J. R. Stobo

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BACKGROUND Imatinib mesylate (IM) induces clinical remission of chronic myeloid leukemia (CML). The Abelson helper integration site 1 (AHI-1) oncoprotein interacts with BCR-ABL and Janus kinase 2 (JAK2) to mediate IM response of primitive CML cells, but the effect of the interaction complex on the response to ABL and JAK2 inhibitors is unknown. METHODS(More)
versus continuous imatinib in chronic phase chronic myeloid leukaemia patients at 5 years follow-up Despite their efficacy in inducing deep and durable responses in chronic phase (CP) chronic myeloid leukaemia (CML) patients, BCR-ABL1 tyrosine kinase inhibitors (TKI) do not eradicate leukaemia stem cells (LSC), as proven by the persistence of BCR-ABL1+(More)
Histocompatibility is necessary for many collaborative and aggressive cell interactions. The sharing of alleles at certain loci of the H-2 region on chromosome 17 of the mouse is essential for optimal interaction of lymphocytes with each other (1-7), with macrophages (8, 9), and with target cells in certain types of cytotoxic killing by T lymphocytes(More)
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