Genetic mapping of a cellular DNA region involved in induction of thymic lymphomas (Mlvi-1) to mouse chromosome 15.

Ca, Kozak; Strauss, P G; Tsichlis, Philip N.

doi:10.1128/mcb.5.4.894

Cited by 33 publications

(11 citation statements)

References 36 publications

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“…The 5.7-kilobase (kb) RNA genome of E26 contains, in addition to partial retroviral gag and env genes, a part of the myb oncogene originally identified in avian myeloblastosis virus (AMV) and an E26-specific sequence, ets (12,13 (18)(19)(20). Hybrids were genetically characterized by G-trypsin banding (21), G-11 staining, and enzyme typing of [20][21][22][23][24][25][26][27][28] isozyme markers previously assigned to human chromosomes at the same passage from which high molecular weight DNA was extracted (20). Genomic DNA was digested with restriction enzymes and subjected to a Southern analysis (22) using the specific v-ets, ets-1, and ets-2 probes described below (15,17).…”

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“…Genomic DNA was digested with restriction enzymes and subjected to a Southern analysis (22) using the specific v-ets, ets-1, and ets-2 probes described below (15,17). Analogous procedures were used to prepare and characterize the rodent-feline hybrid panel, which segregates cat chromosomes (23), and the Chinese hamster-mouse panel, which segregates mouse chromosomes (24 (15). E.1.28 contains 95% of the viral ets sequence (v-ets).…”

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Conserved chromosomal positions of dual domains of the ets protooncogene in cats, mice, and humans.

Watson

McWilliams-Smith

Kozak

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

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The mammalian protooncogene homologue of the avian v-ets sequence from the E26 retrovirus consists of two sequentially distinct domains located on different chromosomes. Using somatic cell hybrid panels, we have mapped the mammalian homologue of the 5' v-ets-domain to chromosome 11 (ETSI) in man, to chromosome 9 (Ets-1) in mouse, and to chromosome D1 (ETSI) in the domestic cat. The mammalian homologue of the 3' v-ets domain was similarly mapped to human chromosome 21 (ETS2), to mouse chromosome 16 (Ets-2), and to feline chromosome C2 (ETS2). Both protooncogenes fell in syntenic groups of homologous linked loci that were conserved among the three species. The occurrence of two distinct functional protooncogenes and their conservation of linkage positions in the three mammalian orders indicate that these two genes have been separate since before the evolutionary divergence of mammals.Transforming genes, or protooncogefles, represent a class of conserved cellular genes that may play an important role in tumorigenesis. They were initially described as transduced RNA segments in transforming retrovirus genomes, and they have also been discovered by focus induction after transfection of mouse 3T3 cells with genomic DNA extracted from human tumors (1-5). The limited number of protooncogenes (%30) described to date has attracted considerable research emphasis as an experimental opportunity to study neoplastic transformation from both genetic and molecular perspectives. Because of these extensive analyses, there are now at least five documented modes of oncogene activation associated with tumorigenesis. These include the following: (i) transduction of portions of protooncogene transcripts by retroviruses, thereby placing the oncogene under regulatory control of strong promoters in the viral long terminal repeats (1-5); (ii) chromosomal insertion of an infecting retrovirus adjacent to a protooncogene, similarly altering their control of transcription (5, 6); (iii) translocation of cellular oncogenes to chromosomal regions of differential regulation (7, 8); (iv) amplification of oncogene-containing segments, thereby increasing the dosage of the oncogene (9-11); and (v) point mutation in the cellular coding sequence (2).The ttTo whom reprint requests should be addressed. 1792The publication costs of this articlv were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

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confidence: 99%

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confidence: 99%

Conserved chromosomal positions of dual domains of the ets protooncogene in cats, mice, and humans.

Watson

McWilliams-Smith

Kozak

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

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“…In (6,7). Recently, a number of mink cell focus-forming (MCF) proviruses were molecularly cloned from mouse lymphoma DNA, and flanking-region probes were used to detect common integration regions in other MuLV-induced lymphomas.…”

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confidence: 99%

“…The hpim gene is expressed as a 3.2-kilobase mRNA in various human cell lines of hematopoietic lineage, most dramatically in the K562 erythroleukemia cell line, which contains a cytogenetically demonstrable rearrangement in the 6p2l region. A characteristic chromosome anomaly, a reciprocal translocation t(6;9)(p21;q33), has been described in myeloid leukemias and could involve the hpim gene.In (6,7). Recently, a number of mink cell focus-forming (MCF) proviruses were molecularly cloned from mouse lymphoma DNA, and flanking-region probes were used to detect common integration regions in other MuLV-induced lymphomas.…”

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“…Tumor induction by this type of insertional mutagenesis was first demonstrated in chickens, in which the majority of bursal lymphomas induced by avian leukosis virus contain proviral integrations near the c-myc oncogene (1,2). The mouse mammary tumor virus proviral genome has been observed to be integrated into distinct chromosomal domains in virally induced mammary carcinoma (3)(4)(5), and in Moloney murine leukemia virus (MuLV)-induced lymphomas in rats, a MuLV provirus is frequently integrated in distinct chromosomal domains (6,7). Recently, a number of mink cell focus-forming (MCF) proviruses were molecularly cloned from mouse lymphoma DNA, and flanking-region probes were used to detect common integration regions in other MuLV-induced lymphomas.…”

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Localization of the human pim oncogene (PIM) to a region of chromosome 6 involved in translocations in acute leukemias.

