Measurement of low pT D0 meson production cross section at CDF II

In this thesis we present a study of the D0 meson (through one of its two-body decay channel, D0 → Kπ) collected by the CDF II experiment at the Tevatron pp ̄ collider at Fermilab. In particular we measured the differential production cross section as a function of the transverse momentum down to pT = 1.5 GeV/c.

Measurement of the differential cross section of tt pairs in pp collision at sqrt(s) = 7TeV with the ATLAS detector at the LHC

In this thesis three measurements of top-antitop differential cross section at an energy in the center of mass of 7 TeV will be shown, as a function of the transverse momentum, the mass and the rapidity of the top-antitop system. The analysis has been carried over a data sample of about 5/fb recorded with the ATLAS detector. The events have been selected with a cut based approach in the "one lepton plus jets" channel, where the lepton can be either an electron or a muon. The most relevant backgrounds (multi-jet QCD and W+jets) have been extracted using data driven methods; the others (Z+ jets, diboson and single top) have been simulated with Monte Carlo techniques. The final, background-subtracted, distributions have been corrected, using unfolding methods, for the detector and selection effects. At the end, the results have been compared with the theoretical predictions. The measurements are dominated by the systematic uncertainties and show no relevant deviation from the Standard Model predictions.

Airway Basal Cell Vascular Endothelial Growth Factor-mediated Cross-Talk Regulates Endothelial Cell Dependent Growth Support of Human Airway Basal Cells

The human airway epithelium is a pseudostratified heterogenous layer comprised of cili-ated, secretory, intermediate and basal cells. As the stem/progenitor population of the airway epi-thelium, airway basal cells differentiate into ciliated and secretory cells to replenish the airway epithelium during physiological turnover and repair. Transcriptome analysis of airway basal cells revealed high expression of vascular endothelial growth factor A (VEGFA), a gene not typically associated with the function of this cell type. Using cultures of primary human airway basal cells, we demonstrate that basal cells express all of the 3 major isoforms of VEGFA (121, 165 and 189) but lack functional expression of the classical VEGFA receptors VEGFR1 and VEGFR2. The VEGFA is actively secreted by basal cells and while it appears to have no direct autocrine function on basal cell growth and proliferation, it functions in a paracrine manner to activate MAPK signaling cascades in endothelium via VEGFR2 dependent signaling pathways. Using a cytokine- and serum-free co-culture system of primary human airway basal cells and human endothelial cells revealed that basal cell secreted VEGFA activated endothelium to ex-press mediators that, in turn, stimulate and support basal cell proliferation and growth. These data demonstrate novel VEGFA mediated cross-talk between airway basal cells and endothe-lium, the purpose of which is to modulate endothelial activation and in turn stimulate and sustain basal cell growth.

Measurements of ttbar Differential Cross Section at the ATLAS Experiment in pp Collisions at sqrt(s)=7TeV and sqrt(s)=8TeV

This PhD thesis presents two measurements of differential production cross section of top and anti-top pairs tt ̅ decaying in a lepton+jets final state. The normalize cross section is measured as a function of the top transverse momentum and the tt ̅ mass, transverse momentum and rapidity using the full 2011 proton-proton (pp) ATLAS data taking at a center of mass energy of √s=7 TeV and corresponding to an integrated luminosity of L=4.6 〖fb〗^(-1). The cross section is also measured at the particle level as a function of the hadronic top transverse momentum for highly energetic events using the full 2012 data taking at √s=8 TeV and with L=20 〖fb〗^(-1). The measured spectra are fully corrected for detector efficiency and resolution effects and are compared to several theoretical predictions showing a quite good agreement, depending on different spectra.

IGF system, CD99 and tumor-specific chromosomal translocations: evaluation of their cross-talk and definition of their role in Ewing sarcoma and prostate cancer

Aberrant expression of ETS transcription factors, including FLI1 and ERG, due to chromosomal translocations has been described as a driver event in initiation and progression of different tumors. In this study, the impact of prostate cancer (PCa) fusion gene TMPRSS2-ERG was evaluated on components of the insulin-like growth factor (IGF) system and the CD99 molecule, two well documented targets of EWS-FLI1, the hallmark of Ewing sarcoma (ES). The aim of this study was to identify common or distinctive ETS-related mechanisms which could be exploited at biological and clinical level. The results demonstrate that IGF-1R represents a common target of ETS rearrangements as ERG and FLI1 bind IGF-1R gene promoter and their modulation causes alteration in IGF-1R protein levels. At clinical level, this mechanism provides basis for a more rationale use of anti-IGF-1R inhibitors as PCa cells expressing the fusion gene better respond to anti-IGF-1R agents. EWS-FLI1/IGF-1R axis provides rationale for combination of anti-IGF-1R agents with trabectedin, an alkylator agent causing enhanced EWS-FLI1 occupancy on the IGF-1R promoter. TMPRSS2-ERG also influences prognosis relevance of IGF system as high IGF-1R correlates with a better biochemical progression free survival (BPFS) in PCa patients negative for the fusion gene while marginal or no association was found in the total cases or TMPRSS2-ERG-positive cases, respectively. This study indicates CD99 is differentially regulated between ETS-related tumors as CD99 is not a target of ERG. In PCa, CD99 did not show differential expression between TMPRSS2-ERG-positive and –negative cells. A direct correlation was anyway found between ERG and CD99 proteins both in vitro and in patients putatively suggesting that ERG target genes comprehend regulators of CD99. Despite a little trend suggesting a correlation between CD99 expression and a better BPFS, no clinical relevance for CD99 was found in the field of prognostic biomarkers.