1974
DOI: 10.1038/bjc.1974.115
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Non-random Chromosome Changes in Human Cancer

Abstract: Summary.-A malignant invasive fibrosarcoma in hamsters and a malignant mammary carcinoma in mice were each challenged with the broad spectrum proteinase inhibitor aprotinin (Trasylol). In both tumour systems, significant anti-tumour effects of aprotinin were observed. Variations in the site and dosage of aprotinin application were made in an attempt to improve the chemotherapeutic response.

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Cited by 10 publications
(4 citation statements)
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“…56 Each alteration, whether an initiating or a progression-associated event, may be mediated through a gross chromosomal change and therefore has the potential to be cytogenetically visible. Although the mechanisms whereby neoplastic cells become less genetically stable and develop specific, nonrandom chromosomal aberrations are poorly understood, it has been hypothesized that some neoplasia-producing mutations may inactivate a repair locus, as one of many pleotrophic effects, thus facilitating later numerical and structural karyotypic change^.^*-^^-^^ Conversely, another hypothesis is that the persistence of the carcinogen in the tumor or simply a nutritional insufficiency in the microenvironment might predispose aberrant cellular division.…”
Section: Discussionmentioning
confidence: 99%
“…56 Each alteration, whether an initiating or a progression-associated event, may be mediated through a gross chromosomal change and therefore has the potential to be cytogenetically visible. Although the mechanisms whereby neoplastic cells become less genetically stable and develop specific, nonrandom chromosomal aberrations are poorly understood, it has been hypothesized that some neoplasia-producing mutations may inactivate a repair locus, as one of many pleotrophic effects, thus facilitating later numerical and structural karyotypic change^.^*-^^-^^ Conversely, another hypothesis is that the persistence of the carcinogen in the tumor or simply a nutritional insufficiency in the microenvironment might predispose aberrant cellular division.…”
Section: Discussionmentioning
confidence: 99%
“…The clonal evolution of kar yotype is in keeping with the prominent chromosome instability typical of malignant cells. Most tumours appear to evolve by non-random losses and/or gains of particu lar homologues, groups or markers [Miles, 1974] . Indeed in animal experiments the appearance of certain markers has been linked to oncogenic causative agents [DiPaolo, 1977],…”
Section: Discussionmentioning
confidence: 99%
“…This interpretation can be made from the karyotypic analysis of a number of human tumor cell lines determined by polymorphic enzyme analysis to be a contamination group Whether the demonstration of a few identical marker chromosomes in two or more cell lines carries sufficient weight to declare them as cross-contaminated has become more problematical as a consequence of recent karyotypic studies of human tumors and tumor cell lines with chromosome banding techniques. These studies have shown that specific translocations and other karyotypic modifications involving a nonrandom selection of chromosomes occur frequently and can be correlated with specific types of cancer (63)(64)(65)(66)(67)(68)(69)(70). Therefore, tumor cell lines derived from tumors of different patients with certain types of cancer could be expected, in some cases, to have certain similar marker chromosomes.…”
Section: Constancy Of Phenotypes Shown Inmentioning
confidence: 99%