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1.
Mapping of the human Blym-1 transforming gene activated in Burkitt lymphomas to chromosome 1 总被引：7，自引：0，他引：7
C C Morton R Taub A Diamond M A Lane G M Cooper P Leder 《Science (New York, N.Y.)》1984,223(4632):173-175
Blym-1, a transforming gene detected by transfection of NIH 3T3 cells with DNA from Burkitt lymphomas, was mapped to the short arm of chromosome 1 (1p32) by chromosomal in situ hybridization. The Blym-1 gene was not physically linked to the cellular myc oncogene or to any of the immunoglobulin gene loci implicated in the characteristic chromosomal translocations in Burkitt lymphoma. 相似文献
2.
Transformation and plasmacytoid differentiation of EBV-infected human B lymphoblasts by ras oncogenes 总被引：7，自引：0，他引：7
S Seremetis G Inghirami D Ferrero E W Newcomb D M Knowles G P Dotto R Dalla-Favera 《Science (New York, N.Y.)》1989,243(4891):660-663
The biological effects of ras oncogene activation in B cells were studied by using amphotropic retroviral vectors to introduce H- or N-ras oncogenes into human B lymphoblasts immortalized by Epstein-Barr virus. Expression of both H- and N-ras oncogenes led to malignant transformation of these cells, as shown by clonogenicity in semisolid media and tumorigenicity in immunodeficient mice. In addition, terminal differentiation into plasma cells was detectable as specific changes in morphology, immunoglobulin secretion, and cell surface antigen expression. This combined effect, promoting growth and differentiation in human lymphoblasts, represents a novel biological action of ras oncogenes and has implications for the pathogenesis of terminally differentiated B-lymphoid malignancies such as multiple myeloma. 相似文献
3.
Individual tumors of multifocal EB virus-induced malignant lymphomas in tamarins arise from different B-cell clones 总被引：10，自引：0，他引：10
M L Cleary M A Epstein S Finerty R F Dorfman G W Bornkamm J K Kirkwood A J Morgan J Sklar 《Science (New York, N.Y.)》1985,228(4700):722-724
Cotton-top tamarins were inoculated with sufficient Epstein-Barr virus to induce multiple tumors in each animal within 14 to 21 days. The tumors consisted of large-cell lymphomas that contained multiple copies of the Epstein-Barr virus genome and generated Epstein-Barr virus-carrying cell lines showing no detectable consistent chromosomal abnormality. Hybridization of tumor DNA with immunoglobulin gene probes revealed that each lymphoma was oligo- or monoclonal in origin and that individual tumors from the same animal arose from different B-cell clones. Thus the virus induced multiple transformation events in tamarins in vivo to cause malignant tumors resembling the Epstein-Barr virus-associated lymphomas of patients with organ transplants. 相似文献
4.
Nucleotide sequence of a human Blym transforming gene activated in a Burkitt's lymphoma 总被引：2，自引：0，他引：2
The nucleotide sequence of a human Blym-1 transforming gene activated in a Burkitt's lymphoma cell line was determined. This sequence predicts a small protein of 58 amino acids that is 33 percent identical to the predicted product of chicken Blym-1, the activated transforming gene of chicken B cell lymphomas. Both the human and chicken Blym-1 genes exhibit significant identity to an amino-terminal region of transferrins. 相似文献
5.
Translocation and rearrangements of the c-myc oncogene locus in human undifferentiated B-cell lymphomas 总被引：61，自引：0，他引：61
R Dalla-Favera S Martinotti R C Gallo J Erikson C M Croce 《Science (New York, N.Y.)》1983,219(4587):963-967
The locus for the cellular myc (c-myc) oncogene in humans is located on the region of chromosome 8 that is translocated to chromosome 14 in cells from most undifferentiated B-cell lymphomas. It is shown in this study that the c-myc locus is rearranged in 5 out of 15 cell lines from patients with undifferentiated B-cell lymphomas, and that the rearrangement involves a region at the 5' side of an apparently intact c-myc gene. In at least three patients, this rearranged region appears to contain immunoglobulin heavy chain mu sequences that are located on chromosome 14. The data indicate that this region contains the crossover point between chromosomes 8 and 14. The break point can occur at different positions on both chromosomes among individual cell lines. 相似文献
6.
Trans-activator gene of HTLV-II induces IL-2 receptor and IL-2 cellular gene expression 总被引：20，自引：0，他引：20
W C Greene W J Leonard Y Wano P B Svetlik N J Peffer J G Sodroski C A Rosen W C Goh W A Haseltine 《Science (New York, N.Y.)》1986,232(4752):877-880
The human T-lymphotropic viruses types I and II (HTLV-I and -II) have been etiologically linked with certain T-cell leukemias and lymphomas that characteristically display membrane receptors for interleukin-2. The relation of these viruses to this growth factor receptor has remained unexplained. It is demonstrated here that introduction of the trans-activator (tat) gene of HTLV-II into the Jurkat T-lymphoid cell line results in the induction of both interleukin-2 receptor and interleukin-2 gene expression. The coexpression of these cellular genes may play a role in the altering T-cell growth following retroviral infection. 相似文献
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8.
