Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C1326912 (tumorigenesis)
 57,481 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
 ...
PMID:Transforming genes of neoplasms induced by avian lymphoid leukosis viruses. 625 8

We constructed lambda recombinants containing the Harvey murine sarcoma virus genome and the thymidine kinase (tk) gene of herpes simplex virus type 1 linked to each other. The tk gene was located in a position downstream from both the long terminal repeat and the src gene of Harvey murine sarcoma virus. The DNAs of the lambda recombinants were used to transfect NIH3T3 mouse fibroblasts in order to obtain Harvey murine sarcoma virus DNA-induced foci of transformed cells. The transformed foci were superinfected with a helper-independent retrovirus, and new individual retrovirus were isolated from the superinfected foci. The new viruses could induce focus formation on NIH3T3 cells and could convert NIH3T3(TK-) cells into TK+ cells by carrying the herpes simplex virus type 1 tk gene into the TK- cells. From virus-infected cells, we isolated nonproducer foci on NIH3T3 cells and TK+ transformants on NIH3T3(TK-) cells containing one such new viral genome coding for the dual properties. The new retroviral sequence in the nonproducer cells could be rescued into virus particles at high titers by superinfection with a helper-independent retrovirus. A hybridization analysis indicated that the recombinant virus contained both the Harvey murine sarcoma virus src sequence and the tk gene sequence in a single RNA species approximately 4.9 kilobases long. We concluded that retroviruses can be used as true vectors for genes other than genes that lead to oncogenesis.
 ...
PMID:Construction and isolation of a transmissible retrovirus containing the src gene of Harvey murine sarcoma virus and the thymidine kinase gene of herpes simplex virus type 1. 627 Mar 59

The immunohistochemical localization of glial fibrillary acidic protein (GFAP) was studied by the peroxidase-antiperoxidase (PAP) method in avian sarcoma virus (ASV)-induced brain tumors in hamsters. One hundred twenty-four tumors including 54 astrocytomas, 64 pleomorphic gliomas, five sarcomas, and one unclassified tumor were stained with anti-GFAP serum. A positive immunostaining was seen in astrocytomas and in pleomorphic gliomas. Sarcomas and an unclassified tumor were negative. These results confirmed that a majority of ASV-induced brain tumors contained neoplastic glial cells, and further suggested that the astrocyte is a main target cell of ASV in the experimental neuro-oncogenesis.
 ...
PMID:The localization of glial fibrillary acidic protein in brain tumors induced in hamsters with avian sarcoma virus. 627 41

Some of the parameters involved in retrovirus-induced oncogenesis were analyzed in newborn mice injected with Moloney-murine leukemia virus (M-MuLV) as well as in adults who received the virus by the intraperitoneal (i.p.) or intrathymic (i.t.) route. The neonatally injected mice were permissive for both viral replication and virus-induced cell-surface antigen expression on thymus cells, peripheral T and B lymphocytes, and macrophages, whereas the M-MuLV was not present in the adult i.p. injected mice. Instead, in i.t. injected mice, the virus was expressed in thymus and peripheral T cells only, but was not detected in tail extracts as assessed by means of the UV-XC plaque assay. Lack of virus spread in adult-treated animals correlated with a prompt humoral and cellular immune response, whereas the highly viremic newborn inoculated mice showed negligible virus-specific antibody production and an extremely low frequency of splenic cytotoxic T lymphocyte precursors. Moreover, immune response in both groups of adult-treated mice efficiently prevented tumor induction by Moloney-murine sarcoma virus (M-MuSV), which has the same antigenic determinants as M-MuLV, its natural helper. In contrast, M-MuSV sarcomas grew progressively in newborn inoculated mice and killed the host. Finally, 80% of neonatally injected mice developed lymphomas, whereas all treated adults remained free of disease for more than 15 months. These findings imply that the immune response may, in fact, prevent retrovirus-induced oncogenesis through restriction of virus replication and/or destruction of virus-infected cells.
 ...
PMID:Role of infectious virus expression and immune response in retrovirus-induced oncogenesis. 632 31

