Articles tagged with Cancer Genomics
University of Virginia researchers have developed a new computational method to map the folding patterns of chromosomes in three dimensions. This will help scientists understand the genetic cause of cancer and advance other areas of medical research.
The scientific community is urged to adopt more inclusive practices in preclinical and basic science research to promote personalized medicine. Researchers highlight the lack of diversity in commonly used human cell lines, which are predominantly of European descent, and emphasize the need for representative cell lines to better unders...
A new machine learning technique, MethSig, analyzes DNA methylation changes in tumor cells to infer which ones are driving tumor growth. The algorithm identifies a small number of cancer-driving events, consistent across patients and tumor types.
Researchers at Cold Spring Harbor Laboratory found that a protein called Asterix/Gtf1 suppresses small specific regions of mobile genetic elements by binding to tRNA molecules. This discovery could lead to understanding how cells protect themselves against these elements and potentially tame an overly restless genome.
Researchers at IRB Barcelona have discovered the HMCES enzyme to be a Achilles heel of some lung tumours with high mutations caused by the APOBEC system. Blocking HMCES is damaging to cancer cells but less so for healthy cells, making it a promising target for future treatments.
Researchers found that tumour samples from over 2,600 patients with different types of cancer contain a high prevalence of genetic diversity within individual tumours. This variation is a challenge for doctors as treatment may not be effective against another subclone, and certain subclones can initiate tumour spread or drug resistance.
A new study by NYU Rory Meyers College of Nursing found that breast cancer survivors with high genomic test scores report higher overall fear and greater perceived consequences compared to those with low scores. Anxiety and emotional response to cancer are the best predictors of fear, explaining 58% of variance in fear of recurrence.
An international study reveals that the MutS protein, known as the guardian of our genome, coordinates the essential DNA repair process from beginning to end. The researchers used cryo-electron microscopy to visualize the protein and describe its mechanism of action.
Researchers have developed an AI system to analyze DNA-sequenced mesotheliomas, revealing similar evolutionary paths that predict aggressiveness and possible therapy. This breakthrough could lead to improved patient outcomes for those with this aggressive form of cancer.
A new study led by University of Maryland researchers found that DNA from tissue samples can be used to accurately predict the age of bats in the wild. The study showed age-related changes to DNA are different between long-lived and short-lived bat species, especially near genes associated with cancer and immunity.
The study demonstrates MEK inhibitors as a promising targeted therapy for basal subtype bladder cancer, highlighting the importance of 3D cell culture drug screening. Established genomic and transcriptomic data are correlated with drug response to identify novel groups of tumors vulnerable to specific drugs.
Researchers have found that short strands of cell-free DNA in urine can indicate a difference between healthy individuals and those with cancer. The DNA fragments are protected from degradation and can provide meaningful information about disease complexity like cancer.
A new review highlights biological differences in prostate cancer development across ethnicities, identifying potential improvements for African American men. The study aims to reduce incidence and mortality rates by leveraging these differences.
A new genomic test helps oncologists determine which patients with recurrent prostate cancer may benefit from hormone therapy, guiding precision medicine efforts. The Decipher test, measuring tumor gene activity, predicts risk of metastasis and death, even after adjusting for other factors.
A new study reveals that errors in chromosome packing may cause B-cell blood cancers. Researchers identified a critical protein called DIS3 that maintains genomic architecture and prevents cancer. The findings could lead to new biomarkers and therapies targeting genome instability.
Lung cancer is a leading cause of death in Singapore and the world, with Asian populations exhibiting distinct genetic alterations. The World Conference on Lung Cancer Singapore presented new data on EGFR mutation and TKI-drug resistance, highlighting the need for targeted treatment approaches.
A recent study published in JAMA Oncology found significant racial disparities in breast cancer prognosis testing among Black women, who have higher recurrence and mortality rates than non-Hispanic white women. The study suggests that genomic tumor tests may require re-calibration to reflect racial differences.