Expression of the 3' terminal region of human T-cell leukemia viruses 总被引：19，自引：0，他引：19
W Wachsman K Shimotohno S C Clark D W Golde I S Chen 《Science (New York, N.Y.)》1984,226(4671):177-179
Human T-cell leukemia viruses (HTLV) are closely associated with some human T-cell leukemias and lymphomas. A unique 3' region of the HTLV genome is believed to be involved in HTLV-induced cellular transformation, although the function of this region has yet to be determined. A subgenomic messenger RNA transcribed from this region of HTLV has now been characterized. These results provide direct evidence for the expression of a novel gene in HTLV. 相似文献
9.
Guanosine triphosphatase activating protein (GAP) interacts with the p21 ras effector binding domain 总被引：97，自引：0，他引：97
A cytoplasmic protein that greatly enhances the guanosine triphosphatase (GTPase) activity of N-ras protein but does not affect the activity of oncogenic ras mutants has been recently described. This protein (GAP) is shown here to be ubiquitous in higher eukaryotes and to interact with H-ras as well as with N-ras proteins. To identify the region of ras p21 with which GAP interacts, 21 H-ras mutant proteins were purified and tested for their ability to undergo stimulation of GTPase activity by GAP. Mutations in nonessential regions of H-ras p21 as well as mutations in its carboxyl-terminal domain (residues 165-185) and purine binding region (residues 117 and 119) did not decrease the ability of the protein to respond to GAP. In addition, an antibody against the carboxyl-terminal domain did not block GAP activity, supporting the conclusion that GAP does not interact with this region. Transforming mutations at positions 12, 59, and 61 (the phosphoryl binding region) abolished GTPase stimulation by GAP. Point mutations in the putative effector region of ras p21 (amino acids 35, 36, and 38) were also insensitive to GAP. However, a point mutation at position 39, shown previously not to impair effector function, did not alter GAP-p21 interaction. These results indicate that GAP interaction may be essential for ras p21 biological activity and that it may be a ras effector protein. 相似文献
10.
Mouse leukemia virus activation by chemical carcinogens 总被引：10，自引：0，他引：10
The induction of lymphomas in C57BL mice by methylcholanthrene, urethan, or diethylnitrosamine was accompanied by the development of murine leukemia viral antigen in most of the lymphoid tumors. The cell-free transmission of lymphomas induced by methylcholanthrene and the development of antibody to murine leukemia virus prior to the detection of overt lymphoma in these mice suggest that unmasking of a latent leukemia virus is an indigenous actuating cause of the lymphomas. 相似文献
11.
A cytoplasmic protein stimulates normal N-ras p21 GTPase, but does not affect oncogenic mutants 总被引：143，自引：0，他引：143
The role of guanine nucleotides in ras p21 function was determined by using the ability of p21 protein to induce maturation of Xenopus oocytes as a quantitative assay for biological activity. Two oncogenic mutant human N-ras p21 proteins, Asp12 and Val12, actively induced maturation, whereas normal Gly12 p21 was relatively inactive in this assay. Both mutant proteins were found to be associated with guanosine triphosphate (GTP) in vivo. In contrast, Gly12 p21 was predominantly guanosine diphosphate (GDP)-bound because of a dramatic stimulation of Gly12 p21-associated guanosine triphosphatase (GTPase) activity. A cytoplasmic protein was shown to be responsible for this increase in activity. This protein stimulated GTP hydrolysis by purified Gly12 p21 more than 200-fold in vitro, but had no effect on Asp12 or Val12 mutants. A similar factor could be detected in extracts from mammalian cells. It thus appears that, in Xenopus oocytes, this protein maintains normal p21 in a biologically inactive, GDP-bound state through its effect on GTPase activity. Furthermore, it appears that the major effect of position 12 mutations is to prevent this protein from stimulating p21 GTPase activity, thereby allowing these mutants to remain in the active GTP-bound state. 相似文献
12.
A point mutation in the c-myc locus of a Burkitt lymphoma abolishes binding of a nuclear protein 总被引：9，自引：0，他引：9
A 20-base pair region in the first intron of the human c-myc gene was identified as the binding site of a nuclear protein. This binding site is mutated in five out of seven Burkitt lymphomas sequenced to date. To investigate the protein-recognition region in greater detail, the abnormal c-myc allele from a Burkitt lymphoma line (PA682) that carries a t(8;22) chromosomal translocation was used. A point mutation in the binding region of the PA682 c-myc DNA abolished binding of this nuclear protein. This protein may be an important factor for control of c-myc expression, and mutations in its recognition sequence may be associated with c-myc activation in many cases of Burkitt lymphoma. 相似文献
13.
