Detection of a human p53-like protein in E. histolytica.
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Animals↗
Biomedical subjects
L M Rangel
Publications and source records attributed to L M Rangel.
Multistep carcinogenesis and genital papillomavirus infection. Implications for diagnosis and vaccines.
Activated cellular oncogenes (myc and ras, for example) and inactivated anti-oncogenes (p53 or Rb) participate in multistep carcinogenesis. In addition, some high risk human papillomaviruses (HPV) are also involved in uterine cervix carcinomas. Typification of HPV is important for clinical diagnosis. Unravelling the complexities of the immune system and understanding the biochemistry and molecular genetics of cellular oncogenes and tumor viruses have opened up new possibilities for vaccination.
Cocarcinogenesis↗
Expression of sequences related to c-myc in Entamoeba.
The evolutionarily conserved proto-oncogene c-myc is involved in both proliferation and differentiation processes of higher eukaryotic cells. We report here the identification and characterization of sequences homologous to c-myc in different Entamoeba species using a fragment of the mammalian c-myc gene as a probe. This probe hybridized with fragments of 3.5 and 3.4 kilobases (kb) in E. histolytica HindIII of EcoRI digested DNA. In E. invadens it recognized fragments of 3.1 and 2.8 kb, and in Laredo strain (reported as E. moshkovskii by Clark and Diamond in 1991) the probe hybridized with fragments of 17 kb. The c-myc probe identified transcripts of 3.3 and 1.5 kb in E. histolytica, transcripts of 1.8 and 1.3 kb in Laredo strain, and transcripts of 3.7, 1.8, 1.5 and 1.1 kb in E. invadens. Antibodies against a highly conserved region of the c-myc protein recognized in E. histolytica polypeptides of 35, 40, and 60 kDa. The expression of the 60 kDa polypeptide was temperature-inducible in Laredo strain. In E. invadens a 110 kDa strong band was detected by the antibodies. Surprisingly, E. invadens myc-like sequences and proteins showed greater homology to mammalian c-myc gene and proteins. Expression of proteins antigenically related to c-myc varied according to the cell cycle phase of E. histolytica. These proteins peaked during D, G1, and S phases and declined during G2.
Animals↗
Heterogeneity in state and expression of viral DNA in polyoma virus-induced tumors of the mouse.
We have examined the state and expression of polyoma viral DNA in representative epithelial and mesenchymal tumors, using a combination of biochemical and in situ methods. Results showed wide variations among tumor types and also in different regions within individual tumors, with respect to copy number of viral DNA, presence or absence of deletions, and expression of early and late viral proteins. Epithelial tumors showed the greatest heterogeneity. High copy free viral DNA, frequently with deletions, was found in all such tumors. A portion of free viral DNA was recoverable as transcriptionally active minichromosomes. Three distinct subpopulations of cells were distinguished by in situ analyses. Type 1 cells showed high copy free viral DNA and expressed the major viral capsid protein VP1; these cells appeared to be at various stages of productive (lytic) viral infection. Some productively infected cells were able to undergo mitosis; in a portion of these cells, VP1 was found in close association with the mitotic spindle. Type 2 cells contained high copy free DNA but did not express VP1; by some unknown mechanism, these cells manifest a post-replication block to late gene expression and lytic infection. Type 3 cells contained only low copy, presumably integrated, viral DNA and expressed no VP1; they thus resemble cells transformed in vitro by the virus. Epithelial tumors contained variable mixtures of these subpopulations, while mesenchymal tumors were composed of Type 3 cells only. Differences in virus-cell interactions are discussed in terms of their possible implications in tumor development.
Animals↗
[Presence of proteins and genes homologous to the c-myc proto-oncogene in Entamoeba].
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Animals↗
Poliovirus-induced modification of host cell RNA polymerase IIO is prevented by cycloheximide and zinc.
Infection of HeLa cells with poliovirus results in a decrease in the level of RNA polymerase IIO, the transcriptionally active form of the enzyme, and a shutdown of host transcription (Rangel, L. M., Fernández-Tomas, C., Dahmus, M. E., and Gariglio, P. (1987) J. Virol. 61, 1002-1006). The effect of cycloheximide on poliovirus-induced modification of host RNA polymerase IIO was investigated. The inhibition of protein synthesis, at sequential stages during viral replication, prevents the modification of both total and chromatin-bound RNA polymerase IIO. Furthermore, the inclusion of zinc at a concentration that inhibits the proteolytic post-translational processing of viral polyprotein also prevents the modification of RNA polymerase IIO. These results suggest that host cell enzyme modification depends on the synthesis and processing of protein(s) encoded by the viral genome.
Cell Transformation, Viral↗
Electron microscopy and biochemical properties of polyamine-compacted DNA.
We have obtained polyamine-compacted DNA and analyzed it by electron microscopy employing the method described by Dubochet, suitable for the study of complexes in which the main interactions are of ionic character. In addition, we have developed a simple biochemical method, based on the action of pancreatic DNase I, to demonstrate the condensation of DNA with spermidine. DNA-spermidine complexes are resistant to the action of DNase I, and there is a strong correlation between the presence of condensed DNA forms, both as toroids and as cylinders, and the insensitivity to DNase I activity. We have also shown that pBR322 DNA-spermidine complexes are transcriptionally active in the presence of Escherichia coli RNA polymerase. This supports the data concerning the biological activity of spermidine-condensed DNA.
DNA↗
Modification of RNA polymerase IIO subspecies after poliovirus infection.
Infection of HeLa cells with poliovirus results in a shutdown of host transcription. In an effort to understand the mechanism(s) that underlies this process, we analyzed the distribution of RNA polymerase IIO before and after viral infection. Analysis of free and chromatin-bound enzyme indicated that there is a significant reduction in RNA polymerase IIO following infection. This observation, together with increasing evidence that transcription is catalyzed by RNA polymerase IIO, supports the hypothesis that poliovirus-induced inhibition of host transcription occurs at the level of RNA chain initiation and involves the direct modification of RNA polymerase II.
Cell Transformation, Viral↗
[Virus and cancer].
There are at least four viruses tightly associated with human cancer: HTLY-I and HTLY-II with certain leukemias, EBV with lymphomas, BHV with hepatocarcinomas and HPV with genital cancer. In this work we discuss some evidences indicating these associations; in particular we emphasize the characteristics of human papillomavirus (HPV), due to its growing importance in the development of uterine-cervix carcinoma and the mortality of Mexican women. The low percentage of infected individuals that develop these neoplasias and the long latency periods observed indicate that both cellular and environmental factors are involved in tumor induction. Among cellular factors, oncogenes (such as myc) and antioncogenes could play important roles in the induction and development of the malignant phenotype. The understanding of these factors could lead to the development of methods for early diagnosis and therapy of cancer.
Burkitt Lymphoma↗