Genome - wide detection of SVs and copy number alterations, which are often pervasive (and clinically relevant)
in tumor genomes
Unlike previous studies, which tracked lymphoma progression by monitoring the sequence of just one cancer - associated protein, CAPP - Seq can identify a much larger range of mutations
in the tumor genome.
In tumor genome processing, we identify discrete coverage levels based on the distribution of the observed normalized coverage levels in the tumor genome.
Not exact matches
To determine how the cells switch from one type to another, they took three human uterine carcinosarcoma samples and sequenced the
genomes of cells
in two parts of each
tumor: the carcinoma and sarcoma components.
«Cancer cells disguise themselves by switching off genes, new research reveals: A
genome - wide map of the genes switched off
in aggressive
tumors reveals a «signature».»
In a study published in Neoplasia, researchers at the Washington University School of Medicine created a map showing which genes were switched on and off in different parts of the tumor, providing a «signature» of these switches throughout the genom
In a study published
in Neoplasia, researchers at the Washington University School of Medicine created a map showing which genes were switched on and off in different parts of the tumor, providing a «signature» of these switches throughout the genom
in Neoplasia, researchers at the Washington University School of Medicine created a map showing which genes were switched on and off
in different parts of the tumor, providing a «signature» of these switches throughout the genom
in different parts of the
tumor, providing a «signature» of these switches throughout the
genome.
«This model was trained on genetic data from human
tumors in The Cancer
Genome Atlas and was able to predict response to certain inhibitors that affect cancers with overactive Ras signaling
in an encyclopedia of cancer cell lines,» Greene said.
«Machine learning finds
tumor gene variants and sensitivity to drugs
in The Cancer
Genome Atlas.»
«Just as normal cells with the same
genome differentiate into many different cell types, a single
tumor characterized by specific genetic mutations can contain many different types of cells — stem - like and more differentiated cells — with the difference being rooted
in their epigenetic information.
With a grant from the Morris Animal Foundation, Antczak, his collaborators Samantha Brooks and Ann Staiger from the University of Florida, and the rest of the team applied a genomewide association study to compare the genetic makeup of horses with and without sarcoid
tumors at more than 50,000 sites
in the equine
genome.
The
genome - wide epigenetic changes clustered
in certain chromatin domains and controlled «gene expression changes that specify different malignant traits, including the ability to form
tumors,» McDonald said.
«Studies like the current one involving rhabdomyosarcoma are giving us a close - up look at the way cancer evolves
in response to treatment,» said study co-author Richard K. Wilson, Ph.D., director of The
Genome Institute at Washington University School of Medicine in St. Louis, where scientists have extensive expertise analyzing tumor recurrence using whole - genome seque
Genome Institute at Washington University School of Medicine
in St. Louis, where scientists have extensive expertise analyzing
tumor recurrence using whole -
genome seque
genome sequencing.
«Based on mutations we found
in the
genome, there is evidence of high levels of oxidative stress
in the
tumors,» Dyer said.
Most of the mutations that drive recurrent
tumors when they pop up elsewhere
in the body were present
in the original
tumor, geneticist Elaine Mardis reported May 9 at the Biology of
Genomes meeting.
This stress, which is notably induced
in pre-cancerous lesions, is characterised by an increased DNA replication rate, which provokes DNA damage and
genome instability, major drivers of
tumor formation.
«One of the major and immediate downstream effects of myc activation is a dramatic increase
in the capacity of affected cells to make protein,» Ruggero said «This,
in turn, leads to increased cell survival and proliferation, and to unstable
genomes that foster additional mutations that turn these abnormal cells into
tumor cells.»
The 15 AACR scientists, who were already
in Washington, D.C., to meet with the U.S. Food and Drug Administration on genetic testing for cancer patients, tossed around ideas including expanding NCI's
tumor genome - sequencing efforts and getting the government to cover the costs of genomic
tumor profiling.
