Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bovine leukemia virus (BLV) single-stranded cDNA was used to study the distribution of DNA sequences in tissues (normal or malignant) from bovine, ovine and human origin. After recycling against normal bovine DNA, BLV (3H) cDNA hybridized with bovine enzootic tumor DNA but did not hybridize with normal bovine DNA. These results indicate that BLV is an exogenous RNA oncogenic virus and confirm that enzootic bovine leukosis (EBL) is an infectious disease. Proviral BLV sequences were also detected in buffy coat cells of animals in persistent lymphocytosis (PL) and carrying antibodies to BLV but no tumors. In animals at the tumor stage of EBL, the proviral sequences were found in buffy coat cells, in solid tumors (lymphosarcomas) and in organs infiltrated with tumoral lymphoid cells but not in apparently normal organs. No hybridization above background was observed between BLV (3H) cDNA and DNAs extracted from buffy coat cells and tumors corresponding to sporadic forms of bovine leukosis and some human leukemias and sarcomas.
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PMID:Distribution of bovine leukemia virus proviral sequences in tissues of bovine, ovine and human origin. 22 85

Infection of differentiated mouse embryo cells by simian virus 40 (SV40) leads to the production of the early mRNAs and the tumor (T) antigens that they encode. In contrast, undifferentiated F-9 murine teratocarcinoma cells do not support these early stages of the SV40 cycle. This block results from the inability to accumulate stable processed early SV40 mRNAs. It has recently been shown that vitamin A and its derivatives can induce in vitro differentiation of stem cells. Undifferentiated F-9 cells, upon treatment with a low concentration of retinoic acid, exhibited pronounced morphologic changes as well as the appearance of the H-2 surface antigens. After differentiation, the susceptibility of F9 cells to SV40 infection could be demonstrated by the appearance of large T and small T antigens, as shown by immunofluorescence and immunoprecipitation. Furthermore, SI nuclease mapping of early SV40 transcripts confirmed the presence of the two spliced early mRNAs. These results indicate that the undifferentiated F-9 stem cells contain the genetic information needed for generating stable processed early SV40 mRNAs but are blocked in the production of functional species.
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PMID:Differentiation as a requirement for simian virus 40 gene expression in F-9 embryonal carcinoma cells. 23 Apr 84

Transplantation of a Moloney sarcoma-virus (MSV-M)-transformed producer cell line (Sac(+)) induced progressively or regressively growing tumours in mice. Progressive growth always occurred after transplantation of an MSV-M non-producer transformant (Sac(-)), whereas the MSV-M released from the producer cells (Sac virus) always induced tumours which regressed. In contrast to the non-producer, the producer transformant Sac(+) as well as Sac virus induced a strong immune response, detected in vitro by cell- and antibody-mediated cytotoxicity assays, and in vivo by transplantation immunity. Implantation of Sac(-) cells led to solid, under-vascularized tumours, consisting histologically of uniform densely packed tumour cells. Sac-virus-induced tumours, however, were very well vascularized and arose by proliferation of different connective-tissue cells. After transplantation of Sac(+) cells, tumours were found to consist of typical tumour cells morphologically similar to Sac(-) cells intermingled with proliferated connective-tissue cells. Cultivation of tumour fragments from Sac(+) and Sac(-) tumours was followed by outgrowth of transformed tumour cells with the properties of the originally implanted cells. Tumour explant cultures from Sac-virus-induced tumours did not lead to growth of stably transformed cells. Co-culture of mouse embryo fibroblasts (MEF) with Sac(+) cells resulted in overgrowth of the transformed cells. Infection of MEF with Sac virus led to transiently transformed cells. It is concluded that Sac(+) cell tumours will resist the strong immune defence mechanisms they induce and grow progressively, if the inoculated cells are able to build up a solid, poorly vascularized nodule in the tissue. This always happens after implantation of 10(6) cells, but only occasionally when fewer cells are inoculated. Sac-virus-induced tumours will always regress owing to the strong immune response. The regression is furthered by the fact that MSV-M infection rarely if ever leads to a stable transformation.
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PMID:Growth pattern of tumours in mice induced by murine Moloney sarcoma-virus and sarcoma-virus-transformed cells. 23 Aug 54

