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Abnormal FHIT transcripts found in both lung cancer and normal lung tissue
Genes chromosomes & cancer, 1999-02, Vol.24 (2), p.105-111
Tokuchi, Yoshio
Kobayashi, Yasuhito
Hayashi, Shin-ichi
Hayashi, Moriaki
Tanimoto, Keiji
Hashimoto, Takehisa
Nishida, Kazunori
Ishikawa, Yuichi
Nakagawa, Ken
Satoh, Yukitoshi
Yamamoto, Mitsunobu
Tsuchiya, Eiju
1999
Volltextzugriff (PDF)
Details
Autor(en) / Beteiligte
Tokuchi, Yoshio
Kobayashi, Yasuhito
Hayashi, Shin-ichi
Hayashi, Moriaki
Tanimoto, Keiji
Hashimoto, Takehisa
Nishida, Kazunori
Ishikawa, Yuichi
Nakagawa, Ken
Satoh, Yukitoshi
Yamamoto, Mitsunobu
Tsuchiya, Eiju
Titel
Abnormal FHIT transcripts found in both lung cancer and normal lung tissue
Ist Teil von
Genes chromosomes & cancer, 1999-02, Vol.24 (2), p.105-111
Ort / Verlag
New York: John Wiley & Sons, Inc
Erscheinungsjahr
1999
Quelle
Wiley-Blackwell Full Collection
Beschreibungen/Notizen
Occurrence of abnormal transcripts of the FHIT (fragile histidine triad) gene has been reported in various types of cancer. On the other hand, aberrant transcripts are sometimes found in non‐neoplastic tissues, so the relationship between the presence of abnormal transcripts of the FHIT gene and cancer pathogenesis is controversial. We investigated alterations in the FHIT locus, detected by nested reverse transcription‐polymerase chain reaction and/or allelic status, in 88 primary lung cancers and normal lung tissues, and 22 normal lung tissues with metastasitic lung cancer as a control. The frequencies of abnormal transcripts were 59% in lung cancer, 35% in paired normal lung, and 64% in normal control lung; the difference in frequencies between lung cancer and paired normal lung was significant, while that between lung cancer and normal control lung was not. Sequence analysis revealed that there were no cancer‐specific abnormal transcripts entirely missing two or more exons, nor were the abnormal transcripts of lung cancer identical with those of paired normal lung in the same individual. Furthermore, we found no correlation between loss of heterozygosity in the FHIT locus and occurrence of abnormal FHIT transcripts. These results suggest that the presence of abnormal FHIT transcripts, in terms of their frequency and variety, is not cancer‐specific in lung carcinogenesis, and the abnormality may be mainly due to abnormal splicing and processing of the transcripts. To estimate the precise function of the FHIT gene, further study of the FHIT protein in lung carcinogenesis is needed. Genes Chromosomes Cancer 24:105–111, 1999. © 1999 Wiley‐Liss, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 1045-2257
eISSN: 1098-2264
DOI: 10.1002/(SICI)1098-2264(199902)24:2<105::AID-GCC2>3.0.CO;2-P
Titel-ID: cdi_pubmed_primary_9885976
Format
–
Schlagworte
Acid Anhydride Hydrolases
,
Female
,
Genetic Markers
,
Humans
,
Loss of Heterozygosity
,
Lung - chemistry
,
Lung - cytology
,
Lung Neoplasms - chemistry
,
Lung Neoplasms - secondary
,
Male
,
Middle Aged
,
Neoplasm Proteins
,
Proteins - isolation & purification
,
Reverse Transcriptase Polymerase Chain Reaction
,
RNA, Messenger - isolation & purification
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