Primary cervical carcinomas show 2 common regions of deletion at 3P, 1 within theFHIT gene: Evaluation of allelic imbalance atFHIT, RB1 andTP53 in relation to survival

Helland, Åslaug; Kraggerud, Sigrid Marie; Kristensen, Gunnar B.; Holm, R.; Abeler, Vera M.; Huebner, Kay; Børresen-Dale, Anne Lise

doi:10.1002/1097-0215(20001015)88:2<217::aid-ijc11>3.0.co;2-i

Cited by 17 publications

(18 citation statements)

References 42 publications

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“…Altogether, these data showed that copy number changes (homo-and hemizygous deletions and amplifications) of either NLJ3-001 or NL3-001 were detected in 29 cases (90.6%). This is significantly higher than it was reported earlier for the whole 3p -around or some more than 70% (Larson et al, 1997a;Wistuba et al, 1997;Braga et al, 1999;Helland et al, 2000). These results lend strong support to the conclusion that these two regions are really hot spots for rearrangements in CCs.…”

Section: Analysis Of Two Critical Regions In 3p213supporting

confidence: 54%

Deletion mapping using quantitative real-time PCR identifies two distinct 3p21.3 regions affected in most cervical carcinomas

et al. 2003

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We report chromosome 3p deletion mapping of 32 cervical carcinoma (CC) biopsies using 26 microsatellite markers located in frequently deleted 3p regions to detect loss of heterozygosity and homozygous loss. In addition, two STS markers (NLJ-003 and NL3-001) located in the 3p21.3 telomeric (3p21.3T) and 3p21.3 centromeric (3p21.3C) regions, respectively, were used for quantitative real-time PCR as TaqMan probes. We show that quantitative real-time PCR is reliable and sensitive and allows discriminating between 0, 1 and 2 marker copies per human genome. For the first time, frequent (five of 32 cases, i.e. 15.6%) homozygous deletions were demonstrated in CCs in both 3p21.3T and 3p21.3C regions. The smallest region homozygously deleted in 3p21.3C was located between D3S1568 (CACNA2D2 gene) and D3S4604 (SEMA3F gene) and contains 17 genes previously defined as lung cancer candidate Tumor suppressor genes (TSG(s)). The smallest region homozygously deleted in 3p21.3T was flanked by D3S1298 and NL1-024 (D3S4285), excluding DLEC1 and MYD88 as candidate TSGs involved in cervical carcinogenesis. Overall, this region contains five potential candidates, namely GOLGA4, APRG1, ITGA9, HYA22 and VILL, which need to be analysed. The data showed that aberrations of either NLJ-003 or NL3-001 were detected in 29 cases (90.6%) and most likely have a synergistic effect (Po0.01). The study also demonstrated that aberrations in 3p21.3 were complex and in addition to deletions, may involve gene amplification as well. The results strongly suggest that 3p21.3T and 3p21.3C regions harbor genes involved in the origin and/or development of CCs and imply that those genes might be multiple TSG(s).

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Section: Analysis Of Two Critical Regions In 3p213supporting

confidence: 54%

Deletion mapping using quantitative real-time PCR identifies two distinct 3p21.3 regions affected in most cervical carcinomas

et al. 2003

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“…Deletions in this region are very frequent in lung and kidney carcinomas and were also observed in a variety of other common tumors, such as breast cancer, head and neck cancer, gastrointestinal cancer, esophageal cancer, and cervical cancer (see Croce et al, 1999;Huebner and Croce, 2001;Wistuba et al, 1997;Fong et al, 1997;Greenspan et al, 1997;Muller et al, 1998;Helland et al, 2000;Zo¨chbauer-Muller et al, 2001b).…”

Section: Chromosome Region 3p142 (Fhit Gene Region)mentioning

confidence: 99%

Tumor suppressor genes on chromosome 3p involved in the pathogenesis of lung and other cancers