In the chemotherapy of infectious diseases, selective toxicity has been achieved by designing curative regimens based on pharmacokinetic data. Selective toxicity of antitumor drugs has been demonstrated for rapidly growing large growth fraction tumors occurring in patients under age 30. In these tumors curative schedules have been achieved by application of animal data relating to cellular and drug kinetics. The attempts to improve chemotherapy of large and small growth fraction tumors by kinetic observations in vivo in humans have been disappointing. Recent evidence suggests that the heterogeneity of cells within tumors has prevented precise observations on the relation of cellular and drug kinetics to improved selective toxicity. The availability of xenografts, flow cytometry, and tumor markers presents an opportunity to isolate subpopulations of tumor cells; to characterize their cellular and drug kinetics; and to correlate these with values obtained in vivo in humans. It should then be possible at long last to examine the potential role of cellular and drug kinetics in devising drug schedules with greater selective toxicity for human cancer.
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PMID:Selective toxicity of anticancer drugs: Presidential Address. 36 60

Infection of mice with Salmonella enteritidis 11RX has been shown previously to cause nonspecific immune stimulation and, consequently, resistance to subsequent challenge with a variety of transplantable tumors. The present study has examined the effect of infection with this organism in a chemical carcinogenesis system. Colonic tumors were induced in LACA and BALB/c x C57BL/6JF1 mice by weekly s.c. injection of 1,2-dimethylhydrazine (15 mg/kg) for 28 weeks. Infection of mice p.o. with live S. enteritidis 11RX at 8-week intervals during 1,2-dimethylhydrazine administration protected both strains against colon tumorigenesis. Significantly fewer infected than control BALB/c x C57BL/6JF1 mice had colonic tumors at or before termination of the experiment (34 or 40 weeks) (p less than 0.001 in all cases). Comparable results were obtained with both male and female mice. The difference in tumor incidence between control and infected LACA mice was not statistically significant, however; the number and size of the lesions was greater in control mice (p less than 0.02). Although it has not been proven that the protective effect is mediated by the immune system, the results are consistent with the operation of a macrophage-mediated surveillance system. It is suggested that enteric infections should be considered as a possible contributing factor in the epidemiology of human colonic cancer.
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PMID:Protective effect of oral Salmonella enteritidis 11RX infection against colon tumor induction by 1,2-dimethylhydrazine in mice. 37 22

A painful intracortical and subperiosteal lesion of the fibula with a 14 year follow-up is reported to regress to a painfree state. Infection is favored in the differential diagnosis. Biopsy with histological and radiographical correlation are essential for exclusion of: osteoid osteoma, osteoblastoma, periostitis, glomus tumor, eosinophilic granuloma, enostosis, hemangioma of bone, giant cell tumor, simple cyst, aneurysmal bone cyst, non-ossifying fibroma, polyostotic fibrous dysplasia, hyperparathyroidism, Paget's disease, localized area of avascular necrosis, stress fracture and even metastatic disease.
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PMID:Intracortical and subperiosteal lesion of unknown etiology. 63 98

A total of 393 platelet transfusions, administered on the pediatric service at the M. D. Anderson Hospital and Tumor Institute between March, 1973, to December, 1974, were reviewed. Of these 64 were administered on indications of hemorrhage or surgery, while 324 were administered prophylactically. In only 33% was an adequate platelet rise seen, and in only 40% of those bleeding was the bleeding controlled. The primary factor precluding the success was the number of previously administered platelet transfusions. Infection, the use of random or single donors, and ABO matching had no effect on the outcome, but this was not accentuated in the bleeding patients. Surprisingly, transfusions in patients with leukemia resulted in greater success than transfusions in patients with solid tumors. The lower the platelet count prior to transfusion, the less likely the transfusion was to be successful.
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PMID:Platelet use in pediatric oncology: a review of 393 transfusions. 64 37

