Articles tagged with Cancer Genomics
Researchers found that bacteria have a 'risk management' strategy to control mutation rate in key genes, decreasing the risk of detrimental mutations. The study provides insights into how disease-causing mutations arise and may be involved in cancer development.
A large-scale genetic study reveals that triple negative breast cancer tumours exhibit a continuum of different types, making them difficult to treat. The discovery highlights the importance of tailoring cancer drug treatment to individual tumour profiles.
The Cancer Cell Line Encyclopedia offers a comprehensive resource for cancer research, integrating gene expression, chromosomal copy number, and pharmacological profiles. This will enable researchers to predict drug sensitivity and improve the success rate of drug development in personalized medicine.
Scientists have identified a paradoxical function of the gene Chk1, which is typically known for its anti-cancer properties. In this study, researchers found that extra copies of Chk1 actually facilitate tumor growth in mice, highlighting the complex role of this gene.
A new study by Ohio State University researchers found that mobile DNA elements, called transposons, can significantly disrupt gene expression and cause biological variation in mice. The study discovered that these elements can influence gene expression even when located far away from the affected gene.
Scientists have identified two novel susceptibility genes, EDIL3-HAPLN1 and ANO6, related to bone formation and cartilage development. The study also confirms the previously reported association with HLA-B*27 variants, suggesting a complex interplay of immune mechanisms.
Two independent research teams identify Fusobacterium in colon cancer tissue, a finding that could lead to new avenues for diagnosis and treatment of the disease. The bacteria were found more often in colon cancer tissues than normal tissue, sparking potential links between infection and colorectal tumors.
NextBio's web-based tools aid in assessing potential drug efficacy and adverse effects by analyzing publicly available genomic data, identifying correlations with gene expression changes and cancer profiles.
Genome-wide studies have identified new genes involved in melanoma susceptibility, including Caspase 8 and ATM gene. The study validates regions and genes already identified as significant for melanoma, reinforcing the role of cell cycle genes like CDKN2A and CDK4.
A team of researchers at Baylor College of Medicine identified a sudden chromosomal catastrophe that occurs early in development, leading to developmental delay and cognitive disorders. The study found that this catastrophe shares similarities with massive genomic rearrangements in cancer.
Researchers have created a method for silencing non-protein-coding genes using zinc finger nucleases. This allows for the study of these genes' molecular and cellular functions, which are thought to play a role in cancer development.
A recent study published in Gastroenterology has identified two distinct genetic subtypes of stomach cancer that respond differently to chemotherapy. The researchers found that one subtype, intestinal-type, is more responsive to certain treatments, while the other, diffuse-type, requires a different approach.
Cancer researcher Peter Duesberg suggests that cancer is a form of speciation, where tumors are new species that operate independently and can grow without host control. This theory could lead to new insights into cancer growth and metastasis, as well as new approaches to therapy.
Researchers from the Broad Institute and Harvard identified genes essential for ovarian tumor growth, including PAX8, which is altered in nearly one-fifth of surveyed tumors. The study's findings have implications for cancer research, suggesting that classification based on genetic mutations may be more revealing than tissue origin.
Researchers developed a novel analysis method to organize genomic cancer data, revealing previously unknown genetic connections and similarities among different types of cancers. The approach uses multiplicity to create three-dimensional models, potentially leading to trials of already approved drugs for additional cancers.
Researchers from UNC Lineberger have contributed to a comprehensive view of cancer genes in ovarian cancer, identifying sets of genes associated with patient survival patterns and potential therapeutic targets.
Researchers discovered that Barrett's esophagus arises from embryonic cells present in all adults, which can rapidly grow and form unusual tissue when the esophagus is damaged by acid reflux. This finding provides a potential target for preventing esophageal cancers.
Researchers have discovered a single communication system that decides the fate of stem cells, paving the way for new stem cell therapies with fewer side effects. The Nodal/Activin pathway can specify a wide range of eventual cell types, offering a major step forward for personalized medicine.
A new online tool, Mouse Phylogeny Viewer, allows researchers to select from 162 strains of laboratory mice for which the entire genome has been characterized. This tool enables scientists to design better experiments by selecting strains with greater genetic diversity, ultimately improving the translation of results to humans.
Job Dekker, an associate professor at UMass Medical School, has been awarded the Young Investigator Award by the American Society for Biochemistry and Molecular Biology. He developed methods to analyze millions of chromosome interactions in parallel, opening a new field of study.
