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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Histochemistry and cell biology 42 (1974), S. 345-349 
    ISSN: 1432-119X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The usual Carnoy fixative (acetic acid: methanol, 1:3) for metaphase preparations removes most histone as well as other nuclear proteins from rat and mouse embryo fibroblasts. Acrylamide gel electrophoresis patterns of fixatives from treated cells and the residual cell pellets show that significant amounts of histones are extracted into the Carnoy fixative. In contrast, formalin treatment fixes histones in the cells and renders them unextractable by the usual procedures. Autoradiographic studies with H3-lysine-labeled cells and electrophoretic analysis of cell extracts and fixative confirm these findings. The demonstration of typical quinacrine and trypsin-G-banding patterns with cells from both fixation procedures suggeststhat chromosomal banding patterns are independent of either the presence or absence of basic histone proteins.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary In an infant with gonadal dysgenesis and somatic anomalies, the internal and external genitalia were female but the gonads contained tubular structures suggesting male differentiation. The karyotype was 46,XY with no evidence of structural aberration or mosaicism. Hormonal metabolism and H-Y antigen expression were assayed in cultured gonadal cells. Although unable to synthesize testosterone, the cultured cells were able to convert it to dihydrotestosterone. H-Y antigen was present, perhaps at a level lower than that in cells from normal XY males. Our observations indicate that a modicum of testicular organogenesis may precede the involution that results in a streak gonad in some cases of gonadal dysgenesis.
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  • 3
    ISSN: 1573-7217
    Keywords: bilateral breast cancer ; genetic predisposition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Our purpose was to determine whether bilateral breast cancer depends upon genetic predisposition to multiple tumors or, alternatively, represents two independent sporadic events. Biological concordance of hormone receptors and histopathology in bilateral tumors, family history of breast cancer, age at diagnosis, and survival were evaluated in 88 patients. The immunoreactivity of paired tumors from 51 patients to six different immunocytochemical markers was compared. Neither histologic patterns nor immunocytochemical reactions showed concordance between bilateral tumors. Absence of concordance (other than for estrogen receptors) and lack of associations with positive family history and early age of onset support an interpretation of independent tumor origins and does not suggest a major role for genetic determinants in the majority of cases of bilateral breast cancer.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Cancer and metastasis reviews 2 (1983), S. 257-293 
    ISSN: 1573-7233
    Keywords: chromosome ; progression ; instability ; rearrangement ; amplification ; specificity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Karyotypic progression may be viewed in at least two ways. One approach seeks evidence for increasing and progressive deviation from the normal chromosome pattern in tumors. The clearest examples, found in some leukemias, are those in which successive karyotypic changes are superimposed on an already aberrant cell population. Evidence of chromosomal progression within solid tumors is far less frequent, possibly because the tumors themselves are at a relatively late stage in their evolution. An alternative approach, therefore, attempts to correlate the extent of karyotypic deviation with other aspects of tumor progression. Recent data, based on classical cytogenetic analyses and flow cytometry, are presented to determine relationships between karyotype and specific origin and morphology of tumors. The predominant theme which emerges, not surprisingly, is that the more deviant chromosome patterns are associated with other measures of increased biologic malignancy. What is surprising is the degree to which these properties are expressed in primary tumors and the relative lack of evidence for further karyotypic evolution with recurrence or metastasis. Examples of genetic instability, evolution through polyploidy, gene amplification, and selection for specific chromosomal rearrangement are found in populations of premalignant and malignant human cells. There is increasing recognition of the importance of tumor-specific chromosome aberrations in the stepwise progression from the normal to the fully neoplastic cell.