From molecularly cloned DNAs of Fujinami sarcoma virus (FSV) and the Schmidt-Ruppin-A strain of Rous sarcoma virus (SRA), viral DNA was constructed in which fps-specific sequences encoded in FSV replaced the src gene of SRA. A 3' fragment of FSV DNA, from an ATG methionine coding sequence 148 base pairs downstream from the gag-fps junction through the long terminal repeat, was joined to cloned SRA DNA at the translation start site for the src gene. The resultant DNA clone contained the splice acceptor site for src mRNA processing in SRA, but contained no src coding sequences from SRA nor any gag sequences from FSV. All genes for the replication of SRA were retained. Transfection of this cloned viral DNA genome into chicken embryo fibroblasts induced morphological transformation of the cells in culture. However, the morphology of the transformed cells was distinct from that observed in cells infected with wild-type FSV. The transformed cells produced a nondefective transforming virus called F36 which contained a hybrid FSV-SRA long terminal repeat. F36-infected cells produced a protein with the expected molecular weight of 91,000, which had an associated protein kinase activity and was immunoprecipitated by antibodies raised against fps gene determinants but not by antibodies raised against gag or src proteins. Injection of F36 virus into 8-day-old chicks produced tumors at the site of inoculation, detectable within 7 days. These results demonstrated that the gag portion of the gag-fps fusion protein of FSV is not required for transformation or tumorigenesis.
 ...
PMID:A fps gene without gag gene sequences transforms cells in culture and induces tumors in chickens. 660 29

The effect of vitamin B-6 deficiency on in vivo host susceptibility to primary Moloney sarcoma virus (MSV)-induced tumor growth and to secondary challenge with MSB sarcoma cells was examined in mice. Female C57BL/6 mice, 6 weeks of age, were fed 20% casein diets with pyridoxine (PN) added at 1, 0.5, 0.1 or 0 mg/kg diet for 21 weeks. After 4 weeks of dietary treatment the mice were challenged with MSV. Vitamin B-6 deficiency resulted in an enhancement of tumor susceptibility as well as an increase in tumor size and regression time. The animals resistant to both MSV and MSV-transformed tumor cells ( MSB ) challenge showed splenic tumor development at necropsy 51 days after MSB challenge. Total incidence of MSV/ MSB /splenic tumors was 2/11, 2/11, 4/10 and 8/11 in animals fed PN 1, 0.5, 0.1 and 0 diets, respectively. Since MSV-induced tumors regressed spontaneously in immunocompetent hosts, the increased susceptibility to MSV oncogenesis in vitamin B-6-deficient animals suggests that reactivity of T cells and/or other effector cells is impaired in vitamin B-6-deficient animals suggests that reactivity of T cells and/or other effector cells is impaired in vitamin B-6 adequacy.
 ...
PMID:The effect of vitamin B-6 deficiency on host susceptibility to Moloney sarcoma virus-induced tumor growth in mice. 672 63

Several groups have shown that the malignant phenotype can be transferred to NIH/3T3 fibroblasts by incorporation of DNA isolated from tumour cell lines. These studies have demonstrated that the transforming activity of DNA isolated from human bladder, lung and colon carcinoma cell lines is related to an alteration of the cellular homologues of the ras genes of Harvey or Kirsten murine sarcoma viruses. It is, however, unclear what relevance these observations have to the multi-stage nature of tumorigenesis in vivo, in which several independent events are required in both humans and experimental animals. The activation of a cellular oncogene in a defined experimental system for the progressive induction of solid tumours has not yet been demonstrated. We report here that high molecular weight DNA from transplanted squamous cell carcinomas induced by sequential treatment of mouse skin with initiators and promoters of carcinogenesis causes morphological transformation of NIH/3T3 fibroblasts at high frequency. The transforming properties are due to the transfer of an activated cellular homologue of the Harvey-ras (rasH) oncogene.
 ...
PMID:Mouse skin carcinomas induced in vivo by chemical carcinogens have a transforming Harvey-ras oncogene. 684 61