Researchers at North Carolina State University used a genetic model of dogs to identify genes involved in human non-Hodgkin lymphoma. The study found that only a few genes were shared between dogs and humans, suggesting that the genetic changes associated with the cancer are much less complex in canines.
Studies reveal Tet protein maintains pluripotency in stem cells by silencing differentiation genes while activating pluripotency genes. The protein's product, 5-hydroxymethylcytosine, plays a crucial role in regulating transcription and is the first genome-wide location of its role in development and disease.
A University of Louisville professor is developing a statistical model that can help determine what prolongs cancer-free survival. The new multi-state model analyzes how diseases progress from one stage to another, allowing for broad inspection of patient patterns and data collection.
Researchers at IDIBELL have identified a small molecule called enoxacin that inhibits tumor growth by activating the 'dark genome' and microRNA molecules, offering new potential for cancer treatment. The study's findings open up new directions for anti-tumor therapy targeting microRNA as a therapeutic target.
A Mayo Clinic research team has pinpointed the function of the MMSET gene, revealing how it enables disease-causing mutations to occur. Normally-functioning MMSET plays a restorative role within the genome, but when impaired, cells lose the correct response to DNA damage.
Researchers identified 27 genes that influence the effectiveness of oxaliplatin in treating colorectal cancer. The study highlights the need for further clinical research to improve treatment outcomes and reduce side effects associated with the drug.
Researchers have documented genetic abnormalities in human embryonic stem cells and induced pluripotent stem cells, including duplications near pluripotency-associated genes and deletions involving tumor suppressor genes. Frequent genomic monitoring of these cell lines is necessary to ensure their stability and clinical safety.
Scientists have identified age-related gene-specific accumulation of DNA methylation that suppresses the critical TGF-beta pathway contributing to ovarian carcinogenesis. This finding provides crucial information for future translational research and may lead to targeted therapeutic interventions.
A team of researchers discovered that mutant enzymes in leukemia create a chemical poison to cause cancer. This finding suggests a new avenue for treating acute myelogenous leukemia and other cancers.
The Salk Institute created the Renato Dulbecco Chair in Genomics and Roger Guillemin Chair in Neuroscience, honoring their groundbreaking research contributions. The $6 million gift from Irwin Jacobs will pay tribute to Drs. Dulbecco and Guillemin's leadership and innovation.
Genomic Systems announces a major breakthrough in treating terminal cancer, citing research published in PNAS that shows an anti-PECAM-1 antibody is effective against three common fatal cancers in mice. The treatment targets normal endothelial cells rather than directly attacking cancer cells.
The $1.5 million grant will fund Ben Major's work to identify functional human genes contributing to specific cellular processes, such as cancer growth and migration. The goal is to develop a low-cost approach to determine gene function in the human genome.
Researchers found a way to shrink tumors in certain cancers by blocking the production of microRNA 380, which disables the P53 gene. This breakthrough provides hope for new treatments and may return cells to normal when blocked.
Two assays, GCR and RQPS, are used to investigate the genetic basis of cancer by measuring chromosomal rearrangements and gene copy numbers. These methods provide insight into pathways that suppress genomic instability in yeast and humans.
A study mapping vitamin D receptor genome-wide connections autoimmune disease and cancer genes reveals novel links of vitamin D with disease predisposition. Vitamin D insufficiency is a growing concern worldwide, especially for individuals genetically predisposed to be sensitive to deficiency.
Researchers have identified a gene, CACGN2, associated with chronic pain susceptibility in humans. The study suggests that genetic variants in this gene may contribute to individual differences in chronic pain experience.
Researchers at Ohio State University found that breast cancer cells can regulate 14 genes simultaneously in response to estrogen-like compounds like BPA. This mechanism may contribute to cancer development and could serve as a marker for studying environmental exposure.
Researchers found genetic risk factors for nasopharyngeal carcinoma (NPC) linked to HLA locus and three new genes TNFRSF19, MDSIEVI1, and CDKN2A/2B. The study advances understanding of NPC's role in southern China's high prevalence.
Researchers discovered that metformin disables the mTOR complex through RAG GTPase, rather than activating TSC proteins via AMPK. This finding raises the possibility of using metformin more widely to treat cancer and diseases linked to TSC deficiency.
Researchers analyzed genetic networks of microRNAs in tumors to understand how interactions go awry in disease. The study found that normal network interactions have become disrupted or rewired in cancer, contributing to disease progression.
