Given a passage with a context and an answer, 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.

Ex Input:
Context: We utilized whole-genome mapping of promoters that are activated by DNA hypomethylation in hepatocellular carcinoma (HCC) clinical samples to shortlist novel targets for anticancer therapeutics. We provide a proof of principle of this approach by testing six genes short-listed in our screen for their essential role in cancer growth and invasiveness.', 'We used siRNA- or shRNA-mediated depletion to determine whether inhibition of these genes would reduce human tumor xenograft growth in mice as well as cell viability, anchorage-independent growth, invasive capacities, and state of activity of nodal signaling pathways in liver, breast, and bladder cancer cell lines.', 'Depletion of EXOSC4, RNMT, SENP6, WBSCR22, RASAL2, and NENF effectively and specifically inhibits cancer cell growth and cell invasive capacities in different types of cancer, but, remarkably, there is no effect on normal cell growth, suggesting a ubiquitous causal role for these genes in driving cancer growth and metastasis. Depletion of RASAL2 and NENF in vitro reduces their growth as explants in vivo in mice. RASAL2 and NENF depletion interferes with AKT, WNT, and MAPK signaling pathways as well as regulation of epigenetic proteins that were previously demonstrated to drive cancer growth and metastasis.
Answer: Our results prove that genes that are hypomethylated and induced in tumors are candidate targets for anticancer therapeutics in multiple cancer cell types. Because these genes are particularly activated in cancer, they constitute a group of targets for specific pharmacologic inhibitors of cancer and cancer metastasis. Clin Cancer Res; 20(12); 3118-32. ©2014 AACR.

Ex Output:
Does genome-wide study of hypomethylated and induced genes in patients with liver cancer unravel novel anticancer targets?


Ex Input:
Context: This study was designed to investigate the effects of simvastatin in a rat model of acute myocardial infarction.', 'Male Wistar rats were anesthetized (thiopentone sodium 120 mg/kg). After a thoracotomy, the left-anterior-descending coronary artery (LAD) was occluded (for 25 min) and reperfused (for 120 min). Area at risk (AR) was determined with Evans Blue dye and infarct size after staining of the area at risk with nitroblue tetrazolium.', 'In rats, which received the vehicle for simvastatin (10% DMSO, 1 ml/kg i.v. at 1 h prior to the occlusion of the LAD), occlusion of the LAD for 25 min followed by reperfusion for 2 hours resulted in an infarct size of 54 +/- 4% (n=7) of the AR. When compared with vehicle, administration of simvastatin (1 mg/kg i.v. bolus administration at 1 h prior to the onset of myocardial ischemia) caused a significant reduction in myocardial infarct size of 39%. LAD-occlusion and reperfusion caused a progressive fall in mean arterial blood pressure (when compared with sham-operated animals). Simvastatin had no significant effect on blood pressure.
Answer: The result indicates that simvastatin, an inhibitor of HMG-CoA reductase and a ligand of PPAR-a and PPAR-g, reduces the tissue necrosis associated with acute myocardial infarction. We propose that statins may be useful in conditions associated with ischemia-reperfusion of the heart and other organs.

Ex Output:
Does simvastatin reduce infarct size in a model of acute myocardial ischemia and reperfusion in the rat?


Ex Input:
Context: To determine whether or not serum adiponectin concentrations are influenced by ovarian hyperstimulation during in vitro fertilization (IVF).', 'This study involved 52 women who were participating in IVF-ET cycles. Adiponectin levels in serum were determined by radioimmunoassay and compared.', 'Serum adiponectin levels fell from Day-basal to Day-hCG (p = 0.047), and then rose on Day-OR and again on Day-7ET (p < 0.001; p < 0.001). Estradiol levels on Day-hCG were significantly and positively correlated with serum adiponectin levels on Day-OR and Day-7ET (r = 0.325, p = 0.019; r = 0.372, p = 0.007). Progesterone levels on Day-OR positively correlated with serum adiponectin levels on Day-basal (r = 0.278, p = 0.046). There was also a positive correlation between progesterone levels on Day-7ET and serum adiponectin levels on Day-OR (r = 0.289, p = 0.038). Multiple linear regression analysis revealed that adiponectin levels on Day-OR and Day-7ET were negatively correlated with age and body mass index after adjustment was made for concomitant diseases.
Answer: To sum up, following gonadotropin treatment, serum adiponectin levels decrease as a result of the negative effect of high estradiol levels on adiponectin production. Conversely, serum adiponectin levels increase following human chorionic gonadotropin treatment.

Ex Output:

Do serum adiponectin levels increase after human chorionic gonadotropin treatment during in vitro fertilization?