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

The production of tumors through solid-state mechanisms has been demonstrated in experimental animals, but foreign body tumorigenesis has not been proven definitively in man. The authors report three patients with angiosarcoma that occurred in intimate association with foreign material retained for prolonged periods. Although several etiologic factors have been defined in angiosarcoma, foreign bodies generally are not appreciated to have this potential. Review of the literature disclosed six cases of angiosarcoma and 40 cases of sarcomas of other histologic types associated with foreign material, with latency periods of from 4 months to 63 years. Implanted foreign material thus should be considered capable of inducing virtually any form of sarcoma in humans.
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PMID:Angiosarcoma associated with foreign body material. A report of three cases. 305 91

The gene encoding the rat brain facilitated glucose transporter protein was cloned and partially sequenced. The transcribed regions encode 10 exons that span about 30 kilobases of genomic DNA. The intron size is markedly biased, the first two significantly greater in length than the seven others. All of the introns are predicted to occur in regions that encode putative extramembranous domains of the protein, consistent with the proposed topology of 12 alpha-helical membrane-spanning segments. In brain, transcription of the glucose transporter gene initiates at two adjacent adenosine residues located about 30 base pairs 3' to a TATA sequence. In addition, there is at least one minor upstream start site. Both transformation of fibroblasts by the oncogenic retrovirus Fujinami sarcoma virus and stimulation of quiescent fibroblasts with serum increase transcription of the glucose transporter gene from identical initiation sites, which are the same as the predominant start sites in brain. The use of the same promoter for increased transcription under both conditions is consistent with the hypothesis that the regulation of gene expression by normal growth and by oncogenesis is mediated by similar or identical pathways.
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PMID:The rat facilitated glucose transporter gene. Transformation and serum-stimulated transcription initiate from identical sites. 319 39

The growth of normal diploid fibroblasts is generally thought to be tightly controlled by exogenous growth factors such as platelet-derived growth factor (PDGF) and epidermal growth factor (EGF). Subversion of a growth factor pathway at a regulatory point is considered to be a key event in neoplastic transformation and tumorigenesis. Thus, simian sarcoma virus has acquired the gene encoding the B-chain of PDGF and there is direct experimental proof that SSV-transformation is mediated by a PDGF-like growth factor. There is accumulating evidence that PDGF-like molecules are also synthesized and released by certain normal cells, suggesting an important role of cellularly produced PDGF in development and tissue regeneration. We now present evidence that a transient expression of the gene encoding the PDGF A-chain, and the synthesis and release of functional A-chain homodimers, is an early event in the prereplicative phase of normal human foreskin fibroblasts exposed to PDGF or EGF. Since these cells are PDGF-responsive, the results imply the existence of a positive autocrine signal that may serve as an amplifier of the mitogenic response under certain conditions.
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PMID:Possible positive autocrine feedback in the prereplicative phase of human fibroblasts. 349 51

This paper reports on the investigation of the effect of medroxyprogesterone acetate (MPA) on foreign body tumorigenesis that resulted from sc implantation of a glass cylinder. Adult BALB/c mice of both sexes bearing the foreign body were separated into groups. Group 1 received 40 mg MPA sc every 2 months during 1 year, in the vicinity of the glass cylinder; group 2 received the same MPA treatment in the contralateral flank; and group 3 received no hormonal treatment. Sarcomas developed in 4 of 39, 9 of 41, and 17 of 39 mice, respectively. With the use of an evaluation based on the number of high-risk mice per time interval, the MPA inhibitory effect was found to be statistically significant in both groups: 26, 53, and 79% tumor incidence, respectively. A decrease in the rate of tumor development also was observed but only in mice treated with MPA in situ. An unexpected side effect of continuous MPA administration in females was the appearance of adenocarcinomas.
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PMID:Inhibitory effect of medroxyprogesterone acetate on foreign body tumorigenesis in mice. 352 97

Four different kinds of data from the 3-methylcholanthrene-induced sarcoma system of the mouse show that the immune system stimulates oncogenesis; i.e., the presence of a tumor-specific immune reaction is a positive aid to tumor development. It seems proper, therefore, to consider cancer, at least in part, an autoimmune disease.
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PMID:The autoimmune nature of cancer. 354 2

