Articles tagged with Cancer Genomics
Researchers have identified silent ancient DNA elements in our genome that, when reactivated, stimulate the immune system to fight cancer. The discovery of ADAR1, an enzyme used by cancer cells to evade detection, opens up a new field of cancer therapies.
Researchers identify lysine acetylation as key regulator of Pif1 helicase, a protein involved in genome stability and cancer. The study's findings could lead to more targeted cancer therapies by fine-tuning drugs to target specific enzymes.
Researchers developed a novel epigenomic approach to detect pancreatic cancer in its early stages using blood draws, identifying distinctive patterns in thousands of genes that serve as biomarkers. This technology has the potential to lead to more timely treatment and improved patient survival.
Scientists at Cold Spring Harbor Laboratory discovered the intricate details of the Origin Recognition Complex (ORC), a crucial protein in human genome replication. ORC changes shape dramatically as it assembles around DNA, with parts twisting and pinching to interact with the molecule.
A team of researchers identified specific therapeutic targets for adenosquamous cancer of the pancreas (ASCP), a deadly form of pancreatic cancer. The study used multiple analysis methods to identify mutations and genomic variants, including FGFR signaling and RORC, which could be targeted by existing drugs.
Scientists at Cornell University's veterinary college have identified the genetic drivers of ovarian cancer, a deadly disease that kills more women than any other cancer. The study reveals that ovarian surface stem cells are more susceptible to mutations, while certain genes can inhibit cancer initiation.
Researchers found widespread imbalances in chromosomal gains and losses between cells taken from different parts of tumors, indicating ongoing evolution and selection for preferred traits. This high-level variation was observed across all tumor types analyzed, with some regions showing mirrored subclonal allele imbalance.
A new database of 40 breast cancer cell lines will help speed the development of new gene-targeted therapies by providing genomic and proteomic information. Researchers aim to identify functional genes that drive cancer growth and develop targeted therapies based on unique gene changes in each patient's cancer.
Researchers from IRB Barcelona have identified 568 cancer driver genes, play specific roles in cell growth regulation, DNA replication, and more. These genes confer malignant cells rapid reproduction, immune evasion, and invasive capabilities.
A study found that younger and female patients accumulate more cancer-causing genetic mutations, making them less visible to the immune system. This selective pressure leads to poorer response rates to immunotherapy.
A recent study published in Nature Genetics analyzed genomic differences between HPV strains causing cervical cancers, revealing distinct characteristics and implications for prognosis. The researchers identified specific patterns associated with aggressive cancers, highlighting the need for further studies on African populations.
Blocking TLKs triggers alternative telomere lengthening system, activating innate immune system and potentially attracting immune cells to combat cancer.
Scientists at IRB Barcelona have discovered a new type of hypermutation called mutation fog, which generates hundreds of mutations in every cell and accumulates in critical genome regions. This process is linked to normal DNA repair and APOBEC enzyme activity, suggesting it may be a major source of cancer mutations.
Researchers discovered that almost 20% of patients with unexplained intestinal polyps had tumors with mutations similar to those caused by colibactin, a bacterial toxin. Regular tooth brushing may have prevented the bacterial infection that triggered these cancer-causing DNA mutations.
Researchers developed a computational algorithm to analyze noncoding mutations across five major pediatric cancers. The study identified 1,137 structural variants affecting over 2,000 genes, highlighting their potential as cancer-causing mutations.
The National Lung Matrix Trial, the world's largest precision medicine clinical trial for NSCLC, matches treatments to genetic changes in cancer. It found that targeted therapy is challenging due to genomic complexity and the need for more sophisticated models.
New research published in Developmental Cell shows that an overabundance of protein PRC1 disrupts genome errors linked to cancer. The protein acts like a viscous glue during cell division, precisely controlling the speed at which two sets of DNA are separated as a single cell divides.
A new study shows that genomic mutation testing using the Idylla automated system can reduce wait times for test results from 15 days to just 5 days. This allows patients to begin treatment for colorectal cancer sooner.
Scientists discovered that DNA lesions caused by chemicals are passed on unrepaired, leading to complex patterns of mutations. This phenomenon, known as lesion segregation, can drive tumor growth and development.
A team of scientists has discovered key factors controlling the genome maintenance and replication of KSHV, a virus responsible for lymphatic vascular cancer. The study reveals that two central proteins regulate gene expression on DNA, supporting tumor formation and representing new therapeutic targets.
