generated by back-splicing exons 2–4 of the TP63 gene is significantly downregulated in nasopharyngeal carcinoma (NPC) tissues. Restoring its expression effectively inhibits NPC cell proliferation and metastasis via engagement with HSP90AB1 to modulate the YAP1/Hippo signaling pathway.
Research highlights shared mechanisms among aging, circadian rhythms, and cancer, including genomic instability, cellular senescence, and chronic inflammation. Modulating circadian rhythms may delay age-related functional decline and serve as a novel strategy to intervene in cancer progression.
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.
Research highlights the interconnected relationship between aging, circadian rhythms, and cancer, with shared mechanisms including genomic instability, cellular senescence, and chronic inflammation. Modulating circadian rhythms may serve as a novel strategy to intervene in age-related functional decline and treat cancer.
Researchers found a biomarker, RNA Polymerase II (RNAPII), associated with tumor aggressiveness and recurrence in meningioma and breast cancers. The study developed a novel profiling technology, Cleavage Under Targeted Accessible Chromatin (CUTAC), to measure gene transcription activity from DNA, which predicted cancer outcomes.
Researchers at Osaka Metropolitan University assessed target genes in canine hepatocellular carcinoma (HCC) to develop molecular targeted therapies. The study identified potential gene targets, including PDGFB, which may improve treatment options for unresectable HCC.
Researchers at KAIST have discovered a molecular switch that can induce cancer reversal by capturing the moment of critical transition before normal cells become irreversibly cancerous. The technology uses single-cell RNA sequencing data and computer simulation analysis to identify the molecular switch.
A new study from Stanford Medicine found that certain short-chain fatty acids produced by gut microbiome digestion have anti-cancer actions. The researchers discovered direct epigenetic changes at specific genes regulating cell proliferation and differentiation, potentially leading to cancer disruption.
Scientists have discovered how a mutated ASXL1 gene disrupts normal blood cell development, leading to diseases such as clonal hematopoiesis and malignant leukemias. The study reveals that mutated ASXL1 causes heterochromatin dysfunction, silencing genes essential for blood cell maturation.
Researchers at Osaka Metropolitan University found that suppression of Pcdh8 is essential for proper notochord elongation in zebrafish embryos. This study may lead to novel tumor therapies in humans due to the gene's role in controlling cell proliferation.
A team of researchers at the University of Toronto has discovered two distinct subtypes of glioblastoma cancer stem cells, each with unique genetic vulnerabilities. By targeting these vulnerabilities, a more effective treatment approach may be developed, improving prognosis for patients with this lethal brain cancer.
A study published in Science Advances has identified key characteristics of multiply recurrent meningiomas (MRMs), a highly aggressive form of brain tumor. Researchers found that MRMs are more numerous, larger and more common in men than women, with increased chromosomal instability and DNA methylation.
A novel network computer model, DiWANN, allows for efficient searches of cancer genetic data, identifying co-occurring mutations and similarities among DNA sequence elements across several types of cancer. The model provides a scalable solution to prioritize possible treatment targets.
Researchers identify key genes involved in osteoblast differentiation, finding positive correlations between WNT10B and these genes, and inverse correlations with WNT5B. The study hypothesizes that the use of WNT activators or inhibitors depends on whether canonical or non-canonical pathways are activated.
Researchers discovered hundreds of potential new cancer driver genes through splicing analysis, expanding therapeutic targets. The study found little overlap between splicing and mutation-driven cancer drivers, revealing a new class of potential cancer drivers that can be targeted independently.
A faulty copy of the ZNRF3 gene can lead to abnormal brain growth and neurological symptoms. The study found a correlation between patients' brain size and the location of mutations in the gene.
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.
Researchers found that hyperactivated neurons drive cancer proliferation and that serotonin uptake by ependymoma cells promotes tumor growth. Inhibiting this process blocked tumor growth, opening doors for drug discovery.
