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rdf:type |
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lifeskim:mentions |
|
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pubmed:issue |
12
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|
pubmed:dateCreated |
2000-3-9
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|
pubmed:abstractText |
The genotype-phenotype relationship of Lynch syndrome displays many enigmatic features which cannot be explained satisfactorily by the prevailing concepts of carcinogenesis and genetic predisposition to cancer. We propose here a new model of carcinogenesis divided into two and only two evolutive phases: a) a preliminary phase starting with the counter-selective loss of mismatch repair function, in which most clones with the RER mutator phenotype are eliminated through apoptosis or an accelerated ageing process; b) an explosive phase that is initiated only if mutations blocking apoptosis and senescence, rapidly acquired during the short life span of the non-transformed RER+ clones, eventually rescue one mismatch repair-deficient cell that gives rise to the malignant clone. Carcinogenesis is proposed here to progress irreversibly and very rapidly once initiated. We shall show how this model provides a meaningful etiologic and pathogenic interpretation of all the curious features of Lynch syndrome.
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pubmed:language |
fre
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0764-4469
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pubmed:author |
|
|
pubmed:issnType |
Print
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pubmed:volume |
322
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1017-31
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:10656143-Adenoma,
pubmed-meshheading:10656143-Adult,
pubmed-meshheading:10656143-Age of Onset,
pubmed-meshheading:10656143-Animals,
pubmed-meshheading:10656143-Apoptosis,
pubmed-meshheading:10656143-Cell Aging,
pubmed-meshheading:10656143-Cell Transformation, Neoplastic,
pubmed-meshheading:10656143-Child,
pubmed-meshheading:10656143-Colonic Neoplasms,
pubmed-meshheading:10656143-Colonic Polyps,
pubmed-meshheading:10656143-Colorectal Neoplasms,
pubmed-meshheading:10656143-Colorectal Neoplasms, Hereditary Nonpolyposis,
pubmed-meshheading:10656143-DNA Repair,
pubmed-meshheading:10656143-Disease Progression,
pubmed-meshheading:10656143-Genes, APC,
pubmed-meshheading:10656143-Genetic Predisposition to Disease,
pubmed-meshheading:10656143-Genotype,
pubmed-meshheading:10656143-Humans,
pubmed-meshheading:10656143-Mice,
pubmed-meshheading:10656143-Microsatellite Repeats,
pubmed-meshheading:10656143-Middle Aged,
pubmed-meshheading:10656143-Models, Biological,
pubmed-meshheading:10656143-Mutagenesis,
pubmed-meshheading:10656143-Organ Specificity,
pubmed-meshheading:10656143-Phenotype,
pubmed-meshheading:10656143-Precancerous Conditions,
pubmed-meshheading:10656143-Risk
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pubmed:year |
1999
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|
pubmed:articleTitle |
[Explanation of enigmas of the Lynch syndrome thanks to a new carcinogenesis model characterized by an unorthodox initiation process].
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pubmed:affiliation |
Unité d'oncologie médicale, Hôpital Laënnec, Paris, France.
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pubmed:publicationType |
Journal Article,
Comparative Study,
English Abstract,
Review
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