Given a question and a context passage, generate the answer having the word or phrase from the context passage. Here, the answer should be a shortest continous span from the passage.

[Q]: Context: Coming off their last-second victory over the Bengals, the Broncos would play their Week 2 home opener against the Cleveland Browns. In the first quarter, Denver would trail early as Browns kicker Phil Dawson got a 22-yard field goal. Afterwards, the Broncos took the lead as quarterback Kyle Orton completed a 2-yard touchdown pass to tight end Tony Scheffler. Cleveland would creep close as Dawson made a 47-yard field goal, but Denver would answer as kicker Matt Prater got a 23-yard field goal in the second quarter and a 38-yard field goal in the third quarter. In the fourth, the Broncos pulled away as fullback Peyton Hillis got a 2-yard touchdown run and running back Correll Buckhalter got a 45-yard touchdown run. 
 Question: Which team scored the first touchdown?
[A]: broncos


[Q]: Context: Chronic myeloid leukemia (CML) is genetically characterized by the presence of the reciprocal translocation t(9;22)(q34;q11), resulting in a BCR/ABL gene fusion on the derivative chromosome 22 called the Philadelphia (Ph) chromosome. In 2-10% of the cases, this chimeric gene is generated by variant rearrangements, involving 9q34, 22q11, and one or several other genomic regions. All chromosomes have been described as participating in these variants, but there is a marked breakpoint clustering to chromosome bands 1p36, 3p21, 5q13, 6p21, 9q22, 11q13, 12p13, 17p13, 17q21, 17q25, 19q13, 21q22, 22q12, and 22q13. Despite their genetically complex nature, available data indicate that variant rearrangements do not confer any specific phenotypic or prognostic impact as compared to CML with a standard Ph chromosome. In most instances, the t(9;22), or a variant thereof, is the sole chromosomal anomaly during the chronic phase (CP) of the disease, whereas additional genetic changes are demonstrable in 60-80% of cases in blast crisis (BC). The secondary chromosomal aberrations are clearly nonrandom, with the most common chromosomal abnormalities being +8 (34% of cases with additional changes), +Ph (30%), i(17q) (20%), +19 (13%), -Y (8% of males), +21 (7%), +17 (5%), and monosomy 7 (5%). We suggest that all these aberrations, occurring in >5% of CML with secondary changes, should be denoted major route abnormalities. Chromosome segments often involved in structural rearrangements include 1q, 3q21, 3q26, 7p, 9p, 11q23, 12p13, 13q11-14, 17p11, 17q10, 21q22, and 22q10. No clear-cut differences as regards type and prevalence of additional aberrations seem to exist between CML with standard t(9;22) and CML with variants, except for slightly lower frequencies of the most common changes in the latter group. The temporal order of the secondary changes varies, but the preferred pathway appears to start with i(17q), followed by +8 and +Ph, and then +19. Molecular genetic abnormalities preceding, or occurring during, BC include overexpression of the BCR/ABL transcript, upregulation of the EVI1 gene, increased telomerase activity, and mutations of the tumor suppressor genes RB1, TP53, and CDKN2A. The cytogenetic evolution patterns vary significantly in relation to treatment given during CP. For example, +8 is more common after busulfan than hydroxyurea therapy, and the secondary changes seen after interferon-alpha treatment or bone marrow transplantation are often unusual, seemingly random, and occasionally transient. Apart from the strong phenotypic impact of addition of acute myeloid leukemia/myelodysplasia-associated translocations and inversions, such as inv(3)(q21q26), t(3;21)(q26;q22), and t(15;17)(q22;q12-21), in CML BC, only a few significant differences between myeloid and lymphoid BC are discerned, with i(17q) and TP53 mutations being more common in myeloid BC and monosomy 7, hypodiploidy, and CDKN2A deletions being more frequent in lymphoid BC. The prognostic significance of the secondary genetic changes is not uniform, although abnormalities involving chromosome 17, e.g., i(17q), have repeatedly been shown to be ominous. However, the clinical impact of additional cytogenetic and molecular genetic aberrations is most likely modified by the treatment modalities used. 
 Question: Which gene fusion is the result of the "philadelphia translocation" or the "philadelphia chromosome" mutation?
[A]: the bcr/abl gene fusion


[Q]: Context: Hoping to rebound from their three-game losing streak, the Raiders flew to Dolphin Stadium for a Week 11 duel with the Miami Dolphins. In the first quarter, Oakland trailed early as Dolphins WR Ted Ginn, Jr. got a 40-yard TD run. In the second quarter, the Raiders responded with kicker Sebastian Janikowski getting a 21-yard field goal. In the third quarter, Oakland started to catch up as DE Jay Richardson sacked QB Chad Pennington in his own endzone for a safety. Miami would answer with RB Patrick Cobbs getting a 10-yard TD run. In the fourth quarter, the Raiders took the lead as Janikowski got a 37-yard field goal, along with WR Johnnie Lee Higgins returning a punt 93 yards for a touchdown. However, the Dolphins sealed Oakland's fate as kicker Dan Carpenter nailed a 38-yard field goal. 
 Question: Which team scored first?
[A]:
dolphins