A distinct TNF-α signaling program has been identified as a key driver of epithelial cancer development, contributing to cell proliferation and invasion. The researchers found that this program is active in both normal tissues and tumors, but its level of activity correlates with tumor aggressiveness.
Researchers investigate chemical modifications to genetic regulation mechanisms, finding that Set8 controls gene activity through a mechanism other than histone modification. This study refines our understanding of genetic regulation relevant to human diseases like cancer.
Researchers at MD Anderson Cancer Center have identified a small molecule compound that restores physiological levels of telomerase reverse transcriptase (TERT), reducing cellular senescence and tissue inflammation. TERT restoration also spurred new neuron formation with improved memory and enhanced neuromuscular function.
A new study using next-generation molecular sequencing and DNA methylation profile analysis identified a rare type of pediatric brain tumor with specific genetic alterations. The tumors were found to be clinically aggressive but some responded well to chemotherapy, highlighting the need for personalized treatment strategies.
Researchers found that miR-377 reduces MYC mRNA levels, leading to increased Bax and PTEN expression and decreased CDK4. This results in induced apoptosis, inhibited proliferation, and arrested cell cycle in prostate cancer cells.
Researchers investigate senescence phenotypes of human corneal endothelial cells upon treatment with ultraviolet (UV)-A. Cells exhibit enlarged morphology, increased β-galactosidase activity and decreased proliferation. UV-A-induced senescent cells show similar gene expression profiles to ionizing radiation (IR)-induced cells.
Researchers discovered that mutations in noncoding regions of cancer-driving genes can alter mRNA abundance, leading to increased or decreased protein production. This discovery may lead to the development of prognostic testing tools and a better understanding of gene regulation mechanisms in cancer progression.
Researchers at Kyushu University identified a new type of tumor cell population, steroids-producing nodules (SPNs), which lead to cortisol-producing adenomas. The study provides clues into the formation and maintenance of the human adrenal cortex.
Researchers have found that alterations in the blood immune system increase cancer risk, and identified over 1,000 genes influencing this regulation. The study also discovered protective roles of certain immune cells against common cancers.
A team of researchers found that diffuse anaplasia (DA) subtype of Wilms tumor grows despite high DNA damage and TP53 mutation, leading to resistance to chemotherapy. The study suggests that DA histology emerges through accumulating DNA damage and CNAs, creating selection pressure for TP53 mutations.
Researchers at Duke University successfully introduced a mutated BRAF gene into rat heart tissue, inducing growth and cell division. However, the approach was associated with significant loss of contractile strength, highlighting the need for precise control over gene activation and delivery.
Researchers developed an mRNA therapeutic that combats ovarian cancer by producing functional p53 protein, shrinking and killing tumors. The treatment is effective against metastases and has shown promise in preclinical studies.
Researchers analyzed LTBR expression levels in various cancers, finding it associated with low patient survival and immune cell infiltration. The study identified LTBR as a potential target for cancer immunotherapy and marker of poor prognosis.
A recent study by Goethe University Frankfurt has identified a mechanism that could be a suitable starting point for developing novel drugs against leukemia cells. The researchers discovered that the mutated NPM1 gene variant drives pro-autophagic activity, enabling cancer cells to recycle their structures and meet their needs.
Researchers have made a breakthrough in understanding the genetic changes that occur during tumor migration, and discovered a drug that can obstruct this process. A new clinical trial at the University of Rochester's Wilmot Cancer Institute will test the effectiveness of the experimental drug NP137.
A team of KAUST researchers has found a critical protein that regulates cell division and proliferation in breast cancer and leukemia. Their work clears the way for the development of targeted drugs by refuting recent challenges to their approach.
Researchers developed a new technique, GoT-Splice, to analyze RNA splicing in individual cells, revealing how mutations in genes controlling this process lead to diseases. The study linked these mutations to specific changes in immature red blood cells and discovered disruptions in the gene BAX.
