| pubmed-article:10984511 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10984511 | lifeskim:mentions | umls-concept:C0027651 | lld:lifeskim |
| pubmed-article:10984511 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
| pubmed-article:10984511 | lifeskim:mentions | umls-concept:C0812198 | lld:lifeskim |
| pubmed-article:10984511 | lifeskim:mentions | umls-concept:C1516669 | lld:lifeskim |
| pubmed-article:10984511 | lifeskim:mentions | umls-concept:C0308269 | lld:lifeskim |
| pubmed-article:10984511 | pubmed:issue | 20 | lld:pubmed |
| pubmed-article:10984511 | pubmed:dateCreated | 2000-11-3 | lld:pubmed |
| pubmed-article:10984511 | pubmed:abstractText | A remarkable instability at simple repeated sequences characterizes gastrointestinal cancer of the microsatellite mutator phenotype (MMP). Mutations in the DNA mismatch repair gene family underlie the MMP, a landmark for hereditary nonpolyposis colorectal cancer. These tumors define a distinctive pathway for carcinogenesis because they display a particular spectrum of mutated cancer genes containing target repeats for mismatch repair deficiency. One such gene is BAX, a proapoptotic member of the Bcl-2 family of proteins, which plays a key role in programmed cell death. More than half of colon and gastric cancers of the MMP contain BAX frameshifts in a (G)(8) mononucleotide tract. However, the functional significance of these mutations in tumor progression has not been established. Here we show that inactivation of the wild-type BAX allele by de novo frameshift mutations confers a strong advantage during tumor clonal evolution. Tumor subclones with only mutant alleles frequently appeared after inoculation into nude mice of single-cell clones of colon tumor cell lines with normal alleles. In contrast, no clones of BAX-expressing cells were found after inoculation of homozygous cell clones without wild-type BAX. These results support the interpretation that BAX inactivation contributes to tumor progression by providing a survival advantage. In this context, survival analyses show that BAX mutations are indicators of poor prognosis for both colon and gastric cancer of the MMP. | lld:pubmed |
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| pubmed-article:10984511 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10984511 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10984511 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10984511 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10984511 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:10984511 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:10984511 | pubmed:author | pubmed-author:ReedJ CJC | lld:pubmed |
| pubmed-article:10984511 | pubmed:author | pubmed-author:YamamotoHH | lld:pubmed |
| pubmed-article:10984511 | pubmed:author | pubmed-author:KrajewskiSS | lld:pubmed |
| pubmed-article:10984511 | pubmed:author | pubmed-author:PeruchoMM | lld:pubmed |
| pubmed-article:10984511 | pubmed:author | pubmed-author:IonovYY | lld:pubmed |
| pubmed-article:10984511 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10984511 | pubmed:day | 26 | lld:pubmed |
| pubmed-article:10984511 | pubmed:volume | 97 | lld:pubmed |
| pubmed-article:10984511 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10984511 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10984511 | pubmed:pagination | 10872-7 | lld:pubmed |
| pubmed-article:10984511 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:10984511 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10984511 | pubmed:articleTitle | Mutational inactivation of the proapoptotic gene BAX confers selective advantage during tumor clonal evolution. | lld:pubmed |
| pubmed-article:10984511 | pubmed:affiliation | The Burnham Institute, La Jolla Cancer Research Center, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA. | lld:pubmed |
| pubmed-article:10984511 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10984511 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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