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  • 1
    Call number: QZ200:527(11)
    Keywords: Neoplasms
    Notes: For online access to this volume please contact the library staff in room D124 (phone 3661, e-mail: http://www.dkfz.de/de/zbib/mitarbeiter/kontakt/fernleihe.php)
    Pages: xli, 2390 p. : ill.
    Edition: 11th ed.
    ISBN: 9781496394637
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  • 2
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    Philadelphia : Wolters Kluwer/Lippincott Williams & Wilkins Health
    Call number: QZ200:528/1
    Keywords: Neoplasms
    Notes: Chapters in this book were originally publ.in "The Cancer Journal: The Journal of Principles & practice of Oncology", Vol. 15.
    Pages: xx, 427 p. : ill.
    ISBN: 9781451103144
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  • 3
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    Philadelphia : Wolters Kluwer/Lippincott Williams & Wilkins Health
    Call number: QZ200:528/2
    Keywords: Neoplasms
    Notes: Chapters in this book were originally publ.in "The Cancer Journal: The Journal of Principles & practice of Oncology", Vol. 16.
    Pages: xx, 556 p. : ill.
    ISBN: 9781451142693
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  • 4
    Call number: QZ200:529(2) ; F065:34
    Keywords: Neoplasms / etiology ; Molecular Biology / methods ; Neoplasms / genetics ; Neoplasms / physiopathology
    Notes: For online access to this volume please contact the library staff in room D124 (phone 3661, e-mail: http://www.dkfz.de/de/zbib/mitarbeiter/kontakt/fernleihe.php
    Pages: xiv, 519 p. : ill.
    Edition: 2nd. ed.
    ISBN: 9781496310637
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    F065:34 departmental collection or stack – please contact the library
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  • 5
    ISSN: 1534-4681
    Keywords: Idoxuridine ; Radiation sensitizers ; Soft tissue sarcomas ; Radiotherapy ; Surgery
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background: Local control remains an important issue in the management of large soft tissue sarcomas. Radiation is the main adjuvant to surgery for local therapy of sarcomas, but it requires relatively high doses, hitherto considered prohibitive in areas such as the retroperitoneum. We developed a preoperative treatment approach to large soft tissue sarcomas that would deliver a high total dose of radiation administered in conjunction with the halogenated pyrimidine radiosensitizer idoxuridine (IdUrd). Methods: Thirty-seven patients with large sarcomas of the head and neck, mediastinum, retroperitoneum, or extremity received three or five cycles of sequential IdUrd infusion (1000–1600 mg/m2/d×5 d) alternating weekly with twice daily radiation (125–150 cGy per dose) and were then evaluated for resection. The delivered preoperative radiation dose was up to 6250 to 7500 cGy. Results: Five patients (14%) had a partial response to preoperative therapy, and 28 of 37 patients underwent successful resection. There were no intra- or postoperative deaths. Local control was achieved in 19 of 28 resected patients, but in only 1 of 6 patients who remained unresectable despite therapy. With a median follow-up of 5.8 years, 28% of patients are alive with no evidence of disease, 17% are alive with disease, and 53% have died of their disease. Conclusions: Using the dose and schedule we employed, resection of large soft tissue sarcomas was possible after high-dose radiation delivered in conjunction with IdUrd. Although local control was acceptable, the high rate of distant failure represents a limitation of any local approach to the treatment of large soft tissue sarcomas and suggests the need for integration of this approach with an effective systemic therapy.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0843
    Keywords: Key words Fluorodeoxyuridine ; Double-strand break ; Cell cycle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The relationship between cell cycle progression and induction of DNA double-strand breaks and cytotoxicity by exposure to fluorodeoxyuridine (FdUrd) was studied in HT29 human colon cancer cells. Fractionation of drug-treated populations by centrifugal elutriation yielded subpopulations having widely divergent abilities to progress through S phase in the presence of the drug. One of these subpopulations, which appeared to undergo coordinated growth arrest, was resistant to FdUrd cytotoxicity and DNA damage. In contrast, the subpopulation which was able to progress furthest through S phase in the presence of FdUrd underwent unbalanced growth arrest (i.e., increase in size and mass out of proportion to DNA synthesis), and displayed both DNA double-strand break formation (assayed by pulsed field gel electrophoresis) and loss of clonogenicity. When cells were elutriated prior to drug treatment, producing fractions enriched in cells at various cell cycle stages, no significant differences in sensitivity to FdUrd-induced cytotoxicity were detected among elutriation fractions. These findings support the model that, in HT29 cells, progression into and through S phase during drug treatment is an important determinant of FdUrd-induced DNA damage and cytotoxicity, but that the cell cycle position at the start of drug exposure is not a critical factor for these effects.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-0843
