No abstract

Radiation-induced acute myeloid leukemias (AMLs) in the mouse are characterized by chromosome 2 deletions. Previous studies showed that a minimal deleted region (mdr) of approximately 6.5 cM is lost from one homologue in chromosome 2-deleted AMLs. An AML tumor suppressor gene is proposed to map within this mdr. In this study, we refine the mdr to a I cM interval between markers D2Mit126 and D2Mit185 by microsatellite analysis of 21 primary radiation-induced F I AMLs. The construction of a partial yeast artificial chromosome (YAC) contig spanning the mdr and the location of six known genes indicated that the 1 cM mdr is homologous to human 11p11-12, a region implicated in some human AMLs. Screening of five cell lines derived from primary radiation-induced AMLs for homozygous loss of microsatellites and genes mapping within the mdr revealed loss of both copies of the hemopoietic tissue-specific transcription factor Sfpi1(PU.1/Spi1) in one cell line. Studies of primary and F1 AMLs failed to implicate Sfpi1 as the AML tumor suppressor gene. YAC contig construction, together with data suggesting that the critical gene flanks Sfpi1, represents significant progress toward identifying an AML tumor suppressor gene.

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We have compared four cell-based tumour vaccine strathe two latter vaccines promoted antitumour activity, tegies in prevention experiments using the B16-F10 melawhereas the vaccines consisting of B7.1-expressing noma model. Two of these are thought to favour the direct tumour cells or the hybrid vaccine failed to provide any antigen presentation pathway (B16-F10 expressing B7.1 antitumour activity. Recently human trials have comand hybrids made between B16-F10 cells and menced using transfection of the B7.1 molecule, as well macrophages) and the other two strategies are thought to as employing the hybrid technology to make tumour-B cell act by an indirect pathway of presentation (allogeneic hybrids or tumour and dendritic cell hybrids. Our results tumour cells and autologous tumour cells combined with a suggest that these approaches could be disappointing in powerful adjuvant (Provax-IDEC Pharmaceuticals)). Only the clinics if not optimised.