By G. Barry Pierce (auth.), Stewart Sell (eds.)
Developmental melanoma items (oncodevelopmental markers, ODM) not just function diagnostic and prognostic signs but in addition can be used to review the character of the carcinogenic technique and the biology of tumors. for a few years oncologists have sought for markers of melanoma cells that will let unequivocal acceptance of melanoma unlike noncancerous tissue. The earliest and nonetheless most generally used approach to identity of melanoma tissue or cells is the structural resemblance of melanoma tissue to fetal or immature tissue. Pathologists not just realize melanoma by way of its morphologic similarity to fetal tissues, but in addition generally can relate the habit of a given tumor to the measure of tissue differentiation. hence, poorly differentiated tumors that resemble fetal tissue ordinarily develop extra swiftly and metastasize ahead of do well-differentiated tumors that extra heavily resemble grownup tissue. in recent times the commonality of fetal and melanoma tissue has been prolonged to items of tumor cells that, could be analyzed by way of biochemical, immunological, or physiological thoughts. Increas ingly, items of melanoma cells just like fetal items are being pointed out and studied. those items variety from cell-surface markers (fetal or differentiation antigens), placental proteins, hormones, and isoenzymes to a large number of goods, akin to carcinoembryonic antigen (CEA), alphafetoprotein (AFP), lymphocyte markers, and nucleic acids, equivalent to tRNA, which are produced in small quantities by way of v vi PREFACE always differentiating cells within the grownup yet in a lot higher quantities through tumors.
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Extra info for Cancer Markers: Diagnostic and Developmental Significance
6. ORIGIN OF TERATOCARCINOMA It has not been a simple matter to elucidate the origin of embryonal carcinoma because there is not a single progenitor cell type for testicular, ovarian, or experimentally produced tumors. Stevens has indicated the cell of origin for each of these tumors and in each situation the origin has now been confirmed. 1. ORIGIN OF SPONTANEOUS TESTICULAR TERATOCARCINOMAS Stevens (1964) plotted the incidence of tumors versus age in strain-129 animals and by extrapolation came to the conclusion that something happened within the testicular tubules on or about the 12th day of gestation that decided whether or not teratocarcinoma would develop.
Similar results have been demonstrated by Boccara and Kelly (1978). , 1977) when compared to lines of differentiated cells isolated from the teratocarcinoma. To determine whether the block to virus infection was due to the inability of the stem cells to uncoat the virus, the infectious component I DNA of SV40 was utilized for infection. Again, the stem cells were refractory to infection with the viral DNA; however, the differentiated cells were infected. In considering the mechanism of block to S V40 and polyoma infection, interferon was considered since SV 40 is known to be sensitive to this cell product.
In view of Stevens' (1962) demonstration of the multifocal 28 G. BARRY PIERCE nature of small teratocarcinomas, it is most probable that the environment is highly selective for clones of tumor cells best able to survive under the conditions. Thus, a single cell type displaying one isoenzymic marker might be expected to survive from this type of selection. We selected teratocarcinomas for their fastest-growing elements by ascites conversion. Invariably, the 402 AVI strain of teratocarcinoma (Pierce and Dixon, 1959b) or the Fekete ovarian teratocarcinoma (Pierce et at, 1960b) underwent simplification of structure until only parietal yolk sac carcinoma remained.