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  • Springer  (3)
  • 1
    Electronic Resource
    Electronic Resource
    Carcinogen-induced liver tumours of Wistar rats: absence of activatedras genes and of N-rasC (1991)
    Springer
    Journal of cancer research and clinical oncology 117 (1991), S. 381-384 
    Details
    ISSN: 1432-1335
    Keywords: ras genes N-rasC ; Rat HCC ; Mutational activation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We examined mutational activation ofras genes in rat liver preneoplasias and tumours induced by diethylnitrosamine andN-methyl-N-nitrosourea (NMU). In accordance with previous reports on H- and K-ras genes, no mutations were detected in the investigated hepatic tumours and prestages suggesting that neither mutations at codons 12, 13 and 61 of H- and N-ras nor a mutation in the last intron of the H-ras gene are involved in initiation and progression of rat hepatocellular carcinomas. In the course of this investigation we found two N-ras genes (N-rasA, N-rasB). Surprisingly N-rasC, which is present in the germ line of Fischer rats, is missing in Wistar rats. This suggests different numbers of germline N-ras genes in members of one species. Two out of eight NMU-induced liver tumours exhibited additional N-ras-related sequences of unknown origin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01612755
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Proliferative heterogeneity of human renal cell carcinomas and prevalence ofras gene point mutations (1996)
    Springer
    Journal of cancer research and clinical oncology 122 (1996), S. 207-213 
    Details
    ISSN: 1432-1335
    Keywords: ras ; Proliferation ; mibl ; Ki-67 ; Renal cell carcinoma ; Tumor heterogeneity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The variable prevalence and a possible stage-dependent increase ofras gene point mutations in human tumors might correspond to clonal growth advantages ofras-activated cells. Tumor areas with activatedras genes might thus differ in proliferative activity from those lackingras gene activation. This hypothesis is studied in a series of human renal cell carcinomas that had been used previously for an analysis of proliferative compartments after post-operative vascular [3H]/[14C]thymidine perfusion [Rabes et al. (1979) Cancer 44: 799–813]. The growth fraction of different subcompartments of these tumors was studied by immunohistochemistry with mib1 antibody, recognizing a fixation- and embedding-resistant epitope of Ki-67 protein. Thirty subpopulations of 14 human renal cell carcinomas that exhibited a broad spectrum of proliferative activity were chosen for an analysis of the prevalence of K-ras point mutations in exon 1 by a mutation-enriching primermediated restriction-fragment-length-polymorphism analysis and/or direct sequencing of polymerase-chain-reaction-amplified material. The combined autoradiographic and immunohistochemical analysis confirmed the intra- and intertumoral proliferative heterogeneity. Compared to [3H]/[14C]thymidine labeling indices, mib1 labeling indices are higher. The ratio of mib1 to [3H]/[14C]thymidine labeling indices varies from 1.9 to 4.1 for the individual tumor subcompartments. However, neither in K-ras codons 12/13 nor in adjacent codons did we detect any mutations in the various tumor compartments. The results suggest that neither mode of proliferation nor type of differentiation is related to K-ras exon 1 point mutations in human renal cell carcinomas.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01209647
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    DNA adducts and cell cycle (1986)
    Springer
    Journal of cancer research and clinical oncology 112 (1986), S. 189-195 
    Details
    ISSN: 1432-1335
    Keywords: DNA adducts ; Cell cycle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cell cycle-dependent differences of transformation sensitivity may be due to alterations in the formation of ultimate electrophilic carcinogens during the cell cycle, preferential primary adduct formation during specific phases of the cell cycle, e.g. binding to single stranded DNA at the replication fork, base-mispairing and mutation of transformation-related genes replicating at critical phases of DNA synthesis, or cell cycle-related differences in the repair of DNA adducts. Some recent data on these subjects are summarized, mainly in context of cell cycle-dependent transformation sensitivity of regenerating rat liver.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00395911
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    Paper (German National Licenses)
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