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.

Input: Consider Input: Cancer cells frequently exhibit resistance to the cytotoxic effect of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Pretreatment of TRAIL-resistant cells with cisplatin sensitizes them to this ligand. Cisplatin also has been shown to enhance adenoviral transgene expression.', 'This study aims to evaluate the ability of cisplatin to enhance the expression and the cytotoxic effect of the tumor-specific adenoviral vector Ad/gTRAIL, which expresses a green fluorescent protein-TRAIL fusion protein.', 'Cultured cancer cells and normal human cells were infected with Ad/gTRAIL with or without cisplatin pretreatment. Adenoviral transgene expression was determined by using flow cytometry to measure green fluorescent protein fluorescence. Cytotoxicity was measured by using thiazolyl blue tetrazolium bromide assays and an apoptosis enzyme-linked immunosorbent assay kit.', 'Green fluorescent protein-TRAIL fusion protein expression was significantly enhanced by cisplatin pretreatment in cancer cells. Cisplatin treatment before Ad/gTRAIL infection resulted in a 2- to 12-fold increase in green fluorescent protein fluorescence intensity across cancer lines. Although Ad/gTRAIL induced mild cytotoxicity in all cancer lines (inhibitory concentration of 50% values of >500 pfu/cell), pretreatment with cisplatin resulted in a dose-dependent enhancement of Ad/gTRAIL-mediated cytotoxicity, as indicated by the drastic reduction of inhibitory concentration of 50% values to 4 to 42 pfu/cell in all cell lines. There was no cytotoxicity noted in normal cells treated with both cisplatin and Ad/gTRAIL.

Output: Does cisplatin enhance apoptosis induced by a tumor-selective adenovirus expressing tumor necrosis factor-related apoptosis-inducing ligand?

Input: Consider Input: Unintentional injuries are the leading cause of death in children, and falls are the most common type of unintentional injury in the US. The incidence of falls from windows, a common cause of death in urban areas, has not been described outside major cities such as New York and Chicago, and rates in urban and suburban areas have not been compared.', 'To estimate the incidence and identify the population at risk for falls from windows among children in Hamilton County, Ohio.', "Retrospective case series identified using Cincinnati Children's Hospital Medical Center (CHMC) Trauma Registry.", 'Hamilton County, Ohio, which has urban and nonurban areas.', 'Children less than 15 years old residing in Hamilton County, Ohio, presenting to CHMC in Cincinnati, Ohio, after a fall from a window between January 1, 1991, and December 31, 1997.', 'Annual incidence by age, race, gender, and residence of those who fell from windows.', 'Over the 7-year study period, 86 (6.3%) of 1,363 falls were from windows. The mortality rate for falls from windows was 4.7%, compared to 0.07% for all other falls presenting to CHMC (P<.0001). Children 0-4 years old had a higher rate of falls than children aged 5-14 (14.6/100,000 vs. 2.0/100,000) (P<.0001). Males were twice as likely to fall as females (P<.016), and black children were three times more likely to fall than non-black children (P<.002). The incidence of falls in the city of Cincinnati was four times that of the non-urban area (P<.0002).

Output: Does childhood injuries and deaths due to fall from windows?

Input: Consider Input: It has previously been shown that gefitinib-treated patients with epidermal growth factor receptor (EGFR) gene amplification or high polysomy had a statistically significant improvement in response, time to progression, and survival in non-small cell lung cancer (NSCLC). Only few studies utilizing anti-EGFR treatment in advanced esophageal adenocarcinomas have been performed and the results have been heterogeneous. The aim of this study was to evaluate EGFR-targeted therapy with gefitinib in esophageal adenocarcinoma with a high EGFR polysomy.', 'Novel esophageal cell lines PT6216 and LN6216c were established from primary tumor and lymph node metastasis of a patient with highly aggressive and metastatic adenocarcinoma. Pathological examination including tumor differentiation and prognostic marker analysis, immunohistochemical EGFR expression analysis, EGFR fluorescence in situ hybridization, and mutation analysis were performed. Response of novel cell lines to gefitinib treatment was evaluated by cell proliferation and vitality assays. Fifty-four esophageal adenocarcinoma specimens were evaluated for EGFR gene copy gain.', 'The primary tumor cell line PT6216 and the lymph node cell line LN6216c show a homogenously high polysomy for EGFR determined by FISH analysis. Cell proliferation and vitality are highly sensitive to the tyrosine kinase inhibitor gefitinib compared to esophageal control cells without a high polysomy for EGFR. High polysomy for EGFR was found in 35 % of patients.
Output: Is esophageal carcinoma cell line with high EGFR polysomy responsive to gefitinib?