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  • 5
    ISSN: 1573-7217
    Keywords: INT2 ; ERBB2 ; amplification ; expression ; breast cancer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The relationships of INT2 and ERBB2 amplification and of ERBB2 overexpression in primary breast tumors to prognostic factors, recurrence, and survival have generated considerable controversy. The rationale for this study is that long-term, recurrence-free survival is a more direct criterion for testing the validity of a tumor marker than correlation either with prognostic factors or with short-term recurrence and survival. We examined the association of recurrence with INT2 and ERBB2 amplification and ERBB2 expression by comparing primary breast tumors from patients surviving without recurrence for ≥ 8.5 years after diagnosis. the LTS group, to tumors from patients recurring within two years, the RR group. The RR (N = 63) and LTS (N = 61) samples were coded and examined for amplification by Southern blotting and for expression by immunohistochemistry. Comparison between the RR and LTS groups demonstrated that INT2 amplification was associated with a significantly (P = 0.018) higher (5.6-fold) risk of recurrence, an association that remained significant after controlling for lymph node (LN), tumor size (TS), and histograde (HG) status. ERBB2 amplification and expression were not associated with a higher recurrence risk. Survival analyses within the RR group, however, demonstrated significantly shorter survival time among cases with than without ERBB2 amplification (P = 0.018, median survival 16 vs 25 months), or ERBB2 expression (P = 0.019, median survival 15 vs 25 months), but not INT2 amplification. Univariate Cox proportional hazards regression models also demonstrated significantly shorter survival among cases with ERBB2 amplification (P = 0.016) or expression (P = 0.049), that remained significant in multivariate analyses (P = 0.022) for ERBB2 amplification. These results indicate a significant positive association between INT2 amplification and risk for tumor recurrence in the RR as compared to the LTS group. The relationship of ERBB2 amplification or overexpression to patient outcome is more complex. ERBB2 amplification and expression have a significant relationship with shorter survival among patients recurrent within two years, but their occurrence in tumors from women surviving without recurrence for ≥ 8.5 years suggests that ERBB2 status is not predictive of shorter survival for all breast cancers.
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  • 6
    ISSN: 1573-7217
    Keywords: xenograft model ; preneoplasia ; MCF10AT
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A workshop on the ‘Research potential of a unique xenograft model of human proliferative breast disease’ was held at the Karmanos Cancer Institute, Wayne State University, Detroit, Michigan, in November of 1998. The accumulated information and current experimental findings on the MCF10AT model of preneoplastic, proliferative breast disease were reviewed. Discussions focused on the relevance of the model to clinical breast cancer and on the most profitable lines of further research to strengthen its utility.
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 30 (1985), S. 134S 
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Conclusions Examination of a relatively small subset of information pertaining to colon tumors indicates that examples in each category (including predisposing markers of chromosomal instability, causally relevant markers, correlation between karyotypic atypia and biological malignancy, and some tumors with no detectable chromosome changes) can all be found. This discussion began with questions about the purposes that markers could serve: some of those questions with reference to colon tumors can be answered. For the most part, the presence of chromosomal aberrations can indeed distinguish between the normal and the tumor cell and, in this sense, help to define the tumor. Moreover, some specific chromosomal alterations appear to be preferentially associated with colon tumors. If the specificity can be better defined, then, like the other specific tumor-chromosome associations, those in colonic mucosa may help to identify and localize gene functions important in the growth, development, or regulation of this specialized tissue. In any event, chromosomal aberrations are of value, not only in confirming the diagnosis, but also by their associations with different behavioral patterns in both malignant and premalignant lesions. Their definition, therefore, may have predictive value for the individual patient. In particular, inability to find such alterations, while it is not evidence of a nontumorous state, in a known malignancy may at least contribute some information about the biology of that particular tumor. The second question was whether markers could be of value in identifying stages in the evolution from a normal to a tumor cell. From the work done thus far on chromosomal instability, it appears likely, when more data are accumulated and the appropriate tests can be standardized, that proof of chromosomal instability may indeed constitute a marker for certain specific tumor-predisposing states. Similarly, the oncogenes, whose normal genomic counterparts are clearly responsible for important functions relating to cell growth and regulation, may prove to be markers for only a limited number of tumors. However, their definition and the resultant contributions to understanding the basic cellular biology of normal and tumor cells should make it possible to identify some of the critical steps that are altered in the multiple pathways leading to tumor.
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