PubMed · 3127797
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R A Roa, T E Carey. 1988. DNA flow cytometry.. https://doi.org/10.1177/019459988809800324
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The DNA content of 30 malignant tumors and their metastases were compared. The DNA indices of tumors (expressed by the mean DNA content of G0.1-phase tumor cells and leukocytes) differ from each other, but in metastases they are almost the same with the values of primary tumors. It can also be observed, if a tumor consisted of more than one subpopulation of tumor cells, the metastatic potential of clones can be different. However, there is no significant relationship between the degree of ploidy and the occurrence of metastasis. The stability of DNA index in tumors and their metastases were used to distinguish two primary tumors even if their histological patterns were very similar. We present an example of the above mentioned phenomena in which the results of DNA analysis is supported by the results of mucin histochemistry and the follow up data.
BACKGROUND: Given the variable natural history of prostate cancer, prognostic parameters are needed to help guide treatment decisions in individual patients. In some series, analysis of DNA ploidy has correlated well with prognosis. This review was performed to determine whether flow cytometry could be used to help guide treatment decisions in patients with localized carcinoma of the prostate. METHODS: Two hundred consecutive patients were observed for a minimum of 10 years after radical prostatectomy. Follow-up information was incomplete in 14 patients, leaving 186 for analysis. Clinically, there were 72% Stage B tumors and 28% Stage A. RESULTS: Sixty percent of patients were alive with a minimum of 10 years of follow-up, and 47% apparently were tumor free. Twenty-two percent died of carcinoma of the prostate and 18% of other causes. The median time until death from prostate cancer was 6.5 years. Seventy-four percent of tumors were diploid on flow cytometry. Fifty-three percent of patients with diploid tumors survived 10 years without recurrence, whereas 20% died of carcinoma of the prostate. Aneuploid tumors were identified in 16% of the total group; 47% of these patients were alive at 10 years, whereas 24% had died of prostate cancer. CONCLUSIONS: Aneuploid tumors have a worse overall prognosis than diploid lesions. However, the correlation is not strong enough to allow treatment decisions on an individual patient basis. Analysis of DNA ploidy was no more accurate than Gleason histologic grading.
Deregulated c-myc expression, as a consequence of translocation of the c-myc gene to one of the immunoglobulin loci, appears to play an important role in the pathogenesis of several B-cell tumors, including Burkitt's lymphoma, mouse plasmacytoma and rat immunocytoma. This study investigated the expression of c-myc and 2 other members of the myc gene family, L- and N-myc, at the mRNA and protein level, and analyzed for possible rearrangements of these genes in the human counterpart to the mouse plasmacytoma--multiple myeloma (MM). Nine well-characterized MM cell lines were examined by using Northern- and Southern-blot analysis and immunoprecipitation. The c-myc gene was found to be highly expressed in most MM cell lines. The level of expression was comparable to that observed in the COLO 320 and HL-60 cell lines, carrying amplified c-myc genes, and to that of B-cell lines with a higher proliferative activity than the MM cell lines. In the U-266 MM cell line, L-myc, but no c-myc mRNA or protein, was found. The L-myc gene was expressed in both early- and late-passage U-266 cells, suggesting that the L-myc expression was not the result of the in vitro cultivation. N-myc was not expressed in any of the MM cell lines. No rearrangements of c-myc or L-myc genes were found. We thus conclude that (a) in contrast to the corresponding mouse and rat B-cell tumors, c-myc is not frequently rearranged in MM; (b) c-myc is highly expressed in most MM lines; and (c) L-myc but not c-myc is expressed in the U-266 MM cell line.