10,826 research outputs found
Measurement of CP asymmetries in decays
The latest measurements of the individual time-integrated CP asymmetry in the
Cabibbo-suppressed decays decays are presented. The results
are based on collision data, corresponding to an integrated luminosity of
, collected with the LHCb detector at centre-of-mass energies of 7
and 8 TeV. A combination of the asymmetries using both prompt and secondary
charm decays is presented ; .
These are the most precise measurements from a single experiment. The result
for is the most precise determination of a time-integrated CP
asymmetry in the charm sector to date, and neither measurement shows evidence
of CP asymmetry.Comment: VIII International Workshop On Charm Physics, 5-9 September, 2016,
Bologna, Ital
Precision measurements of rare kaon decays
We report the recent results on rare kaon decays from the NA48/2 experiment.
The precise measurement of direct photon emission (DE) in the decay K+- -> pi+-
pi0 gamma and its interference (INT), with the INT amplitude being observed for
the first time, has been finalized. This study is based on the full NA48/2 data
set with about 600k reconstructed K+- -> pi+- pi0 gamma decays which is factor
of 30 larger than for previous experiments. Samples of about 7200 reconstructed
K+- -> pi+- e+ e-, and more than 3000 K+- -> pi+- mu+ mu- events, with very
small background contamination, have been collected. The latter is exceeding
the total existing statistics by a factor of five. A precise measurement of the
branching fractions and the form factors of the rare decays K+- -> pi+- l+ l-
has been performed using different theoretical models. The CP violating
asymmetry between K+ and K- in this channel is also measured.Comment: Proceedings to the EPS-HEP09 conference, 4 pages, 2 figure
Direct CPV in two-body and multi-body charm decays at LHCb
The Standard Model predicts CP asymmetries in charm decays of
and the observation of significantly larger CP violation could indicate
non-Standard Model physics effects. During 2011 and 2012, the LHCb experiment
collected a sample corresponding to 3/fb yielding the world's largest sample of
decays of charmed hadrons. This allowed the CP violation in charm to be studied
with unprecedented precision in many two- body and multibody decay modes. The
most recent LHCb searches for direct CP violation are presented in these
proceedings.Comment: 6 pages, Contribution to proceedings of the 8th International
Workshop on the CKM Unitarity Triangle (CKM 2014), Vienna, Austria, September
8-12, 201
Transcriptional landscape of neuronal and cancer stem cells
Tumor mass is composed by heterogeneous cell population including a subset of âcancer stem cellsâ (CSC).
Oncogenic signals foster CSC by transforming tissue stem cells or by reprogramming progenitor/differentiated
cells towards stemness. Thus, CSC share features with cancer and stem cells (e.g. self-renewal, hierarchical
developmental program leading to differentiated cells, epithelial/mesenchimal transition) and these latter are
maintained by the constitutive activation of stemness-promoting signals. CSC could trigger tumor formation,
drive to resistance to conventional therapeutics and underlie patientsâ relapse. Indeed, stem cell signatures
have been associated with poor prognosis in various.
This background makes the identification of CSC molecular features mandatory to highlight the survival inner
working and to design novel CSC specific therapeutic strategies.
Medulloblastoma (MB) is the most common childhood malignant brain tumor and a leading cause of cancerrelated
morbidity and mortality. Current multimodal therapies are effective in about 50% of patients but often
cause long-term side effects, i.e. developmental, neurological, neuroendocrine and psychosocial deficits
(Northcott PA Nature Rev cancer 2012). For many years, MB treated as a single tumor entity despite the
divergent tumor histology, patientsâ outcome and drug sensitivity, and also by the diversity of the stem cell of
origin. Very recently the scenario of human MB has dramatically changed since its heterogeneous biology has
been addressed by high-throughput gene expression analysis (oligonucleotide microarrays) or by the powerful
genomic next-generation sequencing. These led to the identification of four tumor subgroups (WNT, SHH,
Group 3 and Group 4) uncovering the existence of a highly diverse mutational spectra and gene expression.
However a quantitative approach has not yet been applied to the transcriptional landscape of Medulloblastoma
stem cells (MbSC) through RNA Next Generation Sequencing (RNA-Seq) technology. This is a relevant issue,
since RNA-Seq is able to interrogate the genome wide global transcriptome including new transcripts,
alternative spliced isoforms and non-coding RNAs.
Lower rhombic lip progenitors of the dorsal brainstem are considered the trigger cells in WNT tumors; in SHH
subgroup initiation cells are Prominin1+ CD15+ stem cells from the subventricular zone requiring the
commitment to Math1+ granule cell progenitors [GCP] of the external granule cell layer [EGL]; while Math1+ or
Math1- EGL-GCP or Prominin1+/lineage-negative stem cells sustain the MYC driven Group 3.
MbSC derived from SHH tumors and postnatal normal cerebellar stem cells (NcSC) have been reported to
share several features. A key signal for both of them is Hedgehog. Furthermore, both NcSC and MbSC display
up-regulation of stemness genes (e.g Sox2, Nestin, Nanog, Prom1). Finally, constitutive activation of the Shh
pathway by conditional deletion of Ptch1 inhibitory receptor in NcSC, promote medulloblastoma in vivo,
producing a mouse model of the human SHH tumor. Acquisition of stemness features may therefore represent
the first step of oncogenic conversion. Cooperation with additional oncogenic signals is however needed to
enhance MbSC tumorigenicity.
In order to understand the MbSCs transcriptional programs, we analyze by RNA-Seq, MbSC derived from
Ptch1+/- tumors (Ptch1+/- MbSC). This choice, of a genetically determined model of MB, has allowed us to
work with Ptch1+/- MbSC together with appropriate NcSC counterpart, and to analyze biological replicates
doing statistical analysis.
We identify a number of transcripts, annotated ones, novel isoforms, and long non-coding RNAs,
characterizing MbSC and/or NcSC. Some of these genes control stemness or are cancer related and
conserved in human medulloblastomas. Interestingly a subset of them, belonging to cell stress response, are
of prognostic relevance being significantly related to clinical outcome. Correlation of genes expression
characterizing MbSC with survival information from our human medulloblastomas database further
demonstrates the significance of these findings. Our data suggest that the modulation of normal and cancer
stem cell functions observed in vitro is effective in dissecting the transcriptional programs underlying the in
vivo behavior of human medulloblastomas
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