Document 0611
 DOCN  M9640611
 TI    Induction of the WAF1/CIP1 protein and apoptosis in human T-cell
       leukemia virus type I-transformed lymphocytes after treatment with
       adriamycin by using a p53-independent pathway.
 DT    9604
 AU    Gartenhaus RB; Wang P; Hoffmann P; Department of Medicine, Long Island
       Jewish Medical Center, Albert; Einstein College of Medicine, New Hyde
       Park, NY 11040, USA.
 SO    Proc Natl Acad Sci U S A. 1996 Jan 9;93(1):265-8. Unique Identifier :
       AIDSLINE MED/96133918
 AB    The WAF1/CIP1 protein has been identified as a downstream mediator of
       the tumor suppressor p53 in regulating cell cycle progression through a
       G1-phase check-point. Recent work has implicated the functional status
       of p53 as a critical determinant in the apoptotic response of certain
       cell lines to DNA damaging agents. By using human T-cell leukemia virus
       type I-transformed lymphoid cell lines that differ in their level and
       function of wild-type p53, we investigated the induction of WAF1/CIP1
       and apoptosis after exposure to Adriamycin, a genotoxic agent. We found
       that regardless of the p53 status in these cell lines, WAF1/CIP1 RNA was
       rapidly induced in response to Adriamycin treatment. An elevated level
       of WAF1/CIP1 protein was observed as well. Additionally, we demonstrated
       that apoptosis was induced in all cell lines analyzed despite some
       having functionally inactive p53 protein. Our data suggest that a
       p53-independent pathway may play a role in the apoptotic response
       observed in some cell lines after exposure to DNA damaging agents.
 DE    Antibiotics, Anthracycline/*PHARMACOLOGY  Apoptosis/*DRUG EFFECTS  Base
       Sequence  Cell Transformation, Viral  Cells, Cultured
       Cyclins/*BIOSYNTHESIS  Doxorubicin/*PHARMACOLOGY  DNA Damage  DNA
       Primers/CHEMISTRY  Human  HTLV-I  Lymphocytes/*MICROBIOLOGY/PATHOLOGY
       Molecular Sequence Data  Protein p53/PHYSIOLOGY  Support, Non-U.S. Gov't
       JOURNAL ARTICLE

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