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: Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers worldwide. Despite significant progresses in the last decades, the origin of this cancer remains unclear and no efficient therapy exists. PDAC does not arise de novo: three remarkable different types of pancreatic lesions can evolve towards pancreatic cancer. These precursor lesions include: Pancreatic intraepithelial neoplasia (PanIN) that are microscopic lesions of the pancreas, Intraductal Papillary Mucinous Neoplasms (IPMN) and Mucinous Cystic Neoplasms (MCN) that are both macroscopic lesions. However, the cellular origin of these lesions is still a matter of debate. Classically, neoplasm initiation or progression is driven by several genetic and epigenetic alterations. The aim of this review is to assemble the current information on genetic mutations and epigenetic disorders that affect genes during pancreatic carcinogenesis. We will further discuss the interest of the genetic and epigenetic alterations for the diagnosis and prognosis of PDAC. Large genetic alterations (chromosomal deletion/amplification) and single point mutations are well described for carcinogenesis inducers. Mutations classically occur within key regions of the genome. Consequences are various and include activation of mitogenic pathways or silencing of apoptotic processes. Alterations of K-RAS, P16 and DPC4 genes are frequently observed in PDAC samples and have been described to arise gradually during carcinogenesis. DNA methylation is an epigenetic process involved in imprinting and X chromosome inactivation. Alteration of DNA methylation patterns leads to deregulation of gene expression, in the absence of mutation. Both genetic and epigenetic events influence genes and non-coding RNA expression, with dramatic effects on proliferation, survival and invasion. Besides improvement in our fundamental understanding of PDAC development, highlighting the molecular alterations that occur in pancreatic carcinogenesis could provide new clinical tools for early diagnosis of PDAC and the molecular basis for the development of new effective therapies. 
 Question: Which is the molecular mechanism underlying K-ras alterations in carcinomas?
[A]: point mutations


[Q]: Context: Facioscapulohumeral muscular dystrophy (FSHD) is one of the most prevalent adult muscular dystrophies. The common clinical signs usually appear during the second decade of life but when the first molecular dysregulations occur is still unknown. Our aim was to determine whether molecular dysregulations can be identified during FSHD fetal muscle development. We compared muscle biopsies derived from FSHD1 fetuses and the cells derived from some of these biopsies with biopsies and cells derived from control fetuses. We mainly focus on DUX4 isoform expression because the expression of DUX4 has been confirmed in both FSHD cells and biopsies by several laboratories. We measured DUX4 isoform expression by using qRT-PCR in fetal FSHD1 myotubes treated or not with an shRNA directed against DUX4 mRNA. We also analyzed DUX4 downstream target gene expression in myotubes and fetal or adult FSHD1 and control quadriceps biopsies. We show that both DUX4-FL isoforms are already expressed in FSHD1 myotubes. Interestingly, DUX4-FL expression level is much lower in trapezius than in quadriceps myotubes, which is confirmed by the level of expression of DUX4 downstream genes. We observed that TRIM43 and MBD3L2 are already overexpressed in FSHD1 fetal quadriceps biopsies, at similar levels to those observed in adult FSHD1 quadriceps biopsies. These results indicate that molecular markers of the disease are already expressed during fetal life, thus opening a new field of investigation for mechanisms leading to FSHD. 
 Question: Which disease is associated with the ectopic expression of the protein encoded by the gene DUX4?
[A]: fshd


[Q]: Context: Hoping to rebound from a tough loss to the Patriots, the Bills would play their Week 2 home opener in an interconference duel with the Tampa Bay Buccaneers. This would be the first time that Buffalo ever hosted Tampa Bay in a regular season game, having played a preseason game with each other in 1977. In the first quarter, the Bills came out firing as quarterback Trent Edwards completed a 32-yard touchdown pass to wide receiver Lee Evans, safety Donte Whitner returning an interception 76 yards for a touchdown and kicker Rian Lindell making a 31-yard field goal. The Buccaneers would get on the board in the second quarter as quarterback Byron Leftwich completed a 42-yard touchdown pass to tight end Kellen Winslow, while Buffalo replied with Lindell getting a 43-yard field goal. Tampa Bay would close out the half as Leftwich completed an 8-yard touchdown pass to running back Carnell "Cadillac" Williams. After a scoreless third quarter, the Bills began to pull away as Lindell got a 43-yard field goal and Edwards completed a 43-yard touchdown pass to wide receiver Terrell Owens. The Buccaneers tried to rally as Leftwich completed a 6-yard touchdown pass to tight end Jerramy Stevens (with a failed two-point conversion), yet Buffalo closed out the game with Lindell nailing a 20-yard field goal. With the win, the Bills improved to 1-1. 
 Question: Which player had the longest touchdown scoring play?
[A]:
donte whitner