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P53 STATUS AND THE EFFICACY OF CANCER-THERAPY IN-VIVO
Author(s): LOWE SW, BODIS S, MCCLATCHEY A, REMINGTON L, RULEY HE, FISHER DE, HOUSMAN DE, JACKS T
Source: SCIENCE    Volume: 266    Issue: 5186    Pages: 807-810    Published: NOV 4 1994  
Times Cited: 1,200     References: 25     
Abstract: The therapeutic responsiveness of genetically defined tumors expressing or devoid of the p53 tumor suppressor gene was compared in immunocompromised mice. Tumors expressing the p53 gene contained a high proportion of apoptotic cells and typically regressed after treatment with gamma radiation or adriamycin. In contrast, p53-deficient tumors treated with the same regimens continued to enlarge and contained few apoptotic cells. Acquired mutations in p53 were associated with both treatment resistance and relapse in p53-expressing tumors. These results establish that defects in apoptosis, here caused by the inactivation of p53, can produce treatment-resistant tumors and suggest that p53 status may be an important determinant of tumor response to therapy.
Document Type: Article
Language: English
Addresses:
1. MIT, HOWARD HUGHES MED INST, CAMBRIDGE, MA 02139 USA
2. MIT, DEPT BIOL, CAMBRIDGE, MA 02139 USA
3. HARVARD UNIV, SCH MED, JOINT CTR RADIAT THERAPY, BOSTON, MA 02115 USA
4. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA
5. VANDERBILT UNIV, SCH MED, DEPT IMMUNOL & MICROBIOL, NASHVILLE, TN 37232 USA
6. HARVARD UNIV, CHILDRENS HOSP, SCH MED, BOSTON, MA 02115 USA
7. MIT, CTR CANC RES, CAMBRIDGE, MA 02139 USA
Publisher: AMER ASSOC ADVANCEMENT SCIENCE, 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005
Subject Category: Multidisciplinary Sciences
IDS Number: PP753
ISSN: 0036-8075
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