Results for cpg translation from English to Greek

european common proposal, to be adopted by cept/cpg
european common proposal, to be adopted by cept/cpg (ÅõñùðáúêÞ ÊïéíÞ Ðñüôáóç, ðïõ èá åãêñéèåß áðü ôç cept/cpg)

the cpg coordination proved to be reasonably effective at the previous conference in 1995.
Ο συντονισμός της cpg αποδείχθηκε αρκετά αποτελεσματικός κατά τη διάρκεια της προηγούμενης διάσκεψης, το 1995.

member states of the european union work out european common proposals for wrcs in the conference preparatory group (cpg) of the cept.
Τα κράτη μέλη της Ευρωπαϊκής Ένωσης εκπονούν κοινές ευρωπαϊκές θέσεις για τις wrc στα πλαίσια της ομάδας προετοιμασίας της διάσκεψης (cpg) της cept.

it is estimated that cigarette smoking kills over 1 000 000 people each year by causing lung cancer as well as many other neoplasmas. p53 mutations are frequent in tobacco-related cancers and the mutation load is often higher in cancers from smokers than from nonsmokers. in lung cancers, the p53 mutational patterns are different between smokers and nonsmokers with an excess of g to t transversions in smoking-associated cancers. the prevalence of g to t transversions is 30% in smokers' lung cancer but only 12% in lung cancers of nonsmokers. a similar trend exists, albeit less marked, in laryngeal cancers and in head and neck cancers. this type of mutation is infrequent in most other tumors aside from hepatocellular carcinoma. at several p53 mutational hotspots common to all cancers, such as codons 248 and 273, a large fraction of the mutations are g to t events in lung cancers but are almost exclusively g to a transitions in non-tobacco-related cancers. two important classes of tobacco smoke carcinogens are the polycyclic aromatic hydrocarbons (pah) and the nicotine-derived nitrosamines. recent studies have indicated that there is a strong coincidence of g to t transversion hotspots in lung cancers and sites of preferential formation of pah adducts along the p53 gene. endogenously methylated cpg dinucleotides are the preferred sites for g to t transversions, accounting for more than 50% of such mutations in lung tumors. the same dinucleotide, when present within cpg-methylated mutational reporter genes, is the target of g to t transversion hotspots in cells exposed to the model pah compound benzo[a]pyrene-7,8-diol-9,10-epoxide. as summarized here, a number of other tobacco smoke carcinogens also can cause g to t transversion mutations. the available data suggest that p53 mutations in lung cancers can be attributed to direct dna damage from cigarette smoke carcinogens rather than to selection of pre-existing endogenous mutations.bublefish
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