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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Abnormalities of chromosome 1, including trisomy for all or a portion of the long arm, have been frequently reported in many cancers. Anomalies of chromosome 19 are far less common, although a t(1;19)(q23;p13) translocation has been reported in association with pre-B-cell leukemia. We have observed a t(1;19)(q12;p13) translocation in three cases of advanced melanoma, with the translocation chromosome representing an extra dose of 1q in each instance. The breakpoint on 1q was within the centromeric heterochromatin, proximal to the site in pre-B-cell leukemia, but the breakpoint on 19p appeared identical. The gene for human insulin receptor has recently been mapped to this region of chromosome 19 (p13.2-13.3). This gene shares structural and sequence homologies with the epidermal growth factor receptor (erb-B oncogene) and members of the src family of oncogenes, suggesting that alterations in the insulin receptor, resulting from chromosomal translocation, could lead to a role in tumorigenesis. The present findings may permit this possibility to be examined in a neoplasm of neuroectodermal origin.
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PMID:A t(1;19) chromosome translocation in three cases of human malignant melanoma. 394 10

We analyzed the relationship of genetic factors determining the expression of endogenous type-C RNA tumor viruses and other host-gene markers to tumorigenesis. A hybridization experiment was performed with mice of strains AKR/J and C57L, the first filial (F(1)) generation hybrids, the second filial (F(2)) generation hybrids, and the backcrosses to the two parental strains. The results demonstrated a highly significant and predictable association between the expression of complete infectious virus or the viral group-specific (gs) antigen in spleens of young mice and tumorigenesis later in life. Most of the tumors were thymic leukemia and reticulum sarcoma, but other mesenchymal, as well as epithelial, tumors were also observed. Tumors occurred preferentially in gs-antigen- or virus-positive mice of all crosses; in the C57L-backcross and F(2) mice segregating for gs-antigen and virus expression, a few gs-antigen-negative mice developed reticulum cell sarcomas. At the time of their occurrence, the mice were all gs-antigen-positive, and most had virus as well.A minor effect of the major histocompatibility locus, H-2, on leukemogenesis was found in the F(2) mice. Several tumor types were also found that we have never observed in the two parental strains. Our data provide the most direct biological evidence in favor of the viral oncogene theory. Thus, from the presence or absence of expression in early life of splenic gs antigen or virus, we can predict whether or not a tumor is likely to develop later in life. These findings suggest that the genome of endogenous type-C RNA viruses is the major determinant for tumorigenesis although they provide no clues about the factors responsible for the various histological types.
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PMID:Host-gene control of type-C RNA tumor virus expression and tumorigenesis in inbred mice. 435 Nov 80

Quantitative and qualitative electron microscopic studies were performed on the mitochondria of leukemic myeloblasts in 3 patients with myeloblastic leukemia and in 3 patients with myelomonoblastic leukemia. In addition, to confirm the presence of virus-like particles within mitochondria and better understand the interaction between the virus and mitochondrion, a rat embryo tissue culture infected with MSV-MLV (Moloney sarcoma virus-Moloney leukemia virus) was selected for detailed electron microscopic examination. Significant quantitative differences between normal and leukemic human mitochondria were not observed. However, qualitative abnormalities were found in the human leukemic mitochondria and in the tissue culture material. These abnormalities included variable forms of the leukemic mitochondria (twisted, tear-drop and irregular shapes), fewer cristae, disrupted mitochondria with virus-like particles, smaller granules in greater abundance, mitochondrial DNA, and contact between the mitochondrion and the nucleus. The tissue culture material revealed similar changes, but showed more virus particles which were located outside the cells, in intracytoplasmic sacs and within the mitochondria. In addition two striking features were observed in the tissue culture material not seen in the human material: a) Budding from the outer mitochondrial membrane into the mitochondrial matrix and b) virus particles attached to the cristae. Since mitochondria are important organelles in the glycolytic-oxidative phosphorylation pathways, perhaps all of us engaged in cancer research should take a closer look at the Warburg effect and carefully consider extranuclear factors operating in oncogenesis.
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PMID:Leukemic mitochondria. I. Acute myeloblastic leukemia. 452 Mar 28

The susceptibility of 12 mutant strains of Japanese quails to the R strain of avian erythroblastosis virus (AEV) was examined. Three strains, SBPP, PNN and CWE, showed high susceptibility and developed various types of tumors including erythroblastosis, hemangioma and myeloblastic leukemia. In relatively resistant WE strain, increased incidence and various types of tumors were observed by modification of host conditions. These results indicate pluripotential oncogenicity of AEV in quails as well as partial control of AEV-oncogenesis by genetical background of the host.
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PMID:Oncogenecity of an avian erythroblastosis virus in mutant strains of Japanese quails. 609 91

Several transformation-defective (td) mutants of Abelson murine leukemia virus (AbLV) are described. Cells nonproductively infected with such mutants exhibited a high degree of growth contact inhibition, failed to form colonies in soft agar, lacked rescuable transforming virus, and were as susceptible as uninfected control cells to transformation by wild-type (wt) AbLV pseudotype virus. In addition, each of several td AbLV nonproductively infected cell clones analyzed was found to be nontumorigenic in vivo. Biochemical analysis of td mutant AbLV-infected clones revealed levels of expression of the major AbLV translational product, P120, and a highly related 80,000-Mr AbLV-encoded protein, P80, at concentrations analogous to those in wt AbLV-transformed cells. Although the AbLV-specific 120,000-Mr polyproteins expressed in td mutant AbLV-infected clones were indistinguishable from those in wt AbLV-transformed lines with respect to molecular weight and [35S]methionine tryptic peptide composition, they each differed from wt AbLV P120 in their patterns of post-translational phosphorylation. A previously described AbLV-associated protein kinase activity is shown to recognize as substrate a major tyrosine-specific acceptor site(s) contained within a single well-resolved tryptic peptide common to both AbLV P120 and P80. In vitro [gamma-32P]ATP-mediated labeling of this phosphorylation site was reduced to below detectable levels in td mutant nonproductively infected cell clones. These findings establish that the AbLV-encoded polyprotein P120 and its associated protein kinase activity are involved in AbLV tumorigenesis.
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PMID:Abelson murine leukemia virus transformation-defective mutants with impaired P120-associated protein kinase activity. 625 63

