Aberrant transcripts of the FHIT gene are expressed in normal and leukaemic haemopoietic cells.
Aberrant transcripts of the FHIT gene are expressed in normal and leukaemic haemopoietic cells.
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FHIT 基因的异常转录物在正常和白血病造血细胞中表达。
DOI：
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发表时间：
1998
影响因子：
8.8
通讯作者：
Nicholas C. P. Cross
中科院分区：
文献类型：
--
作者：
M. Carapeti;R. C. Aguiar;Heinz Sill;J. M. Goldman;Nicholas C. P. Cross
FHIT基因3p14.2的缺失和明显的转录异常最近在多种实体肿瘤中被报道。为了确定该基因的损害是否也发生在白血病中，我们分析了总共97例患者（慢性髓性白血病，CML，慢性期或原细胞危象，n = 71；新生急性白血病，n = 26）和16例正常人。使用RT-PCR扩增所有病例的完整FHIT转录本。此外，从白血病患者和正常白细胞的几个样本中扩增出比全长产物强度更小的条带。小产物测序显示，它们来自缺乏完整外显子的FHIT转录本。单链构象多态性分析未发现编码序列突变。此外，在36名信息丰富的患者中，没有发现位于FHIT位点的D3S1300或D3S1481标记的杂合性缺失。我们的结论是，FHIT基因和3p14.2的其他未表征的肿瘤抑制基因不太可能参与急性白血病的发病机制或CML从慢性期进展到原细胞危象。此外，缺乏完整外显子的低丰度FHIT转录本并不是恶性细胞所特有的，在没有明显的基因组DNA病变的情况下，不应被视为异常的证据。
Deletions and apparent transcriptional abnormalities of the FHIT gene at 3p14.2 have recently been reported in a wide variety of solid tumours. To determine whether lesions of this gene also occur in leukaemia, we have analysed a total of 97 patients (chronic myeloid leukaemia, CML, in chronic phase or blast crisis, n = 71; de novo acute leukaemia, n = 26) and 16 normal individuals. Intact FHIT transcripts from all cases were amplified using RT-PCR. In addition, smaller size bands that were less intense than the full-length products were amplified from several samples from patients with leukaemia and also from normal leucocytes. Sequencing of the small products revealed that they were derived from FHIT transcripts lacking whole exons. Using single-strand conformation polymorphism analysis, no mutations in the coding sequence were detected in any patient. Furthermore, loss of heterozygosity was not seen in any of 36 informative patients at D3S1300 or D3S1481, markers located within the FHIT locus. We conclude that the FHIT gene and other uncharacterized tumour-suppressor genes at 3p14.2 are unlikely to be involved in the pathogenesis of acute leukaemia or progression of CML from chronic phase to blast crisis. Moreover, low-abundance FHIT transcripts that lack whole exons are not specific to malignant cells and should not be taken as evidence of an abnormality in the absence of demonstrable genomic DNA lesions.
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影响因子：
4.4
作者：
W. Paradee;C. Mullins;Z. He;T. Glover;C. Wilke;B. Opalka;J. Schutte;D. Smith
通讯作者：
W. Paradee;C. Mullins;Z. He;T. Glover;C. Wilke;B. Opalka;J. Schutte;D. Smith
通过肿瘤细胞系中的纯合缺失鉴定出 3p14.2 FRA3B 位点的潜在胃肠道肿瘤抑制基因座。
影响因子：
11.2
作者：
Kastury,K;Baffa,R;Druck,T;Ohta,M;Cotticelli,MG;Inoue,H;Negrini,M;Rugge,M;Huang,D;Croce,CM;Palazzo,J;Huebner,K
通讯作者：
Huebner,K
结直肠癌中 FHIT 基因的评估。
影响因子：
11.2
作者：
Thiagalingam,S;Lisitsyn,NA;Hamaguchi,M;Wigler,MH;Willson,JK;Markowitz,SD;Leach,FS;Kinzler,KW;Vogelstein,B
通讯作者：
Vogelstein,B
FHIT（一种候选抑癌基因）在头颈癌细胞系中频繁出现异常。
DOI：
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发表时间：
1996
期刊：
Cancer research.
影响因子：
--
作者：
Mao,L;Fan,YH;Lotan,R;Hong,WK
通讯作者：
Hong,WK
默克尔细胞癌中异常的 FHIT 转录本。
影响因子：
11.2
作者：
Sozzi,G;Alder,H;Tornielli,S;Corletto,V;Baffa,R;Veronese,ML;Negrini,M;Pilotti,S;Pierotti,MA;Huebner,K;Croce,CM
通讯作者：
Croce,CM