Linked Life Data

8168089

Source:http://linkedlifedata.com/resource/pubmed/id/8168089

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
1994-6-2
pubmed:abstractText
Chronic inflammation of the urinary tract is a significant risk factor for the development of urinary bladder cancer in man. Previously we have shown that acute and chronic inflammation induced by repeated intravesical instillation of killed Escherichia coli (KEC) strikingly enhanced N-methyl-N-nitrosourea (MNU)-initiated bladder carcinogenesis in our heterotopically transplanted rat urinary bladder model. We conducted the present study to determine whether delayed onset of KEC treatment can still enhance carcinogenesis of the MNU-initiated urothelium and whether continuous KEC treatment is necessary for the development of tumors. After the initiation of carcinogenesis in heterotopically transplanted bladders by the instillation of a single dose (0.25 mg) of MNU, animals were divided into several groups, for which weekly KEC treatment (5 x 10(8) cells suspended in 0.5 ml of phosphate-buffered 2.1% NaCl solution) was begun 1, 5, and 18 weeks later and continued until termination of the experiment at 31 weeks. In addition, animals received 4-week KEC treatment, which was started 1 or 5 weeks after MNU administration. Treatment with KEC alone or MNU alone induced few tumors. Maximal tumor development was demonstrated in the group receiving KEC treatment continuously throughout the experimental period. Delaying the onset of continuous KEC treatment by 4 weeks resulted in a significant decrease in the number of tumors (P = 0.006). However, a substantial number of tumors were induced even when KEC treatment was delayed as many as 18 weeks, as compared to tumor development in the group receiving MNU only (P = 0.007). The tumor volume (size) was not different between continuous and short-term KEC treatment groups. We conclude that (a) although a large number of cells undergo promutagenic DNA damage by a single dose of MNU, the amounts are reduced quickly during the subsequent 4 weeks; but that (b) a substantial number of genetically altered cells remain for a long time and can be promoted to tumors when stimulated by a chronic inflammatory stimulus; and that (c) the duration of KEC treatment determines the number, but not the volume, of tumors.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
54
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2630-2
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Persistence of carcinogen-altered cell population in rat urothelium which can be promoted to tumors by chronic inflammatory stimulus.
pubmed:affiliation
Department of Pathology, Northwestern University Medical School, Chicago, Illinois 60611-3008.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.