    Keywords: Key words Gemcitabine (dFdCyd) ; Mitomycin-C (MMC) ; Colorectal cancer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Both gemcitabine (2′,2′-difluorodeoxycytidine; dFdCyd) and mitomycin-C (MMC) are active against several solid malignancies. dFdCyd is an attractive agent for use in combination with drugs which damage DNA and with radiation therapy because of its ability to inhibit DNA replication and repair as well as its radiosensitizing effect. We hypothesized that the repair of MMC adducts in DNA might be inhibited by dFdCyd leading to a synergistic effect. To test this possibility, we studied the effect of combining dFdCyd and MMC in HT29 human colon carcinoma cells in vitro. The cells were exposed to a variety of drug concentration ratios and schedules, then assessed for clonogenic survival. D50 values (drug concentration at which clonogenicity is inhibited by 50%) were calculated, and the interactive effects of the two drugs were evaluated using median effect analysis. In this approach, if the calculated combination index (CI) is <1, 1, or >1, it indicates synergism, additivity, or antagonism, respectively (Chou and Talalay 1984). We found that marked synergy (CI of 0.5–0.7) was produced by concurrent exposure to mitomycin and gemcitabine. In contrast, sequential treatment led only to additivity. These findings suggest that, when combined in an appropriate schedule, the chemosensitizing effect of gemcitabine may be beneficial in the treatment of malignancies which are sensitive to MMC.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-0843
    Keywords: Key words Apoptosis ; Gemcitabine ; p53 ; Radio-sensitization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Purpose: We compared the cytotoxic and radiosensitizing effects of gemcitabine (2′,2′-difluoro-2′-deoxycytidine, dFdCyd), a clinically valuable radiosensitizer, in colon cancer RKO cells which differed in their p53 status. The parental RKO cells, RKO-P, contain wild-type p53 protein. In RKO-E6 cells, the p53 function has been disrupted by transfection of the cells with the human papillomavirus type-16 E6 gene. Results: We found that the RKO-P cells were significantly more sensitive to dFdCyd-mediated cytotoxicity and apoptosis than RKO-E6 cells (IC10 39.3 ± 5.3 nM and 62.0 ± 6.9 nM, respectively). The cytotoxic effect of dFdCyd in RKO-P cells was accompanied by induction of the proapoptotic protein Bax at the time when p53 was induced. In contrast, similar treatment of RKO-E6 cells with dFdCyd resulted in only limited expression of Bax, suggesting that the cytotoxic effect of dFdCyd was mediated, in part, by a p53-dependent apoptosis pathway. We also studied the effect of dFdCyd on radiation sensitivity. We found that at minimally cytotoxic concentrations dFdCyd failed to radiosensitize either RKO-P or RKO-E6 cells, whereas at cytotoxic concentrations equal sensitization was produced. Finally, we assessed the influence of dFdCyd on cell cycle distribution. We found that dFdCyd synchronized RKO-P cells, whereas synchrony was not produced in p53-disrupted RKO-E6 cells. Conclusion: These results suggest that p53 status may influence dFdCyd-mediated apoptosis, cytotoxicity, and cell cycle progression but do not support an important role for p53 in radiosensitization.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1573-0646
    Keywords: gemcitabine ; radiosensitization ; human tumor cells ; chemotherapy ; radiation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Gemcitabine is a nucleoside analogue with excellent clinical activity against solid tumors. Within the cell, gemcitabine is rapidly phosphorylated to its active di-and triphosphate metabolites. Cytotoxicity with gemcitabine appears to be related to multiple effects on DNA replication, where gemcitabine triphosphate can serve as both an inhibitor and substrate for DNA synthesis. Gemcitabine diphosphate inhibits ribonucleotide reductase, producing decreases in cellular dNTP pool levels in a cell-specific manner. These two major characteristics of gemcitabine, reduction in cellular dNTP pools and incorporation into DNA, are features of other antimetabolites antitumor agents which also exhibit radiosensitizing properties. Based on these favorable metabolic characteristics and the clinical activity of gemcitabine in tumor types which are commonly treated with radiation, the ability of gemcitabine to enhance X-radiation induced cytotoxicity was evaluated. Gemcitabine has been shown to be a potent radiosensitizer in a variety of tumor cell lines, including HT-29 colorectal carcinoma, pancreatic cancer, breast, non-small cell lung and head and neck cancer cell lines. Gemcitabine was most effective as a radiosensitizer when administered at least 2 hours prior to irradiation. For most cell lines, radiosensitization was evident at non-cytotoxic concentrations. The extent of radiosensitization increased with both increasing gemcitabine concentration and duration of exposure. Radiosensitization did not require redistribution of cells into a more radiosensitive phase of the cell cycle. The major metabolic effects observed under radiosensitizing conditions were the accumulation of high levels of gemcitabine triphosphate, and a selective decrease in the cellular dATP pool. The pattern of dATP decrease paralleled the increase in radiosensitization, whereas the level of gemcitabine triphosphate was not associated with the enhanced sensitivity to radiation. Compared to other radiosensitizers, the advantage of gemcitabine is that is can induce radiosensitization at concentrations that are 1000 times lower than typical plasma levels obtained with this drug. These studies will be used as guidelines for developing clinical trials of gemcitabine with radiation.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 272 (1978), S. 501-506 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Rat ovarian granulosa cells and mouse myocardial cells respond to cell-specific hormones by cyclic AMP-dependent mechanisms. In coculture, these heterologous cells communicate by means of gap junctions. Exposure of the cocultures to a hormone specific for one cell type causes the heterologous cells ...
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