Biomedical subjects
Publications and source records attributed to J Limon.
Cytogenetic studies on primary hemangiopericytoma tumor cells from a 28 year old woman showed a single karyotypic change: t(13;22)(q22;q11). The relationship of this aberration to previously described abnormalities of chromosome #22 in other solid tumors is discussed.
Detailed chromosome studies, briefly reported previously, from short-term cultures of tumor cells from myxoid liposarcomas are reported. A common reciprocal translocation, t(12;16)(q13;p11), was found in three cases and a complex t(1;12;16)(p11;q13;p11) in the fourth one. This nonrandom primary change, not described before in solid tumors, could characterize the myxoid form of liposarcoma. The involvement of a closely located breakpoint on chromosome #12 in a reciprocal t(3;12)(q28;q14) described in a lipoma in the previous article of this series, suggests a common basis in the biological process of proliferation of tumors sharing a common histogenesis.
A method has been elaborated for obtaining chromosome preparations from different histologic types of human solid tumors and applied to 60 cases. Such tumors were mechanically dispersed, washed by settling and transferred into flasks containing collagenase (200 U/ml) in the growth medium. Tumor pieces were dissociated in enzyme for 16 hours to 6 days, depending on tumor consistency. The majority of the tumors (80%) required 16-24 hours of such treatment. After disaggregation, the suspension of cells was washed by settling and then centrifuged. Cells were cultured for 24 hours to 6 days (85% of tumors), treated with a hypotonic solution in situ and then fixed. Of the 60 tumors, 37 (60%) displayed a sufficient number of metaphases for banding analysis. The success rate depends primarily on the type of tumor: 70% for soft tissue sarcomas, 40% for bladder carcinomas, and 40% for renal adenocarcinomas. This procedure is gentle, requires no special equipment and is applicable for the study of the full spectrum of human solid tumors.
Two histologically benign adipose tumors were found to have clonal karyotypic changes. Del(4), del(6), and inv(13) were present in a fibrolipoma, and t(7;8) in a lipoblastoma. Additional studies are needed of the frequency and malignant potential of lipomas with cytogenetic abnormalities.
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Cytogenetic analysis of two poorly differentiated sarcomas revealed clonal chromosomal rearrangements involving several autosomes and the X chromosome. Both tumors displayed a common abnormality, t(X;18)(q13;p11). This finding is discussed in relation to published X/autosomes translocations in solid tumors.
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Cytogenetic analysis of a primary leiomyosarcoma of the prostate revealed a clonal chromosomal rearrangement involving chromosomes #2, #3, #9, #11, and #19. The results are discussed in relation to the cytogenetic findings in other solid tumors, especially those of the prostate and leiomyosarcoma at other sites.
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The cytogenetic analysis of transplantable in vivo melanotic and amelanotic lines of mouse B16 melanoma was performed. The second line arose by spontaneous alteration of the first one and these lines are the same in the rate of malignant growth during passages in vivo. The melanotic line shows stable near-diploid karyotype with modal chromosome number 41. The amelanotic line is mostly hypotetraploid karyotype with modal chromosome number 76. The balance of the diploids in the melanotic line is disturbed by the fact that chromosome 15 is partially trisomic, chromosome 6 trisomic, and chromosome 13 and X monosomic. Four marker chromosomes were common to both lines: M1-rob(12;12), M2-rob(5;15), M3-minute, M4-inv(1), M5-del-(14q-), but in the amelanotic line in most cases their number was doubled. Additionally, in the amelanotic line other specific aberrations rob(6;6) and rob(16;16) were observed. Both lines had comparable SCE frequencies. Constitutive heterochromatin in amelanotic line revealed the nonrandom deletion of the heterochromatic segments in chromosome 11 and, occasionally in chromosome 19.
The simultaneous presence of chromosome segments with and without sister chromatid differentiation (SCD) in the same metaphase was observed in a human melanoma cell line after BrdU incorporation for 48-72 hr. This phenomenon was related to the time of BrdU incorporation by the cells: i.e., it was not observed after exposure to BrdU for only 17-20 hr. It is proposed, therefore, that the unusual staining pattern is caused through reduced BrdU incorporation by the cells after completing the first division.
Two differently stained regions of lateral asymmetry were observed in the long arm of the human Y chromosome, following FPG staining. The first asymmetry was confined to band q12 of the long arm. The second asymmetrically stained region was located at the junction between bands q11 and q12. In the non-fluorescent Y chromosomes only one region of lateral asymmetry was found at the end of the long arm and its staining properties were similar to the region situated at the junction between q11 and q12 bands in the fluorescent Ys. The two morphologically distinguishable regions of lateral asymmetry are presumed to indicate sites containing different satellite DNAs in the human Y chromosome.
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Isolabeling segments were found in the distal region of the long arm of Y chromosomes derived from human leukocytes grown through two replication cycles in medium containing BrdU and stained by the FPG technique. Three main types of Y chromosome staining patterns were demonstrated: I-Y chromosome with typical SCD, II-Y chromosome with weakly stained distal regions of long arms (isolabeling segments), III-Y chromosome with both terminal regions displaying SCD interrupted by one isolabeled segment. The existence of different types of Y chromosome staining patterns was explained on the basis of the previously described hypothesis of unequal distribution of thymine residues between two DNA polynucleotide chains in the distal part of the long arms of human Y chromosomes.
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Cytofluorimetric measurements of the DNA content in transplantable melanotic and amelanotic tumor cells were carried out. The mean content DNA is higher in the amelanotic cells. The DNA distribution patterns are different in both tumors: there is a distinct stem line of the cells in the melanotic tumors whereas in the amelanotic cells there is a great variability in the DNA content and the stem line of the cells is absent. The correlation between these findings and some biological properties of the melanotic and amelanotic tumors are discussed.