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M Muleris

Publications and source records attributed to M Muleris.

79 records · Page 5Linked to original sources

Chromosomal phylogeny of forty-two species or subspecies of cercopithecoids (Primates Catarrhini).

After comparison of the chromosomes of 42 species or subspecies belonging to Cercopithecinae, Papioninae and Colobidae, a phylogeny based on the sequence of chromosomal rearrangements is proposed for Cercopithecoidea. From their last common ancestor, which possessed 46 chromosomes, a trifurcation gave 3 branches, very unequal as regards chromosomal rearrangements. One, very short, leads to Papioninae. Another, still poorly known, leads to Colobidae. The last branch leads to a further bifurcation, separating 2 groups of Cercopithecinae, with underwent the most active chromosomal evolution. A tentative to reconcile chromosomal, biochemical and morphological data is presented for Papioninae, for which chromosome study alone is not sufficient to construct a cladogram.

Animals↗

[Cytogenetics of Cercopithecus (mona) campbelli. Comparison with other cercopithecus species and man (author's transl)].

The karyotype of C. (mona) campbelli campbelli is described after applying various banding techniques. After comparing this karyotype with those of numerous other Cercopithecus species it becomes possible to situate C. (m.) c. campbelli in the phylogeny of the group. A comparison with the human karyotype, after high resolution banding, shows that both species differ by some forty rearrangements, essentially fissions and inversions. A fission of the chromosome homologous to the human no. 10 occurred in this taxon, thus reproducing a chromosome present in Prosimii and Lagomorpha (rabbit), which can be considered as a reverse mutation.

Animals↗

Chromosomal and enzymatic patterns provide evidence for two types of human colon cancers with abnormal nucleotide metabolism.

Correlated chromosomal and enzymatic studies are reported in a series of 13 human colon cancers. Two distinct chromosomal patterns are found: one with many losses, called monosomic type and another with many gains, called trisomic type. Chromosome 18, which carries the gene for thymidylate synthase (TS) is always missing in the monosomic type, in which TS activity is low. On the contrary, TS activity is high in the trisomic type on the average. The long arm of chromosome 17, which carries the gene for thymidine kinase (TK), is frequently duplicated in both monosomic and trisomic types, in which TK activities are high. It is found that most other deletions affect chromosomes carrying genes for enzymes of the de novo pathways whereas most other gains affect chromosomes carrying genes for enzymes of salvage pathways for synthesis of nucleotides. The importance of this finding is discussed.

Adenocarcinoma↗

Growth dependency of human colon cancer xenograft on organ environment is related with their original clinical stage.

The ability of cancer cells to metastasize might depend on their reduced dependency on the originating tissue. To test this hypothesis, 10 human colorectal carcinomas (CRC) were implanted either onto nude mouse caecum wall (orthotopic site), or into the subcutaneous tissue (ectopic site), and their growth in these sites compared. Prognostic factors were studied: Astler-Coller modified Dukes's stage, loss of chromosome 17p and/or 18q, and their TP53 gene. Early stage CRC [B2 (n = 3) and C1 (n = 1)] were found to grow 1.7 to 3.6 times (p < 0.05, p < 0.008 respectively) more rapidly in the caecum than in subcutaneous tissue. Metastatic stage CRC [C1 (n = 1), C2 (n = 2) or D (n = 3)] grew similarly in both sites, and more slowly than those of the first group. No relationship was found between growth rates, TP53 mutations or karyotypes. Growth rate of non metastatic cancers was slowed down by implantation in a foreign tissue whereas growth of metastatic tumours was similar in both sites, indicating that they do not recognize or need tissue growth factors.

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