instruction:
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.
question:
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?
answer:
the bcr/abl gene fusion


question:
Context: Sir Wilfred Robarts, a famed barrister, has just been released from the hospital in which he stayed for two months following a heart attack. Returning to his practise of law, he takes the case of Leonard Vole, an unemployed man who is accused of murdering his elderly friend, Mrs. Emily French. Vole claims he's innocent, although all evidence points to him as the killer, but his alibi witness, his cold German wife Christine, instead of entering the court as a witness for the defense, becomes the witness for the prosecution and defiantly testifies that her husband is guilty of the murder. Sir Wilfred believes there's something suspicious going on with the case, particularly with Mrs. Vole. 
 Question: How long did Sir Wilfred Robarts stay int he hospital?
answer:
two months


question:
Context: Abdali invaded the Mughal Empire seven times from 1748 to 1767. According to Jaswant Lal Mehta, Durrani aroused the Afghans "religious passions" to fire and "sword into the land of infidels India." He crossed the Khyber pass in December 1747 with 40,000 troops for his first invasion of India. He occupied Peshawar without any opposition. He first crossed the Indus River in 1748, the year after his ascension- his forces sacked and absorbed Lahore. The following year , the Mughal ruler was induced to cede Sindh and all of the Punjab including the vital trans Indus River to him, in order to save his capital from being attacked by the forces of the Durrani Empire. Having thus gained substantial territories to the east without a fight, Durrani and his forces turned westward to take possession of Herat, which was ruled by Nader Shah's grandson, Shah Rukh. The city fell to the Afghans in 1750, after almost a year of siege and bloody conflict; the Afghan forces then pushed on into present-day Iran, capturing Nishapur and Mashhad in 1751. Durrani then pardoned Shah Rukh and reconstituted Khorasan, but a tributary of the Durrani Empire. This marked the westernmost border of the Afghan Empire as set by the Pul-i-Abrisham, on the Mashhad-Tehran road. 
 Question: What relation was Shah Rukh to Nader Shah?
answer:

grandson