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To date, different mutations have been
reported that result in a complete deficiency, including:
two deletions (295¨C298delTCAT and 1897delC), one splice-site mutation (IVS14+IG>A), four missense mutations
(85T>C, 703C>T, 2657G>A, and 2983 G>T), a
deletion of two nucleotides (1039¨C1040delTG), and the
point mutations P86L, S201R, S492L, D949V and H978R
[13]. The 85T>C mutation might be a common polymorphism,
although functional analysis of a recombinantly
expressed human protein carrying the 85T>C mutation
showed no significant residual mutant enzyme activity
[10,14]. An in-depth discussion of the clinical import of
DPD can be found in a number of review articles, and two
examples are provided in Refs. [37,38], which discuss the
role of DPD in cancer therapy with 5FU

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ЦÊÀ¿ñÁú(½ð±Ò+25, ·­ÒëEPI+1): ллÄã 2011-03-11 20:27:42
ÄúÊDz»ÊǰÑһƪDPDµÄ×ÛÊöÒ»µãµãÌùѽ¡£

ĿǰÒѱ¨µÀÓжà¸öÍ»±äµ¼ÖÂÍêÈ«¹¦ÄÜȱʧ£¬ÕâЩͻ±äÓУºÁ½¸öȱʧͻ±ä£¨295¨C298delTCAT and 1897delC£©£¬Ò»¸ö¼ô½ÓλµãÍ»±ä(IVS14+IG>A)£¬4¸ö´íÒåÍ»±ä(85T>C, 703C>T, 2657G>A, and 2983 G>T)£¬Ò»¸öÁ½¸öºËÜÕËáµÄȱʧͻ±ä(1039¨C1040delTG)ºÍ¼¸¸öµãÍ»±äP86L, S201R, S492L, D949V and H978R¡£85T>CÍ»±ä¿ÉÄÜÊÇÒ»¸ö±È½ÏÆÕ±éµÄ¶à̬ÐÔ£¬µ«Ð¯´ø85T>CÍ»±äµÄÖØ×éÈËDPDµ°°×²¢Ã»ÓÐÃ÷ÏÔµÄÍ»±äøµÄ»îÐÔ²ÐÓà¡£´óÁ¿×ÛÊöÒѾ­ÉîÈëÌÖÂÛÁËDPDµÄÖØÒªÁÙ´²×÷Óã¬ÎÄÏ×37£¬38ÖоÍÓÐÁ½¸öÀý×Ó£¬ÕâÁ½Æª×ÛÊöÌÖÂÛÁËDPDÔÚ5FUÖÎÁư©Ö¢ÖеÄ×÷Óá£
2Â¥2011-03-11 10:50:33
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ÒýÓûØÌû:
Originally posted by µØÍ¼ÎÏÅ£ at 2011-03-11 10:50:33:
ÄúÊDz»ÊǰÑһƪDPDµÄ×ÛÊöÒ»µãµãÌùѽ¡£

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