Nagarajan¹,

Louie

Tsujimoto

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

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The human homolog, hpim, of the murine pim-1 gene, which is activated in murine T-cell lymphomas by insertion of retrovirus proviral genomes in the pim-1 region, has been molecularly cloned; the cloned probe has been used to map the hpim locus to human chromosome region 6p2i by somatic cell hybrid analysis and chromosomal in situ hybridization. The hpim gene is expressed as a 3.2-kilobase mRNA in various human cell lines of hematopoietic lineage, most dramatically in the K562 erythroleukemia cell line, which contains a cytogenetically demonstrable rearrangement in the 6p2l region. A characteristic chromosome anomaly, a reciprocal translocation t(6;9)(p21;q33), has been described in myeloid leukemias and could involve the hpim gene.In (6,7). Recently, a number of mink cell focus-forming (MCF) proviruses were molecularly cloned from mouse lymphoma DNA, and flanking-region probes were used to detect common integration regions in other MuLV-induced lymphomas. One clone revealed variations in the molecular organization of the corresponding region in other lymphomas. This murine genetic locus, pim-1, was rearranged in more than 25% of T-cell lymphomas that were derived from different mouse strains and with various MuLVs (8, 9). The murine pim-1 gene is expressed as a 2.8-kilobase (kb) mRNA at low levels in normal lymphoid tissues (10). Proviral integration in the pim-1 locus in MuLV-induced T-cell lymphomas has been reported to be associated with the presence of enhanced levels of pim-1 mRNA, which may range in size from 2.0 to 2.6 kb depending on the site of integration of the provirus (10). Other investigations have observed pim-J expression in replicating murine T cells but not in various murine T-cell neoplasms (11).Because of our interest in oncogenes and potential oncogenes involved in human B-and T-cell neoplasia, we have isolated human genomic sequences homologous to the murine pim-1 gene. To assess involvement of the human pim locus (PIM, hereafter referred to as hpim) in human neoplastic disease, we have determined the location of the hpim gene in the human genome and have determined that our genomic clones do indeed represent an active gene in various cell lines of hematopoietic origin. MATERIALS AND METHODShpim Genomic Clones. The mouse pim-J probe, a 1-kb BamHI fragment of the murine pim-1 genomic clone (8), hybridized to a human 3.6-kb EcoRI fragment and to a human 14-kb Bcl I fragment. Bcl I-digested, size-selected 14-kb DNA from cell line 380 (12) was cloned in EMBL3A X phage vector. A 14-kb clone from the 380 genomic library, hpim5, that hybridized with the mouse pim-1 probe is shown in Fig. 1. The human 3.6-kb, repeat-free EcoRI fragment (phpim5Rl) contained within this 14-kb X phage recombinant was labeled by nick-translation and used as probe in DNA, RNA, and chromosomal in situ hybridization experiments.Cells. Isolation, propagation, and characterization of parental cells and somatic-cell hybrids used in this study have been described (13)(14)(15)(16)(17)(18). All hybrids were characteriz...

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A human chromosome 8 region with abnormalities in B cell, HTLV-I+ T cell and c-myc amplified tumours.

Mengle-Gaw

Rabbitts

1987

The EMBO Journal

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We describe a region of human chromosome 8q24 involved in variant Burkitt's lymphoma translocations, and where an interstitial deletion occurs in an HTLV‐I+ ATL and three c‐myc amplicons terminate. The deletion in the ATL DNA begins within 1.3 kb of the cloned Burkitt's lymphoma translocation breakpoint and ends within 700 bases of the cloned human equivalent of the rat retroviral insertion site, mis‐1. In addition, three c‐myc amplicons terminate in this region and the end of one of these (the colon carcinoma COL0320) maps within 12 kb of the distal end of the ATL deletion. This region is probably approximately 300 kb downstream of c‐myc and the consistent occurrence of abnormalities in this region implies involvement in tumour aetiology in several different cell types.

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Genetic mapping of a cellular DNA region involved in induction of thymic lymphomas (Mlvi-1) to mouse chromosome 15.

Cited by 33 publications

References 36 publications

Conserved chromosomal positions of dual domains of the ets protooncogene in cats, mice, and humans.

Conserved chromosomal positions of dual domains of the ets protooncogene in cats, mice, and humans.

Localization of the human pim oncogene (PIM) to a region of chromosome 6 involved in translocations in acute leukemias.

A human chromosome 8 region with abnormalities in B cell, HTLV-I+ T cell and c-myc amplified tumours.

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