PMID- 9823330
OWN - NLM
STAT- MEDLINE
DCOM- 19981207
LR  - 20071115
IS  - 0008-5472 (Print)
IS  - 0008-5472 (Linking)
VI  - 58
IP  - 22
DP  - 1998 Nov 15
TI  - Frequent aberration of FHIT gene expression in acute leukemias.
PG  - 5182-7
AB  - We analyzed the mRNA expression of the FHIT gene by reverse transcription-PCR 
      (RT-PCR) in 54 cases of acute lymphoblastic leukemia (ALL; 11 cases of T-cell ALL 
      [T-ALL] and 43 cases of non-T-ALL) and 40 cases of acute myeloid leukemia (AML). 
      In 46% of the ALL cases and 55% of the AML cases, FHIT expression was absent or 
      markedly decreased. Only abnormal short bands were detected in 30% of the ALL 
      cases and 5% of the AML cases. Eighteen of 19 abnormal transcripts had the same 
      fusion of exons 2-7, and all lacked the starting codon in exon 5. No obvious 
      normal-sized PCR products were detected in cases exhibiting abnormal transcripts. 
      These findings suggest that the expression of functional FHIT protein was lost in 
      the majority of ALL (76%) and AML (60%) cases. Differential quantitative PCR of 
      exons 3-9 of the FHIT gene and RT-PCR of the PTPRG gene, which is centromeric to 
      the FHIT gene, showed the presence of the target sequences. Fluorescence in situ 
      hybridization analysis using probes covering exons 5 and 8 revealed no difference 
      in the signal patterns between leukemia and normal cells, showing one or two 
      signal doublets in more than 90% of nuclei, and indicated that gross segments of 
      the FHIT gene were not homozygously deleted in these cases. A small number of 
      transcripts with an aberrant fusion between exons 2 and 7 were detected by RT-PCR 
      in the bone marrow cells from four healthy individuals. Granulocytes, 
      lymphocytes, and monocytes in the bone marrow cells of a healthy individual 
      contained transcripts with the same fusion. This unique fusion of exons 2 and 7 
      might be preferentially seen in either neoplastic or normal hematopoietic cells, 
      regardless of their lineage. The finding that FHIT expression was abolished in 
      the majority of leukemia cases might support the hypothesis that the FHIT gene 
      acts as a tumor suppressor, at least in leukemia.
FAU - Iwai, T
AU  - Iwai T
AD  - Third Department of Internal Medicine, Kyoto Prefectural University of Medicine, 
      Japan.
FAU - Yokota, S
AU  - Yokota S
FAU - Nakao, M
AU  - Nakao M
FAU - Nakazawa, N
AU  - Nakazawa N
FAU - Taniwaki, M
AU  - Taniwaki M
FAU - Kimura, T
AU  - Kimura T
FAU - Sonoda, Y
AU  - Sonoda Y
FAU - Kaneko, H
AU  - Kaneko H
FAU - Okuda, T
AU  - Okuda T
FAU - Azuma, H
AU  - Azuma H
FAU - Oka, T
AU  - Oka T
FAU - Takeda, T
AU  - Takeda T
FAU - Watanabe, A
AU  - Watanabe A
FAU - Kikuta, A
AU  - Kikuta A
FAU - Asami, K
AU  - Asami K
FAU - Sekine, I
AU  - Sekine I
FAU - Matsushita, T
AU  - Matsushita T
FAU - Tsuchiya, T
AU  - Tsuchiya T
FAU - Mimaya, J
AU  - Mimaya J
FAU - Koizumi, S
AU  - Koizumi S
FAU - Ohta, S
AU  - Ohta S
FAU - Miyake, M
AU  - Miyake M
FAU - Takaue, Y
AU  - Takaue Y
FAU - Iwai, A
AU  - Iwai A
FAU - Fujimoto, T
AU  - Fujimoto T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Cancer Res
JT  - Cancer research
JID - 2984705R
RN  - 0 (Neoplasm Proteins)
RN  - 0 (Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (fragile histidine triad protein)
RN  - EC 3.6.- (Acid Anhydride Hydrolases)
SB  - IM
MH  - *Acid Anhydride Hydrolases
MH  - Acute Disease
MH  - Adult
MH  - Bone Marrow/metabolism
MH  - Child
MH  - Gene Deletion
MH  - Gene Expression
MH  - Humans
MH  - Leukemia/*genetics
MH  - Leukemia, Erythroblastic, Acute/genetics
MH  - Leukemia, Monocytic, Acute/genetics
MH  - Leukemia, Myeloid, Acute/genetics
MH  - Leukemia, Myelomonocytic, Acute/genetics
MH  - Leukemia, Promyelocytic, Acute/genetics
MH  - Neoplasm Proteins/genetics/*metabolism
MH  - Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics
MH  - Proteins/genetics/*metabolism
MH  - RNA, Messenger/metabolism
EDAT- 1998/11/21 00:00
MHDA- 1998/11/21 00:01
CRDT- 1998/11/21 00:00
PHST- 1998/11/21 00:00 [pubmed]
PHST- 1998/11/21 00:01 [medline]
PHST- 1998/11/21 00:00 [entrez]
PST - ppublish
SO  - Cancer Res. 1998 Nov 15;58(22):5182-7.