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CONTACT:kate@linnean.org
ORGANIZER:Linnean Society of London
DTEND:20080710T200000
DTSTART:20080710T183000
UID:2009-11-28T09:59:18-05:00_543302982@socialweb1
DTSTAMP:20091128T095918
DESCRIPTION:Cancers arise through accumulation of mutations by a somatic ce
 ll that disrupt the mechanisms controlling their proliferation\, death\, di
 fferentiation\, metabolism and interactions with other tissues. All these p
 rocesses are regulated by extracellular signals\, effectively rendering som
 atic cells completely dependent upon their somatic environment for expansio
 n\, location and survival.  Oncogenic mutations preternaturally activate th
 e signaling pathways that convey information provided by these extracellula
 r signals\, so short-circuiting the dependence of somatic cells on their en
 vironments. In cancers\, such rogue cells expand uncontrollably at the expe
 nse of their organismal host\, disrupting the functions and integrity of no
 rmal tissues. Most adult animals are short-lived and post-mitotic\, so the 
 emergence of mutant cells is not a significant problem. By contrast\, cance
 r is an ever-present threat for large\, long-lived regenerative metazoans l
 ike vertebrates: our somatic cells possess all the ingredients for the expe
 ditious evolution of fitter and faster growing variants: significant rates 
 of mutation that drive variation\, strong selection in an environment where
  most cells are arrested or doomed to die\, prodigious numbers (1011-1016 d
 epending on the organism) and plenty of time.  Despite this\, pathological 
 cancers arise in only 1 in 3 individuals during the entire course of their 
 lives. It is believed that cancers are so rare because tumors require multi
 ple\, complementary mutations that each deregulate distinct processes\, suc
 h as proliferation\, survival\, migration\, increased metabolism\, stromal 
 remodeling and angiogenesis. Acquisition of so many independent mutations i
 n any one cell is a protracted and unlikely. It is also thought that cancer
 s are pro-actively suppressed by tumor suppressors\, proteins that mend or 
 ablate nascent cancer cells. However\, these two seemingly simple explanati
 ons raise two vexing questions. First\, if so many distinct processes have 
 to activated for tumor growth\, how is it so easy for normal tissues to do 
 all the same things during development and embryogenesis. Second\, tumor su
 ppression is an evolutionarily recent requirement of long-lived animals yet
  almost all vertebrate tumor suppressors are variants of ancient genes that
  evolved to respond to damage\, stress or checkpoints. How do vertebrate tu
 mor suppressors discriminate between tumor cells\, where they act\, and nor
 mal proliferating cell\, where they do not. Answers to these two questions 
 are emerging and shedding much light on the architecture of cell and tissue
  growth.
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SUMMARY:Keeping cancers at bay the evolutionary way
LAST-MODIFIED:20080707T102100
CREATED:20080415T100633
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