Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2001-8-29
pubmed:abstractText
Five years ago the fragile histidine triad (FHIT) gene including the most common fragile site locus of the human genome, FRA3B, was identified. The gene is altered in many types of cancer and several data support the idea that FHIT has to be considered a tumor suppressor. FHIT abnormalities were investigated in some skin tumors. Fifty-seven per cent of Merkel cell carcinomas displayed abnormal FHIT products but the involvement of FHIT in human non-melanoma skin cancer is still unclear. Because the murine Fhit locus is similar to its human homologue and is altered in cancer cell lines, we have established a strain of Fhit-deficient mice. After N-nitrosomethylbenzylamine treatment, the spectrum of tumors developed by the Fhit-deficient mice was similar to those observed in a familial skin cancer condition, the Muir-Torre syndrome, although there is no clear evidence yet for a relationship of FHIT and the human syndrome. Because cancer cells lacking in FHIT are defective in apoptosis, we propose the Fhit-deficient mouse as a model to understand a possible proapoptotic mechanism deficiency in the human syndrome.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1167-1122
pubmed:author
pubmed:issnType
Print
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
401-4
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:articleTitle
Fragile histidine triad gene and skin cancer.
pubmed:affiliation
Kimmel Cancer Center, Thomas Jefferson University-BLSB, 1050, 233 South 10th Street, Philadelphia, PA 19107, USA.
pubmed:publicationType
Journal Article, Review