Given a passage, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

Overexpression of the human c-MYC (MYC) oncogene is one of the most frequently implicated events in the pathogenesis of hepatocellular carcinoma (HCC). Previously, we have shown in a conditional transgenic mouse model that MYC overexpression is restrained from inducing mitotic cellular division and tumorigenesis in the adult liver; whereas, in marked contrast, MYC induces robust proliferation associated with the very rapid onset of tumorigenesis in embryonic and neonatal mice.', 'Here, we show that non-genotoxic hepatotoxins induce changes in the liver cellular context associated with increased cellular proliferation and enhanced tumorigenesis. Both 5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) and carbon tetrachloride (CCl(4)) cooperate with MYC to greatly accelerate the onset of liver cancer in an adult host to less than 7 days versus a mean latency of onset of over 35 weeks for MYC alone. These hepatotoxin-enhanced liver tumors grossly and histologically resemble embryonic and neonatal liver tumors. Importantly, we found that MYC overexpression is only capable of inducing expression of the mitotic Cyclin B1 in embryonic/neonatal hosts or adult hosts that were treated with either carcinogen.
Do hepatotoxin-induced changes in the adult murine liver promote MYC-induced tumorigenesis?

Polo-like kinase 1 (PLK1) controls the main cell-cycle checkpoints, suggesting utility of its inhibition for cancer treatment, including of highly proliferative pediatric cancer. This preclinical study explored the selective PLK1 inhibitor volasertib (BI 6727) alone and combined with chemotherapy in pediatric malignancies.', 'Inhibition of proliferation was explored in vitro using dimethylthiazol carboxymethoxyphenyl sulfophenyl tetrazolium (MTS) assay. Mice bearing human xenografts were treated with weekly intravenous injections of volasertib.', 'Volasertib inhibited proliferation in all 40 cell lines tested, with a mean half-maximal growth inhibitory concentration of 313 nmol/l (range: 4-5000 nmol/l). Volasertib was highly active against RMS-1 alveolar rhabdomyosarcoma xenografts, resulting in 100% tumor regression. Activity was associated with complete and prolonged G2/M arrest and subsequent apoptotic cell death. Volasertib showed synergistic activity with vincristine but antagonistic effects with etoposide.
Does polo-like Kinase Inhibitor Volasertib exhibit Antitumor Activity and Synergy with Vincristine in Pediatric Malignancies?

The aim of this study was to determine the reasons for which erupted third molars (3M) are extracted in a sample of Mexican patients.', "A retrospective cross-sectional study was performed on a sample of 83 patients attending exodontia (minor oral surgery) clinics of a public university in Mexico (Autonomous University of Hidalgo State). The outcome variable was the reason for extractions using Kay and Blinkhorn's classification. The independent variables were age, gender, arch and tooth number according to the World Health Organization (WHO). For statistical analysis, we used the Chi-squared test in Stata 9.0.", 'Eighty-three patients underwent 150 3M extractions. Mean age was 38.67 13.96 years, and 71.1% were female. The four reasons for 3M extraction were prosthetic (44.0%), followed by orthodontic (24.7%), dental caries (20.0%) and periodontal disease (11.3%). Differences were observed in the reasons for 3M extractions across age groups (p < 0.05). No significant differences existed between men and women (p > 0.05), or the WHO tooth number (p > 0.05).
Are reasons why erupted third molars extracted in a public university in Mexico?