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Description
The Philadelphia chromosome in humans, is on oncogenic translocation between chromosomes 9 and 22 that gives rise to the fusion protein BCR-Abl. This protein is constitutively active resulting in rapid and uncontrolled cell growth in affected cells. The BCR-Abl protein is the hallmark feature of chronic myeloid leukemia (CML) and is seen in Philadelphia-positive (Ph+) acute lymphoblastic leukemia (ALL) cases. Currently, the first line of treatment is the Abl specific inhibitor Imatinib. Some patients will, however, develop resistance to Imatinib. Research has shown how transformation of progenitor B cells with v-Abl, an oncogene expressed by the Abelson murine leukemia virus, causes rapid proliferation, prevents further differentiation and produces a potentially malignant transformation. We have used progenitor B cells transformed with a temperature-sensitive form of the v-Abl protein that allows us to inactivate or re-activate v-Abl by shifting the incubation temperature. We are trying to use this line as a model to study both the progression from pre-malignancy to malignancy in CML and Imatinib resistance in Ph+ ALL and CML. These progenitor B cells, once v-Abl is reactivated, in most cases, will not return to their natural cell cycle. In this they resemble Ph+ ALL and CML under Imatinib treatment. With some manipulation these cells can break this prolonged G1 arrested phenotype and become a malignant cell line and resistant to Imatinib treatment. Cellular senescence can be a complicated process requiring inter-play between a variety of players. It serves as an alternate option to apoptosis, in that the cell loses proliferative potential, but does not die. Treatment with some cancer therapeutics will induce senescence in some cancers. Such is the case with Imatinib treatment of CML and Ph+ ALL. By using the S9 cell line we have been able to explore the possible routes for breaking of prolonged G1 arrest in these Ph+ leukemias. We inhibited the DNA damage sensor protein ataxia telangiectasia mutated (ATM) and found that prolonged G1 arrest in our S9 cells was broken. While previous research has suggested that the DNA damage sensor protein ataxia-telangiectasia mutated (ATM) has little impact in CML, our research indicates that ATM may play a role in either senescence induction or release.
ContributorsDixon, Sarah E (Author) / Chang, Yung (Thesis advisor) / Clark-Curtiss, Josephine (Committee member) / Touchman, Jeffrey (Committee member) / Arizona State University (Publisher)
Created2011
Description
First-semester student retention is a constant priority for undergraduate institutions. The transition to the collegiate level, and to a new scholastic program and format, is frequently challenging academically and socially—for this reason, many first-semester course schedules for incoming freshman undergraduates feature an introductory seminar to ease transition to an undergraduate lifestyle. Arizona State University features a required “Careers in the Life Sciences” course for its first-semester School of Life Sciences students, which has had tractable results in first semester student retention and academic success. Here, we evaluate a component of the seminar, the peer-mentorship program, for its efficacy in students’ first semester experience. Analysis of self-reports from 168 first-semester “mentees” and their 25 mentors indicates frequency of mentee-mentor contact was the best indicator of a higher first semester GPA, comfort with academic resources and study habits, and desire to engage in extracurricular activities and internships. These data indicate that access to a mentor who actively engages and verbally connects with their mentees is a valuable component of first-semester student academic integration and retention.
ContributorsMathews, Ian T. (Author) / Capco, David (Thesis director) / Clark-Curtiss, Josephine (Committee member) / Harrell, Carita (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor)
Created2014-05