Articles tagged with Cancer Genomics
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A massive data analysis has implicated dozens of mutations in breast and prostate cancer development, focusing on non-coding DNA elements. The study provides new insights into the causes and treatment of cancer.
Researchers at Memorial Sloan-Kettering Cancer Center developed a new approach for cancer therapy development using tumor genomic signatures. The study confirms two major hypotheses, showing that a limited number of genetic events cause most tumor subtypes and that oncogenic signatures are largely independent of tissue origin.
Cancer biologists use a new approach to study human tumors by transplanting them into mice with crippled immune systems. The results show high genomic fidelity between the original tumors and transplanted cancer cells in mice, providing insights into drug resistance. This approach may lead to more precise treatment choices and faster d...
Researchers have discovered that non-coding genes are regulated by protein-DNA interactions and can be targeted with more effective drugs. Using high-resolution technology, scientists identified 150,000 complexes along non-coding stretches of DNA in leukemia cell lines.
The EMBO Meeting 2013 conference will feature keynote lectures by prominent scientists, including Kai Simons, Hans Clevers, Sir Michael Stratton, Peter Hegemann, and Georg Nagel. The scientific programme will include sessions on stem cells, cancer genomics, optogenetics, and the search for life beyond Earth.
A comprehensive compendium of mutational processes explains most mutations found in 30 common cancer types, revealing the biological processes responsible. The study identifies a family of enzymes linked to over half of cancer types, and finds that DNA damage from viruses may cause collateral genetic changes.
HudsonAlpha and UAB researchers aim to identify optimal treatments for ER+ breast cancer using tumor genomics. By analyzing genetic data from patients who responded or didn't respond to treatment, they hope to develop targeted therapies.
Singapore scientists have identified genes that are potential targets for therapeutic drugs against aggressive breast cancer. UBASH3B is a protein tyrosine phosphatase that promotes tumor growth and metastasis in triple-negative breast cancer patients.
Researchers have discovered that cancer cells can fuse with blood cells, enabling them to travel through the body and seed new tumors. This breakthrough has major implications for treating metastatic cancers.
A set of proteins involved in the body's natural defenses produces a large number of mutations in human DNA, according to a study led by researchers at the National Institutes of Health. In some cancers, these naturally produced mutations can outnumber all other mutations and account for over two-thirds of tumors.
Researchers propose a new theory linking cancer's evolutionary roots to ancient life forms. If correct, it may transform cancer therapy by revealing a systematic response to stress or physical challenges.
Researchers identified a new molecular pathway involving the gene ZNF365 that may predict worse outcomes for patients with breast cancer. Abnormalities in this pathway can lead to genomic instability and an increased risk of developing tumors.
Fei Li, an assistant professor at NYU, has been selected as a Pew Scholar in the Biomedical Sciences. He will continue his research on centromeres and chromosome structure to understand how changes lead to cancer.
Researchers have discovered HER2 gene abnormalities in 14 different types of solid tumors, including breast, esophageal, and lung cancers. The study suggests that these irregularities may benefit from existing anti-HER2 therapies, providing new treatment options for patients with advanced cancer.
Researchers at Penn Medicine have identified four new genetic variants associated with an increased risk of testicular cancer, with markers found at four loci, including 4q22, 7q22, 16q22.3, and 17q22.
A large-scale genomic analysis identified distinct subtypes of endometrial cancer based on their genomic makeup, which may respond to targeted drugs already being tested in clinical trials. The findings suggest that a significant portion of high-grade endometrioid tumors should be treated more aggressively after surgery.
A new study found that adding genomics-based testing to the standard diagnostic workup could lead to a change in recommended treatment for some women. The research identified four novel genomic-based subtypes of endometrial cancer, which suggest that genetic changes can help guide treatment decisions.
Researchers found that ATRX deficiency leads to increased DNA damage and telomere dysfunction. Mice lacking neural ATRX exhibited systemic endocrine dysfunction and shortened lifespans, mirroring human premature aging disorders.
Scientists at Fox Chase Cancer Center have identified several dozen transcripts known as lincRNAs that are dysregulated in breast cancer. The study found that these lincRNAs are differentially regulated within breast cancer cell lines, indicating their potential role in tumorigenesis or regulation of other cancers.
Moffitt researchers have discovered four new regions of the genome linked to ovarian cancer risk, accounting for approximately 4% of inherited component. The findings are part of a coordinated series of studies involving over 250,000 individuals and provide new insights into the disease.
A UNC-led team has identified four molecular classes of head and neck squamous cell carcinoma (HNSCC), a disease with limited information on its molecular profile. The study confirms the presence of these subtypes and demonstrates their clinical relevance, paving the way for targeted therapies.
A recent study published in Developmental Cell identifies piRNAs as the primary guides for epigenetic factors, controlling gene expression patterns in Drosophila. This breakthrough discovery has significant implications for understanding cancer development and may lead to new therapeutic opportunities.
Early-onset prostate cancers have distinct genetic alterations that link genes normally independent to cancer-causing fusion genes. Androgen hormone receptors are also higher in younger patients, suggesting a potential trigger for the disease.
A recent study found that the epigenetic marker 5-hydroxymethylcytosine (5hmC) plays a vital role in the selective expression of genes, particularly in healthy brain cells. The study also discovered that changes in 5hmC distribution are associated with gene silencing and may contribute to cancer development.
A recent study has identified specific genetic mutations that lead to drug resistance and relapse in childhood leukemia. Researchers found 20 relapse-specific mutations, including a mutation in the NT5C2 gene, which may help doctors detect early signs of relapse and switch treatment strategies.