The team integrated three, complementary gene sequencing approaches to look for mutations
in tumor cells from SS patients: whole -
genome sequencing
in six subjects, sequencing of all protein - coding regions (exomes)
in 66 subjects, and comparing variation
in the number of copies of all genes across the
genome in 80 subjects.
His laboratory develops and deploys new biochemical and computational methods
in functional genomics, to elucidate the genetic basis of human disease and human physiology, and to create and deploy novel techniques
in next - generation sequencing and algorithms for
tumor evolution,
genome evolution, DNA and RNA modifications, and
genome / epigenome engineering.
Rather,
tumors arise from the complex interplay between any number of mutually exclusive abnormal changes
in the
genome, the combinations of which can be unique to each individual patient.
New research led by Li Ding, Ph.D., of Washington University School of Medicine
in St. Louis, shows that current approaches to
genome analysis systematically miss detecting a certain type of complex mutation
in cancer patients»
tumors.
«This development has the potential to enable earlier detection of solid
tumors through a simple blood draw by substantially improving our ability to detect very low quantities of circulating DNA derived from
tumor cells,» says corresponding author Hunter Underhill, M.D., Ph.D., who initiated the research while
in the lab of senior author Jay Shendure, M.D., Ph.D., a professor
in genome sciences at the University of Washington.
But
tumors from patients with distant metastases to the lung and liver showed massive epigenetic changes that mapped to large, blocklike segments of the
genome, both
in the distant metastases themselves and
in the section, or «subclone,» of the primary
tumors they came from.
«The idea of not catching a targetable mutation
in a patient's
tumor is devastating,» said senior author Li Ding, PhD, associate professor of medicine and assistant director of the McDonnell
Genome Institute at Washington University.
Just as no two people possess the same genetic makeup, a recent study has shown that no two single
tumor cells
in breast cancer patients have an identical
genome.
The
tumors»
genomes were then analyzed for genetic mutations, or alterations
in their DNA, by her team and that of Bert Vogelstein, M.D., professor of oncology at the Johns Hopkins University School of Medicine and the co-director of the Ludwig Center at the Johns Hopkins Kimmel Cancer Center.
Hoping to cash
in on personalized cancer therapy, a new company called Foundation Medicine — founded
in part by
genome guru Eric Lander of the Broad Institute — plans to develop tests for genetic glitches
in tumors that make them vulnerable to specific drugs, reports the United Kingdom's Times Online.
By performing a
genome - wide screen
in breast cancer cells, Dr. Oesterreich and her colleagues identified a gene called HOXC10 as one that the cancer seems to modify to allow continued
tumor growth
in patients whose cancer becomes resistant to traditional therapies.
During the last three years the Spanish Consortium for the Study of the
Genome of the Chronic Lymphatic Leukemia, where the researchers of the present study already collaborate, has sequenced the genome of hundreds of patients with the more common leukemia in our society, identifying new mechanisms of tumor progression and new therapeutic ta
Genome of the Chronic Lymphatic Leukemia, where the researchers of the present study already collaborate, has sequenced the
genome of hundreds of patients with the more common leukemia in our society, identifying new mechanisms of tumor progression and new therapeutic ta
genome of hundreds of patients with the more common leukemia
in our society, identifying new mechanisms of
tumor progression and new therapeutic targets.
Until now, scientists have failed to establish a link between the properties of pancreatic cancer, such as its aggressiveness, and changes, i.e. mutations,
in the
tumor's
genome.
This phenomenon could result
in breakage
in the human
genome, and when a breakage impacts important genes, such as
tumor suppressors, it could lead to cancer development.
«It was hard to find a single microRNA
in the human
genome that wasn't differentially turned on or off across different
tumor types
in different tissues,» Golub says.
The new study, a comprehensive analysis of the
genomes of 178 primary cervical cancers, found that over 70 percent of the
tumors had genomic alterations
in either one or both of two important cell signaling pathways.
The National Institutes of Health today announced
in Nature that it has reached an understanding with the family of the late Henrietta Lacks to allow biomedical researchers controlled access to the whole
genome data of cells derived from her
tumor, commonly known as HeLa cells.