A study by Dmitry Gordenin and colleagues found that genomic DNA changes in skin cells accumulate over time, with the amount of damage caused by UV light unrelated to age. Black individuals exhibited less UV damage compared to white donors, possibly due to higher melanin levels.
The study uses a decontamination algorithm to identify the bacteria living in tumors, finding that normal and cancerous organ tissues have distinct microbiota compositions. The researchers also discovered that bacterial information could help diagnose cancer and predict patient outcomes.
Researchers have classified angiosarcomas into three subtypes based on genomic and immune profiles, enabling personalized treatment approaches. The study suggests that checkpoint immunotherapy can be effective for clusters one and three, while tumour-promoting genes in cluster two may be explored as potential targets.
Researchers have identified seven DNA fingerprints that define cancer risk, including a protective germline pattern and six that present a higher risk. The discovery refines the long-held view that lifestyle factors contribute to cancer risk and sheds light on the role of genetics in cancer development.
Researchers identified genomic heterogeneity and immune content scores that predict lethal outcomes in grade 4/5 prostate cancer patients. The study found that approximately 25% of these patients were more likely to benefit from targeted treatment strategies.
Researchers developed a polygenic risk score to assess breast cancer risk in carriers of high-risk mutations. The score provides a more accurate estimate, especially for close relatives, and has the potential to save lives by targeting cancer screening.
A recent study reveals unique mutation patterns in the genes PIK3CA, GNAS, SMAD3, and TSC2 among young patients with appendiceal cancer. These findings suggest potential for targeted therapies, such as alpelisib, which have already been approved for advanced breast cancer.
A new framework helps determine the exact timing of DNA mutations in cancer genomes, enabling more targeted and personalized treatments. By analyzing 22 different algorithms on nearly 300 prostate cancer samples, UCLA researchers identified biases and variability to improve treatment outcomes.
A new whole-body tissue map of 5-hydroxymethylcytosine (5hmC) modifications was published, expanding understanding of a global biomarker for disease diagnosis. The map confirms 5hmC as a prevalent gene activation mark with superb tissue specificity, providing a resource for future diagnostic tests.
A new study has shed light on the role of p53 target gene Zmat3 in lymphoma and lung cancer development. Researchers found that disabling Zmat3 had little impact on tumor development, suggesting that other proteins may be involved in preventing cancer formation.
The UC Santa Cruz Genomics Institute is teaming up with No Stomach For Cancer to release a web portal that combines vast amounts of gene variant data with corresponding clinical data. This collaboration aims to advance science and patient survival by identifying individuals at risk of hereditary stomach cancers.
A team of researchers analyzed 648 DFT1 tumors collected between 2003 and 2018, revealing that early on in the spread of the tumor, five clades emerged, with two dying out while three continued to spread. The study highlights the importance of geography in influencing the movements of devils and their disease.
Researchers at Huntsman Cancer Institute discovered that chromatin remodeling machines have a motor-like component that drives the machine along DNA, disrupting nucleosome beads. The team found cancer-causing mutations in an area of the hub regulating motor activity, leading to improper gene expression and cancer.
A study of patients with cancer who had exceptional responses to therapy has identified molecular changes in their tumors that contribute to these unexpected and long-lasting responses. The researchers used genomic characterizations to uncover genetic alterations that may help understand the mechanisms behind these rare responses.
A new UK study sheds light on the effects of benzopyrene exposure on human cells, revealing new insights into DNA repair mechanisms and their connection to cancer development. The research suggests that understanding these mechanisms could help predict individuals more susceptible to cancer-causing agents.
A team led by Dr. Katherine L. Nathanson has been awarded $5.4 million to continue researching the genetic risk factors of testicular cancer, which affects men aged 15-45 in the US and Europe. The study aims to identify novel susceptibility genes and provide data for surveillance of high-risk individuals.
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.
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.
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 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.