The UAP56/DDX39B protein removes DNA-RNA hybrids from the genome, ensuring correct gene expression and genomic integrity. Researchers at the University of Seville discovered this key function, highlighting the protein's importance in maintaining genome stability.
A study led by Dr. Dharam Kaushik found that the Nox4 protein is associated with high-grade kidney cancer progression and poor survival rates in patients. The research also identified a subgroup of patients who progress rapidly, making them ideal candidates for future targeted therapy studies.
A new predictor for brain cancer patients' life expectancy has been developed using a genome-wide pattern of DNA copy numbers. The pattern identifies patients who survive for a median of three years, three times longer than those without it.
Researchers have identified a new breast cancer gene, RBBP8, that may explain why some young women develop the disease. The study found that mutations in this gene can lead to cancer by damaging DNA and increasing the risk of genetic variants.
Researchers found that ancestry affects variations in hundreds of genes, but most significant differences are tissue-specific. The study analyzed data from 10,678 patients across 33 cancer types, revealing specific organ and tissue-type associations.
Researchers found that cells protect themselves from mechanical stress by not only deforming cell nuclei but also softening the genetic material itself. This mechanism helps prevent DNA damage and disease, including cancer. The study also reveals that healthy stem cells are more resistant to mechanical stretch than cancer cells.
A new study suggests a single cell division error can trigger a cascade of mutational events, generating defining features of cancer genomes. Researchers recreated the BFB cycle in cultured cells and observed an increase in chromothripsis after aberrant chromosome bridge formation.
The study demonstrates that genomic information can identify individuals with a lifetime risk of more than 60% of developing cardiovascular diseases and diabetes. Combining genetic risk data with clinical risk calculators improved the accuracy of current risk estimation approaches.
A new study suggests that rare, damaging inherited mutations can have a significant impact on an individual's healthspan and longevity. Researchers found that people with more ultra-rare protein-truncating variants (PTVs) had shorter lifespans and healthspans, with each additional variant accounting for a six-month reduction in lifespa...
Researchers at the University of Trento identified a new molecular mechanism that determines the fate of cancer cells. The 'switch' protein DHX30 regulates p53's response to treatment, leading to either cell cycle arrest or programmed cell death, with potential applications for solid tumors in the colon, breast, and lung.
Thelma Alessandra Sugrañes, a medical genetics resident, received the David L. Rimoin Inspiring Excellence Award for her platform presentation on age of first cancer diagnosis and survival in Bloom syndrome. The award recognizes her outstanding research on monogenic cancer predisposition syndromes.
Researchers have identified eight new loci that increase a person's risk for squamous cell skin cancer, bringing the total to 22. The study confirmed previously known risk loci while adding new genomic locations, providing insight into genetic associations and molecular pathways involved in skin cancer development.
Researchers have compiled a global catalogue of cancer mutations to help doctors tailor treatments and improve patient outcomes. The study found that 95% of cancer occurrences can be explained by genetic mutations, paving the way for precision medicine.
Butler simplifies genomic data analysis by constantly collecting health metrics and automating self-healing modules. This reduces large project execution times from years to months, improving researcher productivity and efficiency.
Scientists discovered that over 20% of mutations occur in early stages of tumor development, with some changes taking place years or even decades before cancer is diagnosed. These early genetic alterations can be identified using a new method developed by researchers at the Francis Crick Institute.
Researchers have identified 81 distinct mutational signatures in human cancer genomes that can help reveal the origins and development of various types of cancer. These signatures can provide insight into factors that have mutated a cell's genetic material and inform new strategies to prevent, diagnose and treat the disease.
Researchers at the University of Texas MD Anderson Cancer Center have made significant progress in understanding the mitochondrial genome and its role in cancer. The study found that hyper-mutated cases in kidney, colorectal, and thyroid cancers suggest oncogenic impact with signaling pathway activation.
Researchers identified germline mutations in the MBD4 gene as a driver of somatic mutations in cancer genomes, accelerating the clock-like mutational process. This discovery has significant implications for understanding cancer development and may lead to personalized screening and early intervention strategies.
Researchers have completed the most comprehensive study of whole cancer genomes to date, revealing key mutations driving cancer growth. The atlas provides a solid foundation for understanding which genes are damaged in each cancer type.
Researchers found CNVs to be genomic modifiers of ASD/DD risk in individuals with PHTS, providing insight into the disorder's clinical outcomes and potential predictors for medical management. The study suggests CNV burden analysis may aid in predicting clinical outcomes for other clinically heterogeneous disorders.
