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Titolo:
Methylxanthine sensitization of human colon cancer cells to Re-186-labeledmonoclonal antibody
Autore:
Kinuya, S; Yokoyama, K; Kudo, M; Kasahara, Y; Kobayashi, K; Motoishi, S; Onoma, K; Bunko, H; Michigishi, T; Tonami, N;
Indirizzi:
Kanazawa Univ, Sch Med, Dept Nucl Med, Kanazawa, Ishikawa 9208640, Japan Kanazawa Univ Kanazawa Ishikawa Japan 9208640 wa, Ishikawa 9208640, Japan Kanazawa Univ, Sch Med, Dept Pediat, Kanazawa, Ishikawa 9208640, Japan Kanazawa Univ Kanazawa Ishikawa Japan 9208640 wa, Ishikawa 9208640, Japan Kanazawa Univ Hosp, Kanazawa, Ishikawa, Japan Kanazawa Univ Hosp KanazawaIshikawa Japan sp, Kanazawa, Ishikawa, Japan Japan Atom Energy Res Inst, Dept Res Reactor, Radioisotope Lab, Tokai, Ibaraki 31911, Japan Japan Atom Energy Res Inst Tokai Ibaraki Japan 31911 Ibaraki 31911, Japan
Titolo Testata:
JOURNAL OF NUCLEAR MEDICINE
fascicolo: 4, volume: 42, anno: 2001,
pagine: 596 - 600
SICI:
0161-5505(200104)42:4<596:MSOHCC>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
WILD-TYPE P53; GAMMA-RADIATION; INDUCED APOPTOSIS; G(2) DELAY; DNA DAMAGE; CAFFEINE; CYCLE; RADIOIMMUNOTHERAPY; RADIOSENSITIVITY; LINES;
Keywords:
radiosensitization; methylxanthine; Re-186; beta-irradiation; cell cycle;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
37
Recensione:
Indirizzi per estratti:
Indirizzo: Kinuya, S Kanazawa Univ, Sch Med, Dept Nucl Med, 13-1 Takara Machi, Kanazawa, Ishikawa 9208640, Japan Kanazawa Univ 13-1 Takara Machi Kanazawa Ishikawa Japan 9208640
Citazione:
S. Kinuya et al., "Methylxanthine sensitization of human colon cancer cells to Re-186-labeledmonoclonal antibody", J NUCL MED, 42(4), 2001, pp. 596-600

Abstract

Tumor cells lacking the functional p53 suppressor gene may arrest at the G2 phase of the cell cycle after exposure to ionizing radiation, resulting in increased radioresistance. Methylxanthines (MTXs), such as pentoxifylline(PTX) or caffeine (CAF), can inhibit the G2-phase checkpoint arrest of damaged cells and thus radiosensitize them. However, the effect of MTX in cells irradiated with low-dose-rate p-emission is not well understood. Methods:A clonogenic assay was performed with LS180 human colon cancer cells lacking the functional p53 suppressor gene: Cells were irradiated with increasing concentrations of Re-186-mercaptoacetyltriglycine (Re-186-MAG3)-labeled A7 monoclonal antibody against colorectal cancer (0-925 kBq/mL) at 37 degreesC in 5% CO2 for 24 h in the presence or absence of PTX (0-2 mmol/L) or CAF(0-5 mmol/L). The enhancement ratio (ER) with MTX was calculated as a ratio of 50% cell-killing concentration of Re-186-MAG3-A7 in control cells to that in cells treated with PTX or CAF. The cell cycle distribution was analyzed with a flow cytometer. Results: The concentration of 50% cell kill was 474 kBq/mL Re-186-MAG3-A7. Both PTX and CAF dose dependently enhanced the cytotoxicity of Re-186-MAG3-A7: ERs of 0.5 mmol/L PTX, 2 mmol/L PTX, 1 mmol/L CAF, and 5 mmol/L CAF were 1.50, 2.18, 1.54, and 2.63, respectively. Flowcytometry showed that the percentage nonirradiated cells in the G2/M phaseof the cell cycle was 11.3% +/- 1.66%. On the other hand, cells exposed toRe-186-MAG3-A7 accumulated in the G2/M phase of the cell cycle (40.2% +/- 1.46%), which was inhibited by the presence of 1 mmol/L PTX (19.8% +/- 8.12%) or 2 mmol/L CAF (26.9% +/- 6.21%). Conclusion: Cellular modulation of the cell cycle with PTX and CAF radiosensitized LS180 colon cancer cells exposed to Re-186 radiation.

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Documento generato il 02/04/20 alle ore 18:10:54