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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2009-11-25
pubmed:abstractText
p53 is the most commonly mutated tumor suppressor gene in human cancers. In addition to the loss of tumor suppression function and exertion of dominant-negative effects over the remaining wild-type protein, several p53 mutants can gain novel oncogenic functions (gain-of-function, GOF) that actively regulate cancer development and progression. In human endometrial cancer, p53 mutation is more often associated with aggressive nonendometrioid cancer. However, it was unknown if p53 mutants contributed to endometrial cancer progression through the GOF properties.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-11165124, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-11252954, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-11477555, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-11519036, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-11733960, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-11910072, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-14743206, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-15661684, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-15838523, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-16014005, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-16170357, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-16377102, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-1660340, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-16773209, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-17636407, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-19078924, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-19229860, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-7909788, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-7911031, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-8080050, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-8099841, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-8293402, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-8649855, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-8673929, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-8887630, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-9421075, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-9833779, http://linkedlifedata.com/resource/pubmed/commentcorrection/19917135-9927204
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1476-4598
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
8
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
103
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:19917135-Amino Acid Substitution, pubmed-meshheading:19917135-Cell Line, Tumor, pubmed-meshheading:19917135-Cell Movement, pubmed-meshheading:19917135-DNA, Complementary, pubmed-meshheading:19917135-Down-Regulation, pubmed-meshheading:19917135-Endometrial Neoplasms, pubmed-meshheading:19917135-Enzyme Activation, pubmed-meshheading:19917135-Female, pubmed-meshheading:19917135-Humans, pubmed-meshheading:19917135-Mutant Proteins, pubmed-meshheading:19917135-Mutation, pubmed-meshheading:19917135-Neoplasm Invasiveness, pubmed-meshheading:19917135-Phenotype, pubmed-meshheading:19917135-Phosphatidylinositol 3-Kinases, pubmed-meshheading:19917135-Proto-Oncogene Proteins c-akt, pubmed-meshheading:19917135-RNA Interference, pubmed-meshheading:19917135-Receptor, Epidermal Growth Factor, pubmed-meshheading:19917135-Signal Transduction, pubmed-meshheading:19917135-Transfection, pubmed-meshheading:19917135-Tumor Suppressor Protein p53
pubmed:year
2009
pubmed:articleTitle
Elevated expression of p53 gain-of-function mutation R175H in endometrial cancer cells can increase the invasive phenotypes by activation of the EGFR/PI3K/AKT pathway.
pubmed:affiliation
Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, Shanghai, PR China. dongpeix@yahoo.co.jp
pubmed:publicationType
Journal Article
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