Given a context passage, generate a question from the passage such that its answer is shortest continous span from the passage.

Chronic myeloid leukemia (CML) is caused by Bcr-Abl, a constitutively active tyrosine kinase that is the result of a reciprocal translocation between chromosomes 9 and 22 and cytogenetically evident as the Philadelphia chromosome. Imatinib (Glivec, Gleevec), a specific small molecule inhibitor of Bcr-Abl, has become the standard drug therapy for CML, and has dramatically diminished the use of allogeneic stem cell transplantation. Despite unprecedented rates of complete cytogenetic response, residual disease remains detectable in the majority of patients, suggesting that imatinib fails to eradicate leukemic stem cells. In this publication, the current perspectives for CML patients treated with imatinib are reviewed, focusing on the results of both standard and high-dose therapy. Monitoring of time-dependent prognostic factors is reviewed. The reasons imatinib may not be able to eradicate the disease are discussed, and potential strategies to achieve disease elimination are presented. Lastly, resistance to imatinib and the potential of second-generation Abl kinase inhibitors in the setting of clinical resistance are considered.
What tyrosine kinase, involved in a Philadelphia- chromosome positive chronic myelogenous leukemia, is the target of Imatinib (Gleevec)?

You have been badly injured in a car accident. It is necessary to give you a blood transfusion because you lost a great deal of blood in the accident. However, special care must be taken in selecting new blood for you. If the blood is too different from your own, the transfusion could kill you. There are four basic types of blood; A, B, AB, and O. A simple test can make sure of a person's blood type. Everybody is born with one of these four types of blood. Blood type, like hair color1 and height, is received from parents. The four groups must be transfused carefully. A and B cannot be mixed. A and B cannot receive AB, but AB may receive A or B. O can give to any other group; therefore, it is often called the universal donor . For the opposite reason, AB is sometimes called the universal recipient . However, because so many reactions can happen in transfusions , patients usually receive only salt of plasma (liquid part of blood) until their blood can be matched as exactly as possible in the blood bank of a hospital. In this way, it is possible to prevent the transfusion from any bad reactions.
People with type A blood can receive type .

Nuclear receptor co-repressor (N-CoR) plays important role in transcriptional control mediated by several tumor suppressor proteins. Recently, we reported a role of misfolded-conformation dependent loss (MCDL) of N-CoR in the activation of oncogenic survival pathway in acute promyelocytic leukemia (APL). Since N-CoR plays important role in cellular homeostasis in various tissues, therefore, we hypothesized that an APL like MCDL of N-CoR might also be involved in other malignancy. Indeed, our initial screening of N-CoR status in various leukemia and solid tumor cells revealed an APL like MCDL of N-CoR in primary and secondary tumor cells derived from non-small cell lung cancer (NSCLC). The NSCLC cell specific N-CoR loss could be blocked by Kaletra, a clinical grade protease inhibitor and by genistein, an inhibitor of N-CoR misfolding previously characterized by us. The misfolded N-CoR presented in NSCLC cells was linked to the amplification of ER stress and was subjected to degradation by NSCLC cell specific aberrant protease activity. In NSCLC cells, misfolded N-CoR was found to be associated with Hsc70, a molecular chaperone involved in chaperone mediated autophagy (CMA). Genetic and chemical inhibition of Lamp2A, a rate limiting factor of CMA, significantly blocked the loss of N-CoR in NSCLC cells, suggesting a crucial role of CMA in N-CoR degradation. These findings identify an important role of CMA-induced degradation of misfolded N-CoR in the neutralization of ER stress and suggest a possible role of misfolded N-CoR protein in the activation of oncogenic survival pathway in NSCLC cells.
Which is the receptor for substrates of Chaperone Mediated Autophagy?