instruction:
Given a context passage, generate a question from the passage such that its answer is shortest continous span from the passage.
question:
Molecular abnormalities caused by the hybrid Bcr-Abl gene are causally associated with the development and progression of Philadelphia chromosome-positive (Ph(+)) chronic myelogenous leukemia (CML). Imatinib mesylate (STI571), a specific Bcr-Abl tyrosine-kinase signal-transduction inhibitor, has shown encouraging activity in phase I and II studies of CML. Here, we describe the use of imatinib mesylate to treat 75 patients in blast-phase CML (median age, 53 years; 65 with nonlymphoid and 10 with lymphoid blasts), and compare the results with those of a historical control group treated with standard cytarabine-based therapy. Imatinib mesylate was given as oral doses at 300 to 1000 mg per day and was the first salvage therapy for 47 patients. The objective response rate was 52% (39 of 75 patients: 16 had complete and 3 had partial hematologic response; 12 had hematologic improvement; 7 returned to second chronic phase; and 1 had a complete response in extramedullary blastic disease). Response rates were not different between nonlymphoid and lymphoid groups. The cytogenetic response rate was 16% (12 patients: 5 complete, 3 partial [Ph(+) below 35%], and 4 minor [Ph(+), 34% to 90%]). The estimated median overall survival was 6.5 months; the estimated 1-year survival was 22%. Response to therapy (landmark analysis at 8 weeks) was associated with survival prolongation. Compared with standard cytarabine combinations, imatinib mesylate therapy was less toxic and produced a higher response rate (55% versus 29%, P =.001), longer median survival (7 versus 4 months, P =.04), and lower 4-week induction mortality (4% versus 15%, P =.07). Imatinib mesylate is currently being tested in combination with other drugs to improve the prognosis for blast-phase CML.
answer:
What tyrosine kinase, involved in a Philadelphia- chromosome positive chronic myelogenous leukemia, is the target of Imatinib (Gleevec)?


question:
New research shows how kids' brains reorganize as they learn math. All the time you spent memorizing multiplication tables may have made you a better mathematician, according to a new study. A team of scientists from Stanford University, in California, have shown how the brain reorganizes itself as kids learn math. After a certain amount of time spent practicing math, kids can put away the calculator . They don't even need to count on their fingers. They simply know the answers to subtraction , addition, and multiplication facts. The quicker kids can recall basic math facts, the easier it is for them to solve more complicated math problems. The Stanford University researchers observed the brain activity of 28 students aged 7to 9 for the study. They took scans of the students' brains as the students solved math calculations without the help of a calculator, pen or paper. A calculation--three plus four equals seven, for example--flashed on a screen. The students pushed a button to say if the answer was right or wrong. The scientists also recorded the response speed, and what parts of the brain became active as the kids pushed the button. These observations showed a process called fact retrieval . Rather than using their fingers to count, or writing out answers on a piece of paper, the students pulled the answers from memory. It's as if the answers to basic math problems are kept in a long-term storage area in the brain, which was built from repetition. "Experience really does matter," said Dr. Kathy Mann Koepeke. Children make the shift from counting to fact retrieval when they are 8 to 9 years old, the study shows. This is the time when most students are learning basic addition and subtraction. When kids have basic math facts memorized, the brain has more free space to learn more complicated math. This process has benefits for the future. The study shows as kids grow older, their answers rely more on memory and become quicker and more accurate. Less brain activity is devoted to counting. Some children make this shift quicker than others.
answer:
What plays a key role in solving a math problem?


question:
Naive and primed pluripotent states retain distinct molecular properties, yet limited knowledge exists on how their state transitions are regulated. Here, we identify Mettl3, an N(6)-methyladenosine (m(6)A) transferase, as a regulator for terminating murine naive pluripotency. Mettl3 knockout preimplantation epiblasts and naive embryonic stem cells are depleted for m(6)A in mRNAs, yet are viable. However, they fail to adequately terminate their naive state and, subsequently, undergo aberrant and restricted lineage priming at the postimplantation stage, which leads to early embryonic lethality. m(6)A predominantly and directly reduces mRNA stability, including that of key naive pluripotency-promoting transcripts. This study highlights a critical role for an mRNA epigenetic modification in vivo and identifies regulatory modules that functionally influence naive and primed pluripotency in an opposing manner.
answer:

Which properties of the mRNA does N6-methyladenosine (m6A) affect?