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  • 1
    Electronic Resource
    Electronic Resource
    Genetic analysis of breast cancer progression (1996)
    Springer
    Journal of mammary gland biology and neoplasia 1 (1996), S. 139-151 
    Details
    ISSN: 1573-7039
    Keywords: Breast cancer ; tumor progression ; gene amplification ; loss of heterozygosity ; carcinomain situ ; translational applications
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract At the histological level, breast tumors display a variety of morphologic lesions which suggest the existence of an increasingly aberrant pathway of intermediate steps leading to the invasive primary tumor and its metastatic dissemination. In order to obtain direct evidence for this presumed progression, underlying genetic changes must be identified. Analyses of primary breast tumors have revealed a large number of dominant and recessive gene alterations encompassing several cellular attributes and activities. It is quite likely that some of these alterations are of a causal nature and thus enable the tumor to attain distinctive malignant phenotypes, such as, dysregulated proliferation, invasion, angiogenesis, and ability to metastasize. Considerable heterogeneity has been observed in the sequence of acquisition of these genetic changes, which is substantiated by recent comparative analyses between carefully microdissected preinvasive and invasive tumor. The data are evaluated here in the context of existing models of breast cancer progression. Implications and prospects for translational application to the clinic are also discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02013638
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  • 2
    Electronic Resource
    Electronic Resource
    The prognostic value of proliferation indices: a study with in vivo bromodeoxyuridine and Ki-67 (2000)
    Springer
    Breast cancer research and treatment 59 (2000), S. 113-123 
    Details
    ISSN: 1573-7217
    Keywords: breast cancer ; bromodeoxyuridine ; Ki-67 ; nodes ; survival ; S-phase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Proliferation indices are intended to help patients and clinicians make treatment decisions. We have previously demonstrated that a proliferation index based on in vivo labeling of S-phase cells with bromodeoxyuridine (BrdUrd) correlates with Ki-67 labeling index (LI). We now compare the prognostic value of these indices. With written consent, we gave 129 women with biopsy confirmed breast cancer 200 mg/M2 BrdUrd during 30 min immediately preceding surgery. We used IU-4 anti BrdUrd antibody to count the immunohistochemical labeling index (LI) of DNA-incorporated BrdUrd in 2,000 cells and MIB-1 to count Ki-67 (118 cases). Patients received standard surgical and adjuvant treatment. No patients were lost to follow-up and patients were followed a minimum of 2 (median 5.1) years. We compared survival and recurrence in tumors with high vs low labeling indices. We found that women in the low BrdUrd LI group had better disease free survival (92% vs 67% 5-yr DFS p = 0.001) and overall survival (94% vs 70% 5-yr OS, p = 0.0001) than those with a high LI. In comparison, a low Ki-67 index predicted better OS (87% vs 80% 5-yr OS, p = 0.020) and a trend for better DFS (84% vs 72% DFS p = 0.055). The apparent superiority of BrdUrd LI over Ki-67 LI is likely due to chance (p = 0.18). In multivariate survival analyses we found that BrdUrd LI proliferative index significantly improves prediction of DFS or OS even when node status, age or tumor size is in the model. We conclude that markers of proliferation are useful adjuncts in predicting patient prognosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006344010050
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  • 3
    Electronic Resource
    Electronic Resource
    The functional relationship between in vivo bromodeoxyuridine labeling index and Ki-67 proliferation index in human breast cancer (1998)
    Springer
    Breast cancer research and treatment 49 (1998), S. 155-164 
    Details
    ISSN: 1573-7217
    Keywords: breast cancer ; bromodeoxyuridine ; functional relationship ; human study ; in vivo ; Ki-67 ; prognosis ; proliferation markers
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Proliferation indices are used, along with other parameters, to estimate the risk of recurrence of breast cancer for individual patients. Because it is unlikely one index will be practical for all patients, it is important to understand the relationship between various indices of proliferation. For this reason, we compared a proliferation index based on in vivo labeling of S-phase tumor cells with the thymidine analog bromodeoxyuridine (BrdUrd), to a proliferation index based on an estimate of the growth fraction with the MIB-1 antibody to the Ki-67 antigen. With informed consent, we gave 145 patients 200 mg/m2 BrdUrd intravenously just prior to surgical removal of breast cancer. On histology sections, we visually counted S-phase cells which had incorporated BrdUrd using the Br-3 antibody which is specific to DNA-incorporated BrdUrd, and we counted cells in the growth fraction using the MIB-1 antibody to the Ki-67 antigen. We found that both indices were positively correlated with tumor size, number of positive nodes, and tumor grade, and both were negatively correlated with age and estrogen-progesterone receptor positivity. Using a linear functional relationship model, we found that the best (i.e. the maximal) fit between the two indices (correlation coefficient 0.79; p 〈 0.0001) occurred when each index was square root transformed, as is appropriate when counts follow a Poisson distribution. When we used the median as a cutpoint for each index, the classification of 19 percent of data pairs changed depending upon which index was used. We also estimated that the Ki-67 intercept (1.02 ± 0.25) was significantly greater than zero. We conclude that the BrdUrd index of DNA synthesis in S-phase correlates highly with the MIB-1 index of the growth fraction, and both indices correlate well with other parameters of tumor aggressiveness. Because this correlation is driven by concordance of the extremes of high and low counts, clinical comparison will be necessary to determine which is the better prognostic marker for human breast cancer.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1005926228093
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  • 4
    Electronic Resource
    Electronic Resource
    Molecular aspects of early stages of breast cancer progression (1993)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 53 (1993), S. 144-152 
    Details
    ISSN: 0730-2312
    Keywords: Immune surveillance ; loss of heterozygosity ; oncogene ; p53 ; tumor suppressor gene ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: It is clear that breast cancer progression is associated with inactivation of a number of different recessive oncogenes. The most widely evaluated tumor suppressor gene, p53, is mutated in approximately 30-50% of sporadic breast cancers. Mutations usually occur early in malignant progression. Loss of heterozygosity (LOH) studies have identified numerous chromosomal regions where other recessive oncogenes relevant to breast cancer may be located.Each LOH is seen in a varying proportion of breast cancers and may appear either early or late in progression. High-grade ductal carcinoma in situ (DCIS) and invasive carcinoma have similar genetic lesions, showing that aberrations can occur before invasive disease. Direct evidence that the same aberrations can be acquired later in progression comes from a study of multiple metastases from the same patient; other studies found that primary invasive cancers are characterized by marked intratumor heterogeneity for each lesion examined.The model we propose to account for these results hypothesizes that multiple genetic lesions can accomplish each phenotype required for malignancy (i.e., dysregulated proliferation, invasion, angiogenesis, etc.) and that, for a given tumor, at least one aberrant gene for each phenotypic change is stochastically selected. Biological heterogeneity of breast cancer results from the stochastic acquisition of various genetic aberrations. We further propose that the lymphocytic reaction in high-grade DCIS may select for aggressive tumor subpopulations capable of escaping immune surveillance. Another aspect of tumor heterogeneity may be the multiple mechanisms employed by various tumors to escape immune surveillance.
    Additional Material: 1 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240531128
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