Abstract Three primary tumors induced by 3‐MCA in the golden hamster, with a diploid chromosome constitution and a short latency period, were allogeneically transplanted. Three tumor lines with a total of 19 individual transplanted tumors were chromosomally analyzed. None of the originally diploid tumors preserved its chromosomal constitution in allogeneic serial transplantation. A model of heteroploid transformation was established. In two tumor lines the presence of host cells was observed and in one line at advanced passages a new tumor‐cell population occurred with multiple severe chromosomal aberrations derived from the host cells. No specific chromosomal changes could be observed, but each line was characterized by chromosomal markers and a non‐random distribution in some chromosome groups was identified. The spontaneous occurrence of chromosomal aberrations with a very high incidence occurring in the host cells at advanced passages could not be accounted for by direct action of the chemical substance and possible secondary factor/s of a viral or metabolic nature are discussed.
Chromosome banding techniques were used to analyze the chromosomal constitution of hamster cells transformed by chemical carcinogens and fibrosarcomas obtained after injection of the transformed cell lines. Each transformed line is considered unique because each was derived from fetal material from a different pregnant animal. The chromosome modes of the transformed lines and tumors were generally near-diploid. Analysis of bands verified the occurrence of identical banding patterns in the marker chromosomes of transformed lines and tumor-derived cultures, thus providing unequivocal evidence that the fibrosarcomas were produced by the cells that were transformed in vitro and making it possible to recognize 10 marker chromosomes and their origin. Different carcinogens may produce transformations associated with the same specific marker, but not all transformed lines have the same markers even with the same chemical carcinogen. Some markers were found in the tumor-derived culture and not the transformed line or occurred in later passages of both the transformed line and tumor cultures but not in the early passage of these lines. In some transformed cell lines the chromosome number increased but did not involve a specific chromosome group or pair. The incidence of chromosomal deviation in cancer is species dependent and contributes to the characteristics of cancer. Chromosome alterations are responsible for the genotypic changes capable of autonomous growth and thus are considered reflections of secondary alterations. The question whether chromosome changes are the causal factors in carcinogenesis remains unanswered.
The article demonstrates that the Romanian scientist Stefan Odobleja (1902-1978), in his work "Consonantist Psychology" elaborated the principles and laws that are the basis of artificial thinking. The fascination with artificial intelligence began last century, when humanity was very far from the technologies without which we cannot imagine life today. Artificial intelligence refers to the phenomenon where a machine acts like a human mind. The history of artificial intelligence can include the scientist Stefan Odobleja, as the father of artificial thinking, described in his work, which is actually a generalized cybernetics.
In vitro neoplastic transformation of Syrian hamster cells by chemical carcinogens or Simian adeno-7 virus results in cell lines that have rare cells possessing some chromosomes identical to those referred to as premature chromosome condensation or despiralization. These phenomena occurred without the addition of viruses known to promote cell fusion.
Oral 8-methoxypsoralen (8-MOP) plus high-intensity long-wavelength ultraviolet radiation (UV-A) is used clinically to induce remissions of psoriasis and mycosis fungoides. Leukocytes in 8-MOP containing blood receive UV-A exposure when circulating through the dermis during therapy. The present study utilizes an in vitro assay system to permit quantitation and correlation of multiple biological and physical alterations in human lymphoid cells induced by 8-MOP plus UV-A treatment. Additive inhibition of lymphoid cell DNA synthesis by 8-MOP (0.01 to 1 μ g/ml) plus UV-A (1,000 to 29,000 J/m 2 ) was accompanied by a synergistic potentiation of cell killing in the therapeutic exposure range. Reduction in tritiated thymidine ( 3 HTdR) incorporation to 65–70% of control value was associated with normal survival; while 3 HTdR incorporation of less than 50% of control induced by any 8-MOP plus UV-A combination tested was associated with less than 10% survival, 8-MOP-DNA-cross-links were detected by the alkaline elution assay only when 3 HTdR incorporation was reduced to less than 50% of control. The relative number of crosslinks increased proportionately with further 8-MOP plus UV-A-induced reduction in 3 HTdR incorporation. 8-MOP plus UV-A induced at most approximately a 2-fold increase in sister chromatid exchanges (SCE) per chromosome in lymphocytes or lymphoblastoid cells. Increasing 8-MOP plus UV-A exposure resulted in marked toxicity with few cells progressing to second division metaphases and no further increase in SCE's per chromosome. Addition of 13-cis retinoic acid (1 μ g/ml) to the lymphoblastoid cells prior to 8-MOP plus UV-A treatment did not significantly alter the 3 HTdR incorporation or cell survival. These studies dermonstrate that in vitro exposure of human lymphoid cells to therapeutic levels of 8-MOP and UV-A may decrease cellular DNA synthesis, produce DNA 8-MOP interstrand cross-links, reduce cell viability and induce small increases in sister chromosome exchanges.
The utilization of the C band technique for constitutive heterochromatin has permitted further analysis of both normal and marker chromosomes that were found following neoplastic transformation and in tumors derived from the transformed cells. Syrian hamster cells that have been transformed by chemical carcinogens have chromosomes with constitutive heterochromatin characteristic of the species. In addition to the completely heterochromatic short arms of the submetacentric autosomes, the long arms of both X chromosomes and E20 are entirely heterochromatic. Heterochromatin alterations occurred in only 2 different tumor cultures and in no transformed lines and thus are not a causative factor in transformation. The C band technique facilitated the analysis of marker chromosomes.
SUMMARYOur study concerning the replication of the chromosomal complement in the Romanian hamster (Mesocricetus newtoni) allows for the conclusion that the mitotic cycle is about 10–11 hours.Replication of the chromosomal complement develops asynchronously at both inter and intrachromosomal level. One of the X chromosomes in females begins its replication significantly later than its homologue which replicates similarly to autosomes. The long arms of this X chromosome are late replicating while the short arms are very late replicating as well as the corresponding arms of the other X chromosome. In the male, the X chromosome is uniformely very late replicating and the Y chromosome is also late replicating. Some asynchronous phenomenon may be noticed between the two arms.Replication of autosomes is more uniform and generally occurs before that of heterosomes, except for the long arm of the 17th pair and the short arm of some autosomes.The heterosomes duplication in the Romanian hamster is similar to that of other species of hamsters in which the X chromosomes are very large in sizes. It seems, therefore, that in the Romanian hamster also occurred a phenomenon by which the heterosomes are duplicated (OHNO 1967). The simultaneous presence of more sex chromatin, (RAICU et al. 1970) confirms this hypothesis.The existence of some autosomes with both arms completely unlabelled at the end of S phase, suggests that those proceeded from the fusion of some acrocentrics of golden hamsters presenting the same labelling type. In the evolution process of hamsters, the decrease of the chromosome number from 2n = 44 to 2n = 38 was probably achieved besides others, by a Robertsonian mechanism of the acrocentric chromosomes fusion.
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