By George F. Vande Woude (ed.), George Klein (ed.)
Quantity sixty one of "Advances in melanoma study" comprises insurance of the next: molecular ways to melanoma treatment, radiation resistance, melanoma prevention study trials, mammalian gene amplification, retinoblastoma gene functionality, molecular genetic foundation of breast melanoma, and tumour promoting through okadaic acid category compounds.
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Extra info for Advances in Cancer Research, Vol. 61
1990). C. CYTOCENETIC STUDIES By studying chromosomal (cytogenetic) alterations in breast carcinomas, important starting points can be obtained for further, more detailed analysis involving the cloning of genes. , 1988). For most solid tumors, including breast carcinomas, it is difficult to obtain direct chromosome preparations of sufficient quality for a detailed chromosome analysis; it is also difficult to maintain breast carcinoma cells in tissue culture. As a result, a full analysis of all chromosomes has been obtained only for a limited number of breast cancers.
An example of a DCIS overexpressing neu protein is shown in Fig. 2. Sometimes a large-cell DCIS reaches the surface epithelium of the nipple; this is known as Paget’s disease. , 1989). In large-cell DCIS, the tumor cells show frequent mitoses and have marked nuclear atypia. T h e lesions are usually large (several centimeters); since most patients are treated shortly after detection of their DCIS by excision, the normal biologic behavior is not known with certainty. Ductal carcinoma in situ consisting of small cells usually has a cribriform or micropapillary growth pattern.
T h e region deleted includes the p53 gene. , 1989). , 1991). In the various tumor types studied, these point mutations are usually found in exons 5 , 6 , 7 , and 8 and result in amino acid substitutions of residues that are highly conserved during 42 MARC J. VAN DE VIJVER evolution. , 1991). Four different changes in p53 gene configuration may be present in a breast carcinoma: (a) one wild-type allele, one deleted or inactivated allele; (6) both alleles deleted or inactivated; (c) one wild-type allele, one mutated allele; (d) one allele deleted or inactivated, one mutated allele.