In January, TGI and its collaborators published three Nature papers that came online the same day: one on the genetic basis of an aggressive pediatric leukemia, another on genomic and epigenetic analyses of childhood retinoblastoma, and a third on
tumor evolution in relapsed AML.
Not exact matches
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.
«This was a very difficult study to do, but it allowed us to take a snapshot of both the primary
tumor, and the
tumor after it had spread,
in order to trace its
evolution,» said the study's first author Marni Siegel, a graduate student
in the UNC MD / PhD program.
In collaboration with the University College London (UCL) Cancer Trials Centre and the UCL Cancer Institute, Swanton's research group will be following about 850 patients with NSCLC from diagnosis to death as part of a clinical trial to understand
tumor evolution.
«Another model is punctuated
evolution in which CNAs are acquired
in short bursts of crisis, followed by stable clonal expansion that form the
tumor mass.
The research team developed a new method called highly multiplexed single - nucleus sequencing (HM - SNS) to investigate CNA's clonal substructure and
evolution in a cohort of 12 TNBC patients, whose
tumors had been surgically removed prior to further therapy.
Charles Swanton, a cancer geneticist at the Francis Crick Institute
in London, and colleagues analyzed 1,206 clear - cell renal cell carcinoma (ccRCC)
tumor samples from 101 patients as part of the Tracking Cancer
Evolution through therapy (TRACERx) program.
The branched, Darwinian subtype — «if you like, the microevolutionary
tumors,» says Swanton — acquire chromosomal complexity when they lose alleles
in chromosomes 9 and 14 late
in their
evolution.
In a way,
tumor cells are acting somewhat Nietzschean, blindly managing their own cheap oakley
evolution according to the principle â $ œWhatever doesnâ $ ™ t kill me makes me stronger.â $
These findings reinforce many things that we already know: that mutations acquire gradually with age, that most of the mutations
in AML (and likely other
tumors) are random background events not contributing to tumorigenesis, and that subsequent mutation and
evolution can give rise to subclones that ultimately determine cancer progression and response to therapy.
«With 100 million mutations, each capable of altering a protein
in some way, there is a high probability that a significant minority of
tumor cells will survive, even after aggressive treatment,» said study director Chung - I Wu, PhD, professor of ecology and
evolution at the University of Chicago.
Most of the 8,800 annual deaths
in the United States are of patients who relapse with a
tumor that has undergone clonal
evolution at the cytogenetic level.
Tumor heterogeneity in solid tumor cancers impacts clonal evolution and patient outc
Tumor heterogeneity
in solid
tumor cancers impacts clonal evolution and patient outc
tumor cancers impacts clonal
evolution and patient outcomes.
DeconstructSigs: delineating mutational processes
in single
tumors distinguishes DNA repair deficiencies and patterns of carcinoma
evolution
Cellular heterogeneity
in solid
tumor cancers impacts clonal
evolution and patient outcomes.
The loss of HLA often occurred relatively late
in the
tumors»
evolution and resulted
in an expansion of neoantigens within the
tumors, predicted to bind to the lost HLA allele.
Revealed that the loss of the human leukocyte antigen (HLA) locus
in lung cancers is a way these
tumors evade the immune system and allow mutation expansion and branched
evolution within
tumor cells
The application of subclonal reconstruction methods is providing key insights into
tumor evolution, identifying subclonal driver mutations, patterns of parallel
evolution and differences
in mutational signatures between cellular populations, and characterizing the mechanisms of therapy resistance, spread, and metastasis.
Nowell went on to study chromosomal changes
in other
tumors, and this led him to advance the theory of the clonal
evolution of
tumor progression.
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