Researchers discover collisions between DNA duplication and transcription machineries cause chromosomal alterations in tumor cells. Genomic fragile sites are identified as contributing to genome instability throughout evolution.
Two new mutations have been discovered in the 'dark matter' of the cancer genome, occurring in 71 percent of malignant melanoma tumors. The highly recurrent mutations affect a promoter region adjacent to the TERT gene and may contribute to the development of melanoma.
Michael Stratton and Peter Hegemann received the 2013 Louis-Jeantet Prize for their discovery of ion channels activated by light, known as optogenetics, which holds promise for treating neurological diseases. They will use the prize money to continue their research on proteins that can be activated by light.
A study published in PNAS reveals that inflammation enhances the activity of enzyme ADAR1, leading to increased self-renewal and therapeutic resistance in cancer stem cells. Targeting this pathway with a small molecule inhibitor may help prevent relapse and progression of chronic myeloid leukemia.
Bioinformatician Professor Terry Speed has received a 2012 Victoria Prize for Science and Innovation for using statistics to solve biomedical research questions. His work has led to new techniques in cancer, infectious diseases, immunology, and inherited diseases.
Researchers have developed a solution to predict breast cancer cells' response to cancer drugs by analyzing their genomic profiles. The team's solution outperformed 47 other teams in a prediction challenge, taking an encouraging step forward for personalized medicine.
Researchers have successfully genotyped 344 NSCLC specimens with a median turnaround time of 31 days, enabling targeted therapy. This study's findings highlight the potential for large-scale genomic testing to transform lung cancer treatment.
Scientists have discovered that a gene switch regulates the expression of genes and promotes cancer development, according to a study published in Science. The study found that removing a specific region containing a genetic variant increased resistance to tumor formation in mice.
Researchers found that TFIIB halts general transcription when DNA damage occurs, enabling cells to prioritize repair and support p53's tumor-suppressing functions. This process allows p53 to bypass the need for TFIIB phosphorylation, activating its target genes vital for DNA damage response.
PARG, a molecule involved in DNA repair, has been found to regulate gene expression and modulate cell transcriptional activity. This discovery highlights the potential of targeting PARG in cancer treatment.
Researchers are investigating how constantly evolving chemical modifications in our DNA and proteins cause our genome to stay healthy or develop diseases. Epigenome changes over time can affect which genes are turned on, leading to Leukemia and cancers of the colon and ovaries.
A study by NIH/National Cancer Institute reveals shared genomic features between high-grade serous ovarian cancer and one subtype of breast cancer. This similarity suggests that the two cancers share a common molecular origin, facilitating comparison of therapeutic data.
A new study found that smokers with lung cancer have 10 times more genetic mutations than those who have never smoked. The researchers identified over 3,700 mutations across all patients and found at least one mutated gene in each non-smoking patient that can be targeted with existing drugs.
The CNIO group is part of the Gencode project, creating a reference geneset from Encode data. This effort has mapped four million 'switches' controlling human cell and tissue gene activity, revealing a complex web of interactions.
Researchers created the most comprehensive study of Epstein-Barr virus genome interactions with its human host. The EBV atlas describes over 60 human transcription factors and highlights the extensive coevolution of the virus, pointing toward possible targets for future cancer and anti-viral drugs.
A study on sea lampreys reveals that they undergo programmed genome rearrangement and gene loss during early development, sealing away potentially deleterious genes. This discovery builds on previous research and may provide insights into how vertebrate genomes remain stable, with potential implications for human health.
The study found that the absence or downregulation of the LRP1B gene is associated with chemoresistance in high-grade serous ovarian cancer. Additionally, tumors that initially responded to chemotherapy but later became resistant evolved further than those that were resistant from the outset.
Researchers identified a previously unknown subtype of Ewing sarcoma with genetic factors related to long-term survival. A specific gene change between primary and metastatic stages may lead to better treatment.
Researchers have analyzed 125 genome analyses of medulloblastomas, identifying frequent and characteristic genomic alterations that may lead to developing new diagnosis and treatment methods. Cells with four sets of chromosomes have been found in several types of cancer, including childhood brain tumors.
Researchers identified distinct cancer signatures linked to treatment response in breast tumors, which could help personalize treatment for patients. The study found mutations in genes like TP53 and MAP3K1 associated with good response to aromatase inhibitors, while others like MALAT1 predicted poor outcomes.
Researchers identify nine new genes that drive breast cancer development, highlighting the genetic diversity of the disease. The study provides insights into the consequences of this diversity and its implications for treatment.
Researchers at University of Edinburgh discovered an enzyme that corrects the most common mistake in mammalian DNA replication, including accidental incorporation of RNA. This discovery could have broad implications for autoimmunity and cancer research.
Researchers identified new functions of cohesin SA1 relevant to human disease, including efficient chromosome duplication and regulation of gene expression during embryonic development. This work offers new clues to understand the pathologies observed in CdLS patients and may lead to a better understanding of cancer.
A $4.5 million grant will fund the search to find new ways of treating glioblastoma multiforme (GBM), the most common type of primary brain tumors. The study aims to discover new medicines that can precisely target tumors, shrinking or eliminating them with minimal harm.
Cold Spring Harbor Laboratory Press announces new licensing arrangements with Genome Research authors. Authors can now retain copyright and license their work for 6 months, after which it will be made freely available under a Creative Commons License.
Researchers have announced GenomeSpace, a software environment that brings together a wide range of genomic analysis tools and data sources. The platform enables seamless transitions between tools, allowing biologists to carry out projects from start to finish without manual conversions or programming skills.
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.