The study highlights the efficacy of Bluestar Genomics' 5-hmC signal detection technology for detecting breast, lung, pancreatic, and prostate cancer from a single blood draw. The technology demonstrated high performance in classifying samples with high Area Under the Curve measures.
Researchers have compiled a genome reference database of thousands of healthy older Australians, providing a powerful framework to identify new disease-causing gene variants. The database shows genetic changes associated with ageing, including shorter telomeres and less mitochondrial DNA, which may predict health outcomes for individuals.
A Northwestern University team discovered how chromatin folds at the single-cell level, revealing a 3D forest structure. This finding could help scientists understand chromatin's role in cancer and other diseases.
A GW-led consortium has received a $2.2 million grant to develop BioCompute Object Specification Project standards for genomic data analysis, aiming to streamline data exchange between researchers, pharmaceutical companies, and the FDA. The project's goal is to facilitate personalized medicine by comparing and building on genomic data.
A team of researchers at the University of Colorado Boulder has solved the structure of the Facilitates Chromatin Transcription (FACT) protein, a key player in DNA packaging and gene expression. The discovery sheds light on how this protein maintains the integrity of chromatin during transcription, replication, and DNA damage repair.
Scientists at University of Utah Health have discovered new genetic elements that could help control obesity and metabolic disorders. Hibernating mammals have evolved short non-coding DNA snippets near genes linked to obesity in humans.
Researchers have discovered 37 essential FOXA1 binding sites in T47D cells, which act as enhancers to regulate gene expression. The team also developed a machine learning model to predict important transcription factor binding sites, offering promising insights into cancer biology and potential clinical applications.
Researchers have developed a new CRISPR-Cas9 protein, SaCas9-HF, to increase the precision of genome editing. The new variant shows high accuracy in targeting human cells without compromising on-target efficiency.
Researchers have developed a high-resolution visual map of the RSC complex, a crucial regulator of chromosome structure and gene expression. This study provides new insights into how RSC-like complexes are involved in cancer development and has implications for understanding chromosomal genes in healthy and cancer cells.
Researchers identified four distinct immune-based subtypes of kidney cancer, which could help predict patient survival and response to treatment. The study also found that certain tumor microenvironment signatures were associated with better or worse overall survival.
A team of researchers, including CeMM PI Joanna Loizou, will study DNA-damage response systems using cutting-edge technologies. The six-year project aims to create integrated genetic and physical maps of DNA repair pathways in human cell types.
A novel cancer-driving mutation discovered in the human genome's non-coding regions can drive multiple types of cancer, including brain, liver and blood cancers. The mutation could be used to develop novel treatments for patients with these difficult-to-treat diseases.
Researchers at Mount Sinai Hospital have discovered the near-atomic-resolution structure of DNA polymerase delta, a crucial enzyme in genome replication. The team also mapped mutations associated with cancers and other diseases.
Researchers found that high blood sugar levels in diabetes can cause DNA damage and reduce its repair, increasing the risk of certain cancers. The study suggests that controlling blood sugar levels could be an effective way to reduce cancer risk in diabetics.
Researchers analyzed genomic data from 317 MCC patients and found two distinct populations with different genetic profiles and treatment responses. Immunotherapies showed high effectiveness in both groups, with better response rates when given early treatment.
Researchers explore new tools and strategies to interpret multiomics data, revealing insights into bacterial strains and cancer phenotypes.
The freely available data set includes unique comparisons of almost 1,000 cancer cell lines' responses to 453 licensed and experimental drugs. The dataset offers a rich resource for cancer scientists to discover more about how cancer cells work and generate new therapeutics and drug combinations.
University of Birmingham researchers found that the BRCA1 gene changes shape to protect vulnerable DNA until copying machinery can be restarted. This discovery could help understand how cancers develop and potentially identify new ways to suppress tumors.
A new study from the University of California, Irvine, reveals that many recurrent cancer mutations are not drivers of cancer progression but rather passenger hotspots. The research identified APOBEC3A as a key player in creating these hotspot mutations, which can be targeted for novel cancer therapies.
A study by Massachusetts General Hospital found that DNA single strands can be highly sensitive to mutation by gene-editing enzymes. Many mutations occur in genes unrelated to cancer development, highlighting the need to distinguish between 'driver' and 'passenger' mutations.