These findings suggest that IVL represents a high-grade non-Hodgkin's lymphoma (NHL) with a propensity for systemic dissemination, and that CR and long-term survival may result in patients treated with aggressive combination chemotherapy.

Immunoablative high-dose cyclophosphamide without stem-cell rescue can induce complete remission in patients with refractory, severe autoimmune disease. Reemergence of marrow function is similar to that seen after autologous transplantation and does not carry the risk for reinfusion of autoaggressive lymphocytes with the autograft.

There seems to be a clinical graft-versus-HL effect associated with allo BMT. Allo BMT for HL also seems to have a lower risk of secondary AML/MDS than auto BMT. Thus, allo BMT warrants continued study in HL.

We analyzed in detail the structure of the L-myc gene isolated from human placental DNA and characterized its expression in several small-cell lung cancer cell lines. The gene is composed of three exons and two introns spanning 6.6 kilobases in human DNA. Several distinct mRNA species are produced in all small-cell lung cancer cell lines that express L-myc. These transcripts are generated from a single gene by alternative splicing of introns 1 and 2 and by use of alternative polyadenylation signals. In some mRNAs there is a long open reading frame with a predicted translated protein of 364 residues. Amino acid sequence comparison with c-myc and N-myc demonstrated multiple discrete regions with extensive homology. In contrast, other mRNA transcripts, generated by alternative processing, could encode a truncated protein with a novel carboxyterminal end.The L-myc gene was first isolated from a human small-cell lung cancer (SCLC) cell line, where it was detected by the presence of gene amplification and its sequence homology to c-myc and N-myc (42). Our initial studies showed that this gene was located in human chromosome region lp32 and was frequently expressed with and without gene amplification in human SCLC cell lines. Given the abundant evidence of a role for deregulated c-myc or N-myc expression in several tumor types and their transforming activity in transfection assays (15,31,53,56,59), it seemed possible that deregulated expression of L-myc might be significant in the pathogenesis of SCLC.C-myc and N-myc both have three exons, including an apparently untranslated exon 1, and several areas of nucleotide sequence homology (4,29,55). Comparison of their predicted amino acid sequences reveals several discrete, highly conserved domains. Although the biochemical function of c-myc or N-myc remains unknown, both genes code for nuclear phosphorylated proteins of short half-life and both bind to DNA (22,23,46). These similarities suggest that c-myc and N-myc are functionally related. Recently, c-myc, N-myc, and L-myc were found to have different patterns of expression in developing murine tissues, with L-myc expressed selectively in fetal lung, brain, and kidney and in adult lung but not other tissues examined (61). This was in contrast to the widely distributed expression of c-myc in many tissues and more similar to the restricted expression of N-myc. These findings suggested that the temporal and tissue-specific expression of N-myc and L-myc is important in mammalian development.In this paper we describe the primary structure of the human L-myc gene and in so doing characterize its transcriptional unit, identify open reading frames, and examine its expression in SCLC. The topology of the L-myc gene is similar to those of c-myc and N-myc, with the major open reading frame sharing several areas of substantial amino acid sequence homology to the other myc family members interspersed with regions of unique sequence. In contrast to * Corresponding author. c-myc and N-myc, however, L-myc transcripts undergo a complex se...

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