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It is surprising, and even disappointing, that there have been very
few meetings and published volumes resulting from these meetings
that focus attention upon all of the groups of DNA tumor viruses.
Historically, separate meetings were held each year for the
adenovirus-SV40-polyoma researchers, the herpes viruses, hepatitis
B virus and the papillomaviruses. It was as if these four virus
groups were four fields of study developing independently with a
literature and culture of their own. When a virologist crossed the
field from the adenovirus group to the herpesvirus or
papillomaviruses, he or she was lost to their former group because
of the structure of separate meetings and remote literature. This,
of course, has resulted from historical accident and is being
rectified by the rapid progress made in our understanding of how
these viruses contribute to the causation of cancer in animals and
humans. It was pre cisely because of these factors that it was time
to hold a meeting and publish its proceedings on the subject of
transforming proteins of DNA tumor viruses. For the first time, DNA
tumor viruses were defined as all of the virus groups that can
contribute to cancer in animals with the exception, unfortunately,
of the . poxviruses. The purpose of the meeting was to bring
together scientists who rarely attend meetings together but
actually work on the same problems with different viruses.
The p53 tumor suppressor gene--the "guardian of the
genome"--protects cells against genotoxic stress but is mutated in
many cancers. It encodes one of a family of transcription factors
(p53, p63, and p73) that regulate cell proliferation,
differentiation, senescence, and cell death. Mutations in p53 allow
cells to escape normal growth controls and thereby contribute to
tumor malignancy.
Written and edited by experts in the field, this collection from
Cold Spring Harbor Perspectives in Biology provides a comprehensive
review of the functions of the p53 family. The contributors examine
the normal roles of these transcription factors, the regulatory
mechanisms that control p53 activity, and the part played by p53
mutations in tumorigenesis. They also discuss the evolution of the
p53 family, which may originally have arisen to protect the
integrity of the germ line. This collection also covers the
structure of p53 and its isoforms, model systems for analyzing p53
function, studies of p53 polymorphisms, and therapeutic approaches
aimed at targeting p53 defects in cancer.
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