Thin-needle aspiration cytology is a well-known minimally invasive technique that is used in the diagnosis of neoplastic disease. The same biopsy technique provides a means for immediate identification of actinomycosis. Aspiration specimens may be used for morphologic studies, as well as for microbiologic isolation. The diagnostic histologic feature of sulfur granules remains intact with this cytologic aspiration technique. This technique is a safe, simple, and rapid means of diagnosing actinomycosis and appears to have value in the diagnosis of other infectious diseases as well.
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PMID:Cervicofacial actinomycosis. Rapid diagnosis by thin-needle aspiration. 68 14

Acquired resistance can be defined as a qualitative alteration of the genetic material of a cell which is phenotypically correlated with a measurable decrease of the cell's sensitivity against one or several chemotherapeutic agents. There are two basic genetic mechanisms which can lead to the emergence of resistance: mutation and the acquisition of additional genetic material from another cell. Both forms of resistance play an important role in clinical situations: the emergence of resistance by mutation occurs in tumor cells and can also lead to therapeutic problems in antimicrobial chemotherapy. In bacteria, however, acquisition of resistance plasmids represents the dominating mechanism which is responsible for most therapeutic problems in the clinical environment. The different genetic mechanisms involved in the emergence of resistance are paralleled -- at least in bacteria -- by two principally different groups of biochemical mechanisms implementing resistance. Mutations lead to alterations of single cell constituents such as the cell membrane or cellular receptors necessary for the binding of the antimicrobial agent. This form of resistance is biochemically characterized by the inaccessibility of the cell interior for a particular compound or by the modification of an intracellular binding site which loses its affinity for the chemotherapeutic agent. Resistance plasmids on the other hand code for enzymes which inactivate the antibiotic (beta-lactamases, aminoglycosideinactivating enzymes, chloramphenicol-acetyltransferase); In some cases, they direct the synthesis of proteins which affect cell permeability (tetracycline) or isoenzymes which have a lower affinity for the inhibitor (trimethoprim). Resistance against antibiotics can be inducible; In these cases the regulatory mechanisms involved are stable genetical traits as resistance itself; Using chloramphenicol, beta-lactam-antibiotics and aminoglycosides as examples, it is demonstrated that resistance data gathered early in the development of a new drug are of little value in estimating the clinical potential of a new compound. Information on the rate at which resistance develops, on the pattern according to which it emerges ("single step" or "multi step") and on cross-resistance patterns is important in the characterization of a new drug but is often invalidated by later findings obtained in the clinical environment; The problem appears somewhat simpler if a new drug is a member of an already known class of compounds, e.g. a beta-lactam or an aminoglycoside. In such cases our knowledge of frequent enzymatic inactivation mechanisms provides a basis not only for the evaluation of an existing drug, but also for the synthesis of new derivatives.
Infection 1976
PMID:Parameters of acquired resistance and their role in the evaluation of new chemotherapeutic drugs. 78 Feb 82

The cell mediated immunity as expressed by 2,4 DNCB skin sensitivity was measured in 50 healthy Iranian orphans of the age from 15 years. Complete records of the development of these children from birth were available. Children with severe gastroenteritis leading to marasmus and temporary thymic atrophy during the first 6 months of life showed a persistent atopy 1-5 years later. Less severe disease during this time lead to hyporesponsiveness. Similar stress after the 6th month of life did not lead to persistent changes in their cell mediated immunity. The implications of this for the epidemiology of neoplasia and infectious disease are discussed.
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PMID:Persistent cell mediated immune-deficiency following infantile stress during the first 6 months of life. 81 13


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