HNF transfection with chondrosarcoma DNA results in the development of a sarcoma cell surface-associated epitope

Kumari, H.Lalitha; Shuler, Charles F.; Mannix, Daniel G.; Milo, George E.

doi:10.1016/0014-4800(90)90041-b

Cited by 2 publications

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“…Recently, we reported that one AIG positive premalignant cell line derived from a squamous cell carcinoma (SCC) (SCC-83-01-82) could be converted to a tumorigenic phenotype following treatment with methylmethane sulfonate (MMS) Milo et al, 1990). Similarly, treatment of AIG positive osteosarcoma and bladder carcinoma phenotypes with carcinogens led to the development of the tumorigenic phenotype (Kumari et al, 1989;Kumari et al, 1990). A tumorigenic phenotype is defined as a phenotype that in nude mice produces a progressively growing tumor -> 2.0 cm in diameter.…”

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Conversion of premalignant human cells to tumorigenic cells by methylmethane sulfonate and methylnitronitrosoguanidine

et al. 1992

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Nine human tumor cell lines derived from both epithelial and mesenchymal tumors exhibited either an anchorage-independent growth non-tumorigenic phenotype or an anchorage-independent tumorigenic phenotype. Transformed epithelial cell lines with the non-tumorigenic phenotype could be converted to a progressively growing tumor phenotype following treatment with either methylmethane sulfonate (MMS) or N-methyl-N'-nitro-N-nitro-soguanidine (MNNG). In contrast, sarcoma derived cell lines with a non-tumorigenic phenotype could be converted to a progressively growing tumor phenotype only with MNNG. SV40 immortalized HET-1A non-tumorigenic phenotype cells could be converted to a progressively growing tumorigenic phenotype, infrequently, when treated with MNNG, but not MMS. Progressively growing tumors produced by either MMS or MNNG treated non-tumorigenic phenotypes exhibited metastatic potential in nude mice. Chemically treated HET-1A cells acquired the ability to produce tumor in mice but the tumor did not exhibit metastatic potential. In contrast, populations of tumorigenic cells were not rendered more biologically aggressive after treatment with either MMS or MNNG; i.e., the latency period for tumor development was not accelerated and the tumors did not exhibit metastatic potential. These results suggest that the biological effects of MMS and MNNG on non-tumorigenic, tumorigenic and immortalized cell lines are phenotype specific.

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Conversion of premalignant human cells to tumorigenic cells by methylmethane sulfonate and methylnitronitrosoguanidine

et al. 1992

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“…The stages of progressive development of carcinogen-transformed cells are consistent with the concept of multistage development of cancer cells in vivo. We have shown (Milo et al, i987;Kumari et al, 1990) that carcinogen-induced changes in vitro result in the development of phenotypic characteristics in cells that are similar to some of the characteristics of cells derived from a human tumor. We have observed that cells treated in vitro will exhibit either the expression of a tumor-associated cell surface antigen, anchorage-independent growth, cellular invasiveness, or tumorigenicity.…”

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A conundrum in molecular toxicology: Molecular and biological changes during neoplastic transformation of human cells

et al. 1995

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The process of multistage carcinogenesis lends itself to the concept that the effects of carcinogens are mediated through dose-related, multi-hit, linear changes. Multiple in vitro model systems have been developed that are designed to examine the cellular changes associated with the progression of cells through the different stages in the process; however, these systems may have inherent limitations due to the cell lines used for these studies, the manner of assessing the effects of the carcinogens, and the subsequent growth and differentiation of the exposed cells. Each of these variables results in increasing levels of uncertainty relative to the correlation of the events with the actual process of human tumor development. Therefore, the prediction of the ultimate effect of any carcinogen is difficult. Moreover, relationships between individual biological endpoints resulting from carcinogen treatment appear at best to be approximations. The presence of an activated carcinogen inside the cell can give rise to multiple outcomes, only some of which may be critical events. For example, site-specific modification of the 12th and 13th codons of H-ras is different than that in the adjacent 14th and 15th codons. It is interesting to speculate what effect these differences might have on a biological outcome, e.g., transformation to anchorage-independent growth. The use of different model systems to examine the effects of activated carcinogens also creates additional problems. Comparisons of in vitro transformed cells with similar cells isolated from human tumors indicate that the culture environment appears to influence the expression of a particular phenotype, in that human tumor cells in culture express many of the same parameters as those found in cells transformed with carcinogens in vitro. If the process of transformation is linear, then less aggressive phenotypes should progress to a more aggressive transformed stage. However, in carcinogen-transformed human cells, the populations exhibit phenotypic diversity in that many of the transformed cells differentiate and fail to continue to divide in culture. Historically, we have assumed only a limited role for epigenetic modulation of molecular changes that occur during progression; however, our data suggest quite strongly that nonmalignant tumor populations can be converted to a more malignant phenotype without additional mutations taking place and, conversely, malignant populations can be downregulated to a nontumorigenic phenotype. Tumor cell plasticity is not only a fundamental characteristic of diverse types of human tumors, but also appears as an integral characteristic of carcinogen-transformed cells in vitro.

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HNF transfection with chondrosarcoma DNA results in the development of a sarcoma cell surface-associated epitope

Cited by 2 publications

References 20 publications

Conversion of premalignant human cells to tumorigenic cells by methylmethane sulfonate and methylnitronitrosoguanidine

Conversion of premalignant human cells to tumorigenic cells by methylmethane sulfonate and methylnitronitrosoguanidine

A conundrum in molecular toxicology: Molecular and biological changes during neoplastic transformation of human cells

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