Oncogenic avian retroviruses can be classified into three groups: sarcoma viruses, acute leukaemia viruses and lymphoid leukosis viruses (LLVs). Sarcoma and acute leukaemia viruses transform fibroblasts and/or haematopoietic cells in culture and induce tumours with short latent periods in infected birds. In contrast, LLVs do not transform cells in vitro and require long latent periods before formation of neoplasms in vivo. The most frequent neoplasm induced by LLVs is malignant lymphoma of the bursa of Fabricius, but LLVs also induce other neoplasms, including sarcomas, nephroblastomas and erythroblastosis. The genomes of both sarcoma and acute leukaemai viruses contain specific genes responsible for viral oncogenicity, whereas the genome of LLVs apparently includes only genes required for virus replication. The genetic basis for the low oncogenic potential of LLVs is therefore obscure. The present experiments indicate that LLV-induced tumours contain transforming genes that can be detected by transfection of NH 3T3 mouse cells. These transforming genes are not linked to LLV DNA sequences, suggesting that oncogenesis by LLVs may result from indirect activation of cellular transforming genes.
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PMID:Transforming genes of neoplasms induced by avian lymphoid leukosis viruses. 625 8

Sera of breast cancer patients from the United States, India, East Africa and China as well as from their families and from healthy women were assayed for antibodies reactive with the murine mammary tumor virus (MuMTV). Detection was by an enzyme-linked immunoassay recently developed in our laboratory. In the women with breast cancer, 62% of the East Africans, 28% of the Indians, 19% of the Americans but only 5% of the Chinese had antibody to MuMTV. Among healthy women, 21% of the Africans, 3% of the Americans and 5% of the Chinese possessed this antibody. Several family members of breast cancer patients, males as well as females, had increased levels of MuMTV antibody. The MuMTV-reactive antibody was removed by absorption with MuMTV, deglycosylated MuMTV and gp52, the major MuMTV envelope protein. It was not absorbed out by murine leukemia viruses, red blood cells from various species, fetal calf serum or carbohydrates. The results suggest that there may be more than one form of breast cancer, definable by reactivity to MuMTV. The murine mammary tumor virus (MuMTV) is the etiological agent of breast cancer in mice. The induction of mammary tumorigenesis, however, is dependent upon the genetic makeup, hormonal status, and diet of the infected mouse. Thus, even in a situation where a known single cause for breast cancer exists, disease manifestation is subordinate to diverse factors in the individual host.
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PMID:Geographic and family studies of immunological responses to antigens of the murine mammary tumor virus in sera of patients with breast cancer. 626 56

Radiation leukemia virus (RadLV)-induced lymphomas of C57BL mice display the appearance of novel proviral sequences at common sites of their DNAs. These results are compatible with the hypothesis of viral oncogenesis by promotor insertion. Radiation-induced tumors do not acquire detectable novel provirus, suggesting that activation of a transforming gene proceeds by a mechanism distinct from the former.
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PMID:[Common proviral integration sites in C57BL mouse lymphoma induced by mouse radiation leukemia virus and absence of novel proviral sequences in DNA from radiation-induced lymphoma]. 629 4

Similarly to other mammalian and avian retroviruses that lack a transforming gene, moloney murine leukaemia virus (MoMuLV) causes no morphological transformation in infected tissue culture cells. However, following injection in an appropriate animal host, MoMuLV induces mainly thymic lymphomas after a long latency period. A common characteristic of neoplasms induced by retroviruses lacking transforming genes is their clonal origin. Here we have generated MoMuLV-induced rat thymic lymphomas and confirmed their clonal nature. Furthermore, we took advantage of the clonality of these tumours to investigate the specificity of provirus integration in the tumour DNA. We reasoned that if several independently derived thymic lymphomas would contain the provirus integrated in the same region of cellular DNA, this would be a strong indication that this integration event is a contributing factor in oncogenesis. The results indicate that there is indeed a cellular DNA region (termed the MLVI-1 locus) that serves as the substrate for proviral DNA integration in 5 out of 16 tumours we examined.
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PMID:A common region for proviral DNA integration in MoMuLV-induced rat thymic lymphomas. 630 Jun 84

We have examined the patterns of heavy-chain immunoglobulin gene rearrangement and provirus integration in seven murine leukemia virus-induced thymic leukemias from AKR/J mice. In five of the seven tumors examined, there were between two and five rearrangements of the heavy-chain immunoglobulin J (JH) segment. Except for one case, the rearranged JH segments are present in less than one copy per cell, indicating that these tumors contain subpopulations of thymocytes with differing JH rearrangements. Nevertheless, each tumor is probably of monoclonal origin because the cells in a given tumor contain a common set of randomly integrated murine leukemia proviruses. Our results indicate that the JH segments rearranged within a few cell divisions after tumor cell proliferation began and may, therefore, identify a specific stage in T-cell differentiation when tumorigenesis occurs.
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PMID:Monoclonal AKR/J thymic leukemias contain multiple JH immunoglobulin gene rearrangements. 632 69


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