The Chinese hamster embryo fibroblast cell line CHEF/18 is readily transfected by plasmid DNA. In the present transfection studies with CHEF/18 cells, focus formation induced by plasmids containing the mutant human c-Ha-ras gene EJ was compared with that of control plasmids without the EJ insert. The focus-forming activity of the transfected plasmid J132, a recombinant of the Harvey murine sarcoma virus LTR and the normal human c-Ha-ras1 in pBR322, also was assessed. Foci were recovered after transfection with either pSV2gpt or pSV2neo at about 10% the frequency obtained with the EJ-containing plasmids, and J132 gave a similar frequency, all well above background obtained with salmon sperm DNA. Whereas foci from transfection with EJ-containing plasmids contained the EJ DNA, no plasmid DNA was detected in either tumorigenic or tumor-derived cells from foci transfected with pSVgpt, pSVneo, or J132. Evidence that genomic changes were induced by plasmid transfection is based on finding chromosomal aberrations in all expanded foci and tumor-derived cells examined. The results suggest the occurrence of "hit-and-run" tumorigenesis induced by transient plasmid transfection.
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PMID:Plasmid-induced "hit-and-run" tumorigenesis in Chinese hamster embryo fibroblast (CHEF) cells. 385 18

Tumorigenic and nontumorigenic mutants induced by a single 5'-bromodeoxyuridine (BrdU) treatment of a nonproducer (NP) tumorigenic cell line were isolated and characterized. Among the cloned derivatives were examples of virus-free and sarcoma virus-producing cell lines. Oncogenicity did not correlate with production of virus or ease of rescue of the sarcoma genome. All lines, including nononcogenic derivatives, retained the sarcoma genome. Phenotypic reversion of some cell mutants was observed after in vivo inoculation or long term in vitro cultivation. The M-50T cell line, obtained from a tumor induced by M-50 cells, had a sarcoma genome rescuable by direct superinfection; this was only achieved with parental M-50 cells by a cell fusion rescue technique. The M-43-2T cell, obtained from a single small static tumor induced by otherwise nononcogenic M-43-2 cells, shed sarcoma virus and became tumorigenic. M-58-4-48 became tumorigenic after passage 48 of the M-58-4 line, which was originally nontumorigenic. These observations of phenotypic reversion demonstrate that the presence of the sarcoma gene in cells is an essential but not sufficient condition of tumorigenesis.
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PMID:Mutants of nonproducer cell lines transformed by murine sarcoma virus. II. Relationship of tumorigenicity to presence of viral markers and rescuable sarcoma genome. 412 9

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

Avian myelocytomatosis virus (MC29V) is a retrovirus that transforms both fibroblasts and macrophages in culture and induces myelocytomatosis, carcinomas, and sarcomas in birds. Previous work identified a sequence of about 1,500 nucleotides (here denoted onc(MCV)) that apparently derived from a normal cellular sequence and that may encode the oncogenic capacity of MC29V. In an effort to further implicate onc(MCV) in tumorigenesis, we used molecular hybridization to examine the distribution of nucleotide sequences related to onc(MCV) among the genomes of various avian retroviruses. In addition, we characterized further the genetic composition of the remainder of the MC29V genome. Our work exploited the availability of radioactive DNAs (cDNA's) complementary to onc(MCV) (cDNA(MCV)) or to specific portions of the genome of avian sarcoma virus (ASV). We showed that genomic RNAs of avian erythroblastosis virus (AEV) and avian myeloblastosis virus (AMV) could not hybridize appreciably with cDNA(MCV). By contrast, cDNA(MCV) hybridized extensively (about 75%) and with essentially complete fidelity to the genome of Mill Hill 2 virus (MH2V), whose pathogenicity is very similar to that of MC29V, but different from that of AEV or AMV. Hybridization with the ASV cDNA's demonstrated that the MC29V genome includes about half of the ASV envelope protein gene and that the remainder of the MC29V genome is closely related to nucleotide sequences that are shared among the genomes of many avian leukosis and sarcoma viruses. We conclude that onc(MCV) probably specifies the unique set of pathogenicities displayed by MC29V and MH2V, whereas the oncogenic potentials of AEV and AMV are presumably encoded by a distinct nucleotide sequence unrelated to onc(MCV). The genomes of ASV, MC29V, and other avian oncoviruses thus share a set of common sequences, but apparently owe their various oncogenic potentials to unrelated transforming genes.
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PMID:Avian retroviruses that cause carcinoma and leukemia: identification of nucleotide sequences associated with pathogenicity. 624 77


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