From Marginalized to Maximized Opportunities for Diverse Youths With Disabilities: A Position Paper of the Division on Career Development and Transition

Current secondary education and transition practices have created differential education and employment outcomes by gender, race and ethnicity, socioeconomic status, and disability classifications. These differential outcomes result in economic and social marginalization of far too many students with disabilities. Transition education practices need to respond to these differential outcomes and provide targeted, systematic, and long-term opportunities for all students to attain individually and family-determined postschool goals. This position paper recommends an ecological framework for considering the multiple systems that influence transition education and postschool outcomes for diverse youths with disabilities. The authors argue for educators, researchers, and policy makers to attend to social, political, economic, educational, and cultural contexts in developing effective interventions and improving postschool outcomes.Yeshttps://us.sagepub.com/en-us/nam/manuscript-submission-guideline

An insertional mutagenesis screen identifies genes that cooperate with Mll-AF9 in a murine leukemogenesis model

Patients with a t(9;11) translocation (MLL-AF9) develop acute myeloid leukemia (AML), and while in mice the expression of this fusion oncogene also results in the development of myeloid leukemia, it is with long latency. To identify mutations that cooperate with Mll-AF9, we infected neonatal wild-type (WT) or Mll- AF9 mice with a murine leukemia virus (MuLV). MuLV-infected Mll-AF9 mice succumbed to disease significantly faster than controls presenting predominantly with myeloid leukemia while infected WT animals developed predominantly lymphoid leukemia. We identified 88 candidate cancer genes near common sites of proviral insertion. Analysis of transcript levels revealed significantly elevated expression of Mn1, and a trend toward increased expression of Bcl11a and Fosb in Mll-AF9 murine leukemia samples with proviral insertions proximal to these genes. Accordingly, FOSB and BCL11A were also overexpressed in human AML harboring MLL gene translocations. FOSB was revealed to be essential for growth in mouse and human myeloid leukemia cells using shRNA lentiviral vectors in vitro. Importantly, MN1 cooperated with Mll-AF9 in leukemogenesis in an in vivo BM viral transduction and transplantation assay. Together, our data identified genes that define transcription factor networks and important genetic pathways acting during progression of leukemia induced by MLL fusion oncogenes