B Rajput S F Degen E Reich E K Waller J Axelrod R L Eddy T B Shows 《Science (New York, N.Y.)》1985,230(4726):672-674
A panel of human-mouse somatic cell hybrids and specific complementary DNA probes were used to map the human tissue plasminogen activator and urokinase genes to human chromosomes 8 and 10, respectively. This result is in contrast to a previous assignment of a plasminogen activator gene to chromosome 6. As neoplastic cells produce high levels of plasminogen activator, it is of interest that aberrations of chromosome 8 have been linked to various leukemias and lymphomas and that two human oncogenes, c-mos and c-myc, have also been mapped to chromosome 8. 相似文献
14.
The chromosomal basis of human neoplasia 总被引：85，自引：0，他引：85
J J Yunis 《Science (New York, N.Y.)》1983,221(4607):227-236
High-resolution banding techniques for the study of human chromosomes have revealed that the malignant cells of most tumors analyzed have characteristic chromosomal defects. Translocations of the same chromosome segments with precise breakpoints occur in many leukemias and lymphomas, and a specific chromosome band is deleted in several carcinomas. Trisomy, or the occurrence of a particular chromosome in triplicate, is the only abnormality observed in a few neoplasias. It is proposed that chromosomal rearrangements play a central role in human neoplasia and may exert their effects through related genomic mechanisms. Thus, a translocation could serve to place an oncogene next to an activating DNA sequence, a deletion to eliminate an oncogene repressor, and trisomy to carry extra gene dosage. 相似文献
15.
Marx J 《Science (New York, N.Y.)》2000,289(5485):1670-1672
The use of microarrays--slides or chips systematically dotted with DNA from thousands of genes--to determine gene expression patterns is providing a wealth of new information that should aid in cancer diagnosis and ultimately in therapy. In the past several months, researchers in several labs have used microarray technology to identify specific subtypes of a variety of cancers, including leukemias and lymphomas, the dangerous skin cancer melanoma, and breast cancer. In some cases, they can determine which cancers are likely to respond to current therapies and which aren't. In addition, the studies are giving researchers a fix on which genes are important for the development, maintenance, and spread of the various cancers, and are thus possible drug targets. 相似文献
16.
McPherson JP Lemmers B Chahwan R Pamidi A Migon E Matysiak-Zablocki E Moynahan ME Essers J Hanada K Poonepalli A Sanchez-Sweatman O Khokha R Kanaar R Jasin M Hande MP Hakem R 《Science (New York, N.Y.)》2004,304(5678):1822-1826
Mus81-Eme1 endonuclease has been implicated in the rescue of stalled replication forks and the resolution of meiotic recombination intermediates in yeast. We used gene targeting to study the physiological requirements of Mus81 in mammals. Mus81-/- mice are viable and fertile, which indicates that mammalian Mus81 is not essential for recombination processes associated with meiosis. Mus81-deficient mice and cells were hypersensitive to the DNA cross-linking agent mitomycin C but not to gamma-irradiation. Remarkably, both homozygous Mus81-/- and heterozygous Mus81+/- mice exhibited a similar susceptibility to spontaneous chromosomal damage and a profound and equivalent predisposition to lymphomas and other cancers. These studies demonstrate a critical role for the proper biallelic expression of the mammalian Mus81 in the maintenance of genomic integrity and tumor suppression. 相似文献
17.
Cortisone-treated mice were inoculated with vaccinia virus, and then five paintings of methylcholanthrene were applied over the site of inoculation. In 70 percent of the mice, tumors developed at the site of inoculation, and 35 percent of the mice, with and without skin tumors, also developed lymphomas. Identically treated control mice that were vacciniaimmune developed a significantly lower incidence (38 percent) of both skin tumors and lymphomas 相似文献
18.
Involvement of the bcl-2 gene in human follicular lymphoma 总被引：69，自引：0，他引：69
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水稻丙二烯氧化物合成酶基因OsAOS1的表达研究 总被引：1，自引：0，他引：1
茉莉酸(Jasmonate,JA)为植物病虫害抗性反应中重要的信号分子,茉莉酸类物质生物合成途径中的关键酶为丙二烯氧化物合成酶(Allene oxide synthase,AOS)。已知水稻AOS基因家族包括4个成员,Os-AOS1～OsAOS4。已有研究表明,水稻OsAOS2基因的过量表达提高了内源PR1基因的表达、增强了水稻对稻瘟病的抗性。本研究分析了OsAOS1基因表达的组织和器官特异性以及外源JA处理对OsAOS1基因表达的影响,同时利用转基因技术研究了OsAOS1基因在调控内源PR1基因表达中的作用。研究结果表明:OsAOS1基因表达的组织和器官特异性不同于OsAOS2基因;外源JA处理诱导OsAOS1基因的瞬时表达,然而OsAOS2基因的诱导表达延迟;OsAOS1过量表达抑制烟草中内源PR1基因的表达。据此推测OsAOS1基因可能不参与依赖于PR1的抗病反应。 相似文献