RESUMO
Lutetium oxyorthosilicate (LSO) or lutetium yttrium oxyorthosilicate (LYSO) are the scintillator materials most widely used today in PET detectors due to their convenient physical properties for the detection of 511 keV annihilation photons. Natural lutetium contains 2.6% of 176Lu which decays beta to excited states of 176Hf producing a constant background signal. Although previous works have studied the background activity from LSO/LYSO, the shape of the spectrum, resulting from ß-particle and γ radiation self-detection, has not been fully explained. The present work examines the contribution of the different ß-particle and γ-ray interactions to provide a fuller comprehension of this background spectrum and to explain the differences observed when using crystals of different sizes. To this purpose we have shifted the continuous ß-particle energy spectrum of 176Lu from zero to the corresponding energy value for all combinations of the isomeric transitions of 176Hf (γ-rays/internal conversion). The area of each shifted ß-spectrum was normalized to reflect the probability of occurrence. To account for the probability of the γ-rays escaping from the crystal, Monte Carlo simulations using PENELOPE were performed in which point-like sources of monoenergetic photons were generated, inside LYSO square base prisms (all 1 cm thick) of different sizes: 1.0 cm to 5.74 cm. The analytic distributions were convolved using a varying Gaussian function to account for the measured energy resolution. The calculated spectra were compared to those obtained experimentally using monolithic crystals of the same dimensions coupled to SiPM arrays. Our results are in very good agreement with the experiment, and even explain the differences observed due to crystal size. This work may prove useful to calibrate and assess detector performance, and to measure energy resolution at different energy values.
RESUMO
BACKGROUND: Lung squamous cell carcinomas (SqCCs) occur at higher rates following arsenic exposure. Somatic DNA copy-number alterations (CNAs) are understood to be critical drivers in several tumour types. We have assembled a rare panel of lung tumours from a population with chronic arsenic exposure, including SqCC tumours from patients with no smoking history. METHODS: Fifty-two lung SqCCs were analysed by whole-genome tiling-set array comparative genomic hybridisation. Twenty-two were derived from arsenic-exposed patients from Northern Chile (10 never smokers and 12 smokers). Thirty additional cases were obtained for comparison from North American smokers without arsenic exposure. Twenty-two blood samples from healthy individuals from Northern Chile were examined to identify germline DNA copy-number variations (CNVs) that could be excluded from analysis. RESULTS: We identified multiple CNAs associated with arsenic exposure. These alterations were not attributable to either smoking status or CNVs. DNA losses at chromosomes 1q21.1, 7p22.3, 9q12, and 19q13.31 represented the most recurrent events. An arsenic-associated gain at 19q13.33 contains genes previously identified as oncogene candidates. CONCLUSIONS: Our results provide a comprehensive approach to molecular characteristics of the arsenic-exposed lung cancer genome and the non-smoking lung SqCC genome. The distinct and recurrent arsenic-related alterations suggest that this group of tumours may be considered as a separate disease subclass.
