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.

Context: The Fox River flows from north to south in its first section. The Upper Fox River begins as a small stream northeast of Pardeeville. It flows southwest towards Portage and comes within 2 miles of the Wisconsin River before turning north. After flowing past Montello, the river goes northeast until reaching Lake Butte des Morts. Here it is joined by the tributary Wolf River before entering the west side of Lake Winnebago at Oshkosh. The Upper Fox flows for a total of 142 miles . The Lower Fox begins at the north end of Lake Winnebago, where it flows north past Neenah, Menasha, and Appleton as it begins its 40-mile course northeast towards Lake Michigan. The river drops around 164 feet over this short stretch. Prior to the construction of European-style dams after 1850, the river had many sizable rapids. The Lower Fox ends after flowing through the city of Green Bay and into Lake Michigan through Green Bay. Altogether, the Fox-Wolf watershed drains an area of about 6,429 square miles , giving the Fox an average discharge rate of 4132ft3/s into the bay. 
 Question: Where does the Fox river go first, flowing North to South, Montello or Lake Butte des Morts?
montello

Context: Chronic myeloid leukemia (CML) is characterized by the presence of the Philadelphia chromosome, which is associated with a balanced translocation involving chromosomes 9 and 22 to produce a fusion gene (bcr-abl) that gives rise to a constitutively activated Abl tyrosine kinase. This kinase led to the discovery of several small-molecule inhibitors, imatinib being the first and most successful of these. Resistance to imatinib results in some patients from Abl kinase point mutations. Overcoming imatinib resistance represents one of the biggest challenges facing clinicians in the modern management of CML. In this review, we discuss the current understanding of CML pathophysiology and mechanisms of imatinib resistance and how advancing this knowledge has led to the design of novel therapies in the area of blastic phase CML and Philadelphia chromosome-positive acute lymphoblastic leukemia with previous imatinib failure. 
 Question: What tyrosine kinase, involved in a Philadelphia- chromosome positive chronic myelogenous leukemia, is the target of Imatinib (Gleevec)?
bcr-abl

Context: Spinocerebellar ataxia type 3 (SCA3) is the most frequent inherited cerebellar ataxia in Europe, the US and Japan, leading to disability and death through motor complications. Although the affected protein ataxin-3 is found ubiquitously in the brain, grey matter atrophy is predominant in the cerebellum and the brainstem. White matter pathology is generally less severe and thought to occur in the brainstem, spinal cord, and cerebellar white matter. Here, we investigated both grey and white matter pathology in a group of 12 SCA3 patients and matched controls. We used voxel-based morphometry for analysis of tissue loss, and tract-based spatial statistics (TBSS) on diffusion magnetic resonance imaging to investigate microstructural pathology. We analysed correlations between microstructural properties of the brain and ataxia severity, as measured by the Scale for the Assessment and Rating of Ataxia (SARA) score. SCA3 patients exhibited significant loss of both grey and white matter in the cerebellar hemispheres, brainstem including pons and in lateral thalamus. On between-group analysis, TBSS detected widespread microstructural white matter pathology in the cerebellum, brainstem, and bilaterally in thalamus and the cerebral hemispheres. Furthermore, fractional anisotropy in a white matter network comprising frontal, thalamic, brainstem and left cerebellar white matter strongly and negatively correlated with SARA ataxia scores. Tractography identified the thalamic white matter thus implicated as belonging to ventrolateral thalamus. Disruption of white matter integrity in patients suffering from SCA3 is more widespread than previously thought. Moreover, our data provide evidence that microstructural white matter changes in SCA3 are strongly related to the clinical severity of ataxia symptoms. 
 Question: Which is the protein implicated in Spinocerebellar ataxia type 3?

ataxin-3