Zabarovsky¹,

2002

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Loss of heterozygosity (LOH) involving several chromosome 3p regions accompanied by chromosome 3p deletions are detected in almost 100% of small (SCLCs) and more than 90% of non-small (NSCLCs) cell lung cancers. In addition, these changes appear early in the pathogenesis of lung cancer and are found as clonal lesions in the smoking damaged respiratory epithelium including histologically normal epithelium as well as in epithelium showing histologic changes of preneoplasia. These 3p genetic alterations lead to the conclusion that the short arm of human chromosome 3 contains several tumor suppressor gene(s) (TSG(s)). Although the first data suggesting that 3p alterations were involved in lung carcinogenesis were published more than 10 years ago, only recently has significant progress been achieved in identifying the candidate TSGs and beginning to demonstrate their functional role in tumor pathogenesis. Some of the striking results of these findings has been the discovery of multiple 3p TSGs and the importance of tumor acquired promoter DNA methylation as an epigenetic mechanism for inactivating the expression of these genes in lung cancer. This progress, combined with the well known role of smoking as an environmental causative risk factor in lung cancer pathogenesis, is leading to the development of new diagnostic and therapeutic strategies which can be translated into the clinic to combat and prevent the lung cancer epidemic. It is clear now that genetic and epigenetic abnormalities of several genes residing in chromosome region 3p are important for the development of lung cancers but it is still obscure how many of them exist and which of the numerous candidate TSGs are the key players in lung cancer pathogenesis. We review herein our current knowledge and describe the most credible candidate genes.

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“…Score 0 was defined as absent or lost expression, scores 1-3 were defined as markedly reduced FHIT expression and scored 4-9 were considered as normal expression. [35][36][37] …”

Section: Immunohistochemical Staining For Fhit Proteinmentioning

confidence: 99%

High throughput tissue microarray analysis of FHIT expression in diffuse large cell B-cell lymphoma from Saudi Arabia

et al. 2006

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Recent studies have suggested a potential prognostic role of alterations of the fragile histidine triad (FHIT) gene in diffuse large B-cell lymphoma. To evaluate possible mechanisms of FHIT inactivation and to further clarify its potential prognostic relevance, we analyzed a set of 114 diffuse large B-cell lymphoma with clinical follow-up information. Tissue microarrays were analyzed by immunohistochemistry for protein expression, and corresponding DNA samples were analyzed for FHIT promotor hypermethlyation. Reduced or absent FHIT expression was found in 75 of 114 diffuse large B-cell lymphoma (66%), but was unrelated to clinical tumor stage or patient prognosis. FHIT promotor hypermethylation was observed in 29 of 93 (23%) interpretable diffuse large B-cell lymphoma. Hypermethylation was not significantly correlated to protein expression loss, which could be explained by competing mechanisms for FHIT inactivation in a substantial fraction of non FHIT hypermethylated diffuse large B-cell lymphoma. Hypermethylation was significantly associated with poor prognosis of diffuse large B-cell lymphoma patients and predominantly seen in nongerminal center diffuse large B-cell lymphoma (27%), but less frequent (13%) in germinal center diffuse large B-cell lymphoma. In summary, these data suggest that promotor hypermethylation is responsible for reduced FHIT expression in a substantial subset of diffuse large B-cell lymphoma, which is primarily composed of nongerminal center subtype with poor patient prognosis.

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Primary cervical carcinomas show 2 common regions of deletion at 3P, 1 within theFHIT gene: Evaluation of allelic imbalance atFHIT, RB1 andTP53 in relation to survival

Cited by 17 publications

References 42 publications

Deletion mapping using quantitative real-time PCR identifies two distinct 3p21.3 regions affected in most cervical carcinomas

Deletion mapping using quantitative real-time PCR identifies two distinct 3p21.3 regions affected in most cervical carcinomas

Tumor suppressor genes on chromosome 3p involved in the pathogenesis of lung and other cancers

High throughput tissue microarray analysis of FHIT expression in diffuse large cell B-cell lymphoma from Saudi Arabia

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