Researchers create accurate tumor models using 3D bioprinting and a bioink made from Laponite, improving bonding and cross-linking capabilities. The study shows that Laponite enhances biological signaling in the tumor microenvironment, increasing cell viability and promoting anti-tumor drug development.
Scientists have identified the mechanisms behind how SOX9, a pioneer factor, reprograms adult epidermal stem cells to form cancerous tissues. By activating SOX9, researchers can induce basal cell carcinoma-like structures and study the underlying epigenetic processes.
A study published in Cancer Research identifies a novel mechanism by which liver cancer develops, involving the aberrant activation of the Wnt signaling pathway and the gene GREB1. The research reveals that GREB1 is responsible for integrating conflicting cellular states of differentiation and proliferation, leading to tumor promotion.
Researchers have discovered a new genetic culprit in canine bladder cancers, with implications for early detection and targeted treatments. The study found that 13 out of 28 cases had a different type of mutation, which could lead to more precise treatment options.
Researchers discover that inhibiting a gene crucial for DNA production can significantly reduce destructive cell proliferation and disease progression in pulmonary hypertension. This finding presents a potential treatment target for the condition, which affects females aged 30-60 with limited treatment options.
A new review paper discusses the role of CDK4 in regulating the cell cycle and its involvement in cancer. The study highlights the importance of CDK4/6 inhibitors as treatments for ER+ breast cancer and their potential utility in multiple tumor types.
A study using mRNA and miRNA expression profiles identified molecular signatures that can differentiate muscle invasive bladder cancer patients who respond to neoadjuvant chemotherapy from those who do not. The research found distinct gene pathways and subtypes associated with response, which may lead to more effective treatment delivery.
A new epigenetics drug, tazemetostat, has been found to stop bladder cancer growth by activating the immune system, not just inhibiting tumors. The drug targets the EZH2 gene and is being tested in clinical trials for late-stage bladder cancer.
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 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.
Researchers at Harvard Medical School and Brigham and Women's Hospital identified hundreds of cancer-driving genes with unique sensitivities in various tissues. The study suggests that tissue type plays a crucial role in cancer genetics and may impact the effectiveness of treatments.
Researchers have developed a molecular sensor that can detect and eliminate cells with mutated TP53 genes, which are responsible for 50% of all human tumors. The sensor initiates cell death if the gene is non-functional, preventing tumor formation at an early stage.
The study reveals that TLK2 is vital for placenta and embryo viability in mice, with implications for human intellectual disabilities. The researchers found that mutations in the TLK2 gene may cause impaired placental function, leading to insufficient oxygen during development and potential neurological disorders.
Scientists at Hokkaido University found that ARL3 facilitates STAT3 transport into the nucleus, regulating gene expression and cell proliferation. This discovery offers promising candidates for novel therapies targeting STAT3-related diseases.
A study published in Genes & Development found that inhibiting the MLL1 enzyme prevents age-related inflammation and cancer. Researchers discovered that MLL1 is critical for regulating gene expression and is commonly mutated in human cancers, leading to increased inflammation and tissue degeneration.
Researchers discovered that blocking proteins produced by the MYC oncogene can halt ovarian cancer cell proliferation. Using RNA interference, they silenced c-Myc and L-Myc proteins in lab cultures with amplified MYC, preventing cancer cell growth.
Researchers at Ohio State University's Comprehensive Cancer Center discovered that mice can develop normally with just one of the four E2f genes. The study suggests that the location and timing of gene activity play a crucial role in development, contradicting previous assumptions about cancer-causing gene regulation.
Researchers at the University of Helsinki discovered that tightly organized epithelial cells can suppress malignant cell proliferation, with a focus on the LKB1 tumor suppressor gene. The study found that epithelial cells lacking LKB1 protein form disorganized structures enabling cancer genes to drive proliferation.
Researchers Drs Sun and Arceci find that loss of PASG gene results in reduced genomic methylation and premature aging in mice. The study reveals a potential model for studying aging and epigenetic regulation, with implications for cancer predisposition and therapeutic targeting.