A number of virus and chemical carcinogen-transformed cell lines were generated in tissue culture and analyzed for growth control phenotypes prior to and following tumorigenesis in appropriate hosts. The cell lines include those of mouse, rat, human, and Syrian hamster, transformed by papovaviruses and adenoviruses (DNA) or murine (RNA) tumor viruses. Cell lines were assayed for: (a) multinucleation or uncontrolled nuclear division (UND+) and uncontrolled DNA synthesis in cytochalasin B (CB) medium; and (b) the continuation of DNA synthesis in media containing reduced (0.5%) amounts of serum. All or nearly all lines of DNA virus transformants exhibited UND+ and high frequencies of DNA-synthetic cells in CB medium. Two lines of SV40-transformed hamster cells also showed UND+ following tumorigenesis in weaning hamsters. In addition, DNA virus transformants showed the ability to continue DNA synthesis unabated in low-serum medium. In contrast, the mouse sarcoma virus (MSV)-transformed lines exhibited varying degrees of controlled nuclear division and reduced DNA synthesis in CB medium, both prior to and following tumorigenesis. However, the reduction in DNA-synthetic cells was often not as great as that found in untransformed cells. Results similar to the RNA virus transformants were observed with hamster cells transformed by chemical carcinogens. Nearly all of the MSV-transformed lines showed significantly reduced levels of DNA synthesis in low-serum medium as was found in untransformed cells. One cell line, KA31, was followed through three consecutive in vivo tumorigenic passages, but these cells did not acquire UND+ or the ability to continue DNA synthesis in low-serum medium. These results suggest that many MSV- and carcinogen-transformed rodent cells exhibit transformation phenotypes at levels barely above those of normal cells and markedly less than those of DNA virus transformants, and yet they are tumorigenic.
 ...
PMID:In vitro growth control phenotypes of transformed rodent cells prior to and following tumorigenesis. 684 75

The properties of an unusual mouse tumor capable of extremely rapid and widespread spontaneous metastatic growth were recently described; this tumor, called MDAY-D2, at first appeared to be an H-2Kk loss variant of an (A X DBA/2)F1 (H-2KkDd) sarcoma called MDAY and was obtained by serial ip passage of MDAY in DBA/2 (KdDd) mice. The studies described here were concerned with the analysis of the origin of MDAY-D2; i.e., was it a true variant or a newly induced DBA/2 tumor? Several approaches were used, most of which exploited defined cell surface alloantigenic systems as natural genetic markers. The results indicated that MDAY-D2 was indeed a newly induced DBA/2 tumor and, furthermore, that MDAY was a homozygous A-strain tumor, probably a T-cell lymphoma. Thus a) MDAY was found to be Ly-1.2+, Ly-2.2+, and Thy-1.2+, but Ly-6.2-, whereas the opposite pattern was observed with MDAY-D2; b) MDAY possessed the private and public H-2 specificities associated with H-2k and H-2Dd, but not H-2Dk [i.e., it typed as an A-strain (H-2a) tumor, not as (A X DBA/2)F1]; c) MDAY-D2 possessed private and public specificities associated with H-2Kd and H-2Dd and was found to be H-2Kk-negative [i.e., it typed as a DBA/2 (H-2d) tumor]; d) serial injection of clonally derived ouabain-resistant H-2Kk-positive MDAY cells into DBA/2 hosts led to the rapid development of an MDAY-D2 (H-2d-positive) tumor that was fully ouabain-sensitive. Several findings did not support a contaminant theory to explain induction of MDAY-D2. The rapid induction of a tumor after injection of allogeneic tumor cells may have importance in relation to oncogenesis, tumor variant formation, and tumor progression. The results showed that tumor cells themselves can be potent carcinogens.
 ...
PMID:Carcinogenicity of tumor cell populations: origin of a putative H-2 isoantigenic loss variant tumor. 692 20

Sarcomas were induced by sc implantation of unplasticized polyvinylchloride-vinylacetate films in gonadectomized and normal male and female CBA/H mice. Gonadectomy did not demonstrably influence tumor incidence and tumor latencies in males but significantly prolonged tumor latencies in females. The results suggest that estrogen influences the pace of foreign-body tumorigenesis in CBA/H mice.
 ...
PMID:Effects of gonadectomy on foreign-body tumorigenesis in CBA/H mice. 698 25


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>