The researchers were able to replicate this finding by comparing the healthy thyroid tissues
in GTEx to 500 samples taken from thyroid
tumors, compiled by The Cancer
Genome Atlas, and giving support to the extensive impact of FOXE1 on cellular state.
In particular, he wanted to study the
genomes of marbled crayfish to uncover basic mechanisms underlying epigenetics, the binding of molecules to DNA that can drive
tumor growth and help cancer spread.
They used the gene - editing CRISPR / Cas9 technique to sift the
genomes of melanoma cells for changes that made
tumors resistant to being killed by immune T cells, which are the main actors
in the immune system response against infections and cancer cells.
As the cost of DNA sequencing continues to plummet, the lab will move ever closer to a once - elusive goal: economically processing every patient's complete
genome in both
tumors and healthy cells.
This approach allows us to detect, with high confidence, changes
in circulating
tumor DNA across a large part of the
genome without information from
tumor tissue,» said Dr. Razavi.
Sequencing RNA, not just DNA, could help doctors predict how prostate cancer
tumors will respond to treatment, according to research published
in the open access journal
Genome Biology.
Scientists have discovered a new «mastermind fusion gene» may be associated with a rare cancer - causing
tumor — pheochromocytomas («pheo») and paragangliomas, according to a study published Feb. 13
in Cancer Cell, by researchers at the Uniformed Services University (USU) and the National Cancer Institutes» The Cancer
Genome Atlas.
The Yale - led study performed whole exome sequencing ¬ — a technique for sequencing all the expressed genes
in a
genome ¬ — on TNBC
tumors to identify mutations
in specific genes or pathways that may indicate response or resistance to the standard of care, which is anthracycline / taxane (ACT) chemotherapy.
Next year, NCI will wind up The Cancer
Genome Atlas (TCGA), a huge project piloted
in 2006 that is systematically searching
tumors for genetic changes involved
in cancer.
Possible successor to The Cancer
Genome Atlas would scale up the search for rare mutations
in tumors
His group uses
genome - wide and gene - specific DNA methylation analysis to identify aberrantly silenced
tumor suppressor genes
in B cell leukemias and lymphomas.
Sequencing the whole
genome of a prostate
tumor, says co-author Levi Garraway, a physician and biologist at Harvard Medical School
in Boston, allowed the researchers to see «biology that would have been invisible with any other method.»
In these experiments, Berger and colleagues show that somatic PREX2 mutations identified through whole - genome sequencing of human melanoma can contribute to enhanced lethality of tumor xenografts in nude mice (Figure 3B, S6B, and S6C; Berger et al., 2012
In these experiments, Berger and colleagues show that somatic PREX2 mutations identified through whole -
genome sequencing of human melanoma can contribute to enhanced lethality of
tumor xenografts
in nude mice (Figure 3B, S6B, and S6C; Berger et al., 2012
in nude mice (Figure 3B, S6B, and S6C; Berger et al., 2012).
This analysis discovered an average of 97 structural rearrangements of the
genome per
tumor, and some 9,653 mutations of various types
in 5,712 genes.
In addition, the study, led by investigators in The Cancer Genome Atlas (TCGA) Research Network, revealed four novel tumor subtypes, while also identifying genomic similarities between endometrial and other cancer types, including breast, ovarian, and colorectal cancer
In addition, the study, led by investigators
in The Cancer Genome Atlas (TCGA) Research Network, revealed four novel tumor subtypes, while also identifying genomic similarities between endometrial and other cancer types, including breast, ovarian, and colorectal cancer
in The Cancer
Genome Atlas (TCGA) Research Network, revealed four novel
tumor subtypes, while also identifying genomic similarities between endometrial and other cancer types, including breast, ovarian, and colorectal cancers.
We developed SomaticSniper to detect somatic mutations
in whole -
genome sequencing data while allowing for
tumor contamination of normal cells that occurs
in some types of leukemia.