Researchers at Ohio State University discovered that microRNA-155 can silence genes protecting against DNA mutations, contributing to cancer progression. The study suggests miR-155 expression may be a key stratification factor in cancer prognosis and treatment.
Singapore scientists have made significant breakthroughs in understanding early embryonic development using single cell gene expression analysis. The study resolves debates on cellular differentiation events and highlights the importance of fibroblast growth factor signalling in cell fate decisions.
Cancer genetics expert Bert Vogelstein will review the landscape of cancer genome research and its applications. He predicts that early detection and prevention will be key to reducing cancer deaths in the future.
Researchers at USC have identified a distinct molecular subtype of glioblastoma multiforme (GBM) associated with improved clinical outcomes, including median survival time of over three years. The discovery was made using epigenomics and has potential implications for targeted drug treatments.
Dr. Von Hoff, TGen's Physician-in-Chief, has been recognized with the David A. Karnofsky Memorial Award and Lecture at ASCO's Annual Meeting. He is a renowned physician-scientist who has contributed to developing numerous anticancer agents.
A new study found that one in three early-stage breast cancer patients felt they didn't fully understand their genomic test result discussions, while a quarter experienced distress. The study suggests there is room for improvement in communicating cancer recurrence risks and treatment decisions with patients.
A large-scale study reveals over 100 genomic sites with missing or duplicated DNA in tumors, uncovering novel cancer genes and genetic abnormalities shared across multiple cancers. The study highlights the importance of common genomic alterations in driving cancer growth.
Researchers at the Genome Institute of Singapore have made a significant breakthrough in understanding gene expression and regulation by developing a novel technology called ChIA-PET, which successfully mapped long-range chromatin interactions throughout the human genome.
Researchers have identified heterochromatin, a gene-poor compartment of DNA, as the key to explaining reproductive isolation. Odysseus, a fruit fly gene, has been found to interact with rapidly evolving DNA in heterochromatin, leading to hybrid sterility.
Researchers aim to understand the 'language' of the human genome by linking proteins to their genomic blueprints. The goal is to enhance efforts to solve pressing health issues like heart disease and cancer.
The M.D. Anderson team will use a systems biology approach to analyze multi-gene pathways and combinations of pathways in cancer. The goal is to generate molecular portraits of cancers to personalize therapy choices and improve cancer risk assessment.
A team of Duke and Singapore scientists have discovered a new way to classify gastric cancers based on the signaling pathways used to grow and spread. This new system may lead to more effective treatments and improved long-term survival for patients, as it allows for stratification according to tumor pathway profiles.
The University of North Carolina has been awarded a $13-20 million Cancer Genome Atlas Grant to better understand the mechanisms responsible for uncontrolled growth of cancer cells. The project aims to develop a comprehensive catalog of genetic and genomic changes in cancers, which could fuel rapid advances in cancer research.
Researchers at Johns Hopkins University developed a highly sensitive test using quantum dots to detect DNA methylation, an early warning sign of cancer. The test could alert people at risk and help doctors determine the effectiveness of cancer treatments.
Researchers at the University of North Carolina have decoded the entire structure of an HIV genome, revealing intricate patterns and structures that play a previously unappreciated role in the virus's lifecycle. This breakthrough opens doors for further research and potential antiviral drug development.
A study has pinpointed a genetic link for increased risk of urinary bladder cancer, finding that people with a specific variant have a 30-40% higher risk. The research suggests potential for targeted prevention and early treatment efforts to save lives.
A new region of the genome associated with an increased risk of melanoma has been identified by researchers at Leeds University and IDIBAPS, funded by the European Commission. The study found a link between this region and skin pigmentation, as well as two previously identified regions linked to melanoma risk.
A team of researchers from Ben-Gurion University discovered a link between the mitochondria genome and an increased susceptibility to complex diseases like cancer. The study analyzed 98 unrelated individuals and found that certain mutations, which were advantageous in ancestral environments, are now associated with disease.
Researchers at UNC have redefined the process of X-inactivation, a genetic phenomenon that helps females avoid toxic genes. The new findings suggest Xist gene's role is more nuanced, and its absence may not trigger X-inactivation but rather allow genes to become active again.
Scientists have identified novel epigenetic markers in melanoma that can be used to develop new treatments. The markers, which are alterations to DNA chemical modifications, were found to be correlated with gene repression and can be reversed by treating cancer cells with a drug called decitabine.