FHIT gene alterations in esophageal cancer and ulcerative colitis (UC)

Zou, Tong; Lei, Jiao; Shi, Ying; Yin, Jing; Wang, Suna; Souza, Rhonda F.; Kong, Dehe; Shimada, Yutaka; Smolinski, Kara N.; Greenwald, Bruce D.; Abraham, John M.; Harpaz, Noam; Meltzer, Stephen J.

doi:10.1038/sj.onc.1201169

Cited by 34 publications

(17 citation statements)

References 13 publications

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“…In each of the 20 cases (15 prostate tumors, four normal prostate tissue specimens and total RNA from a pool of 62 normal human prostate tissues) a major FHIT-speci®c full-length product, containing the complete FHIT coding region, was observed. These results matched those obtained on colorectal and esophageal cancers (Thiagalingam et al, 1996;Zou et al, 1997).…”

Section: Discussionsupporting

confidence: 88%

Molecular analysis of the FHIT gene in human prostate cancer

et al. 1998

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A variety of studies suggest that the FHIT gene, which encompasses the fragile site at 3p14.2, is a candidate tumor suppressor gene in several forms of human cancer. To determine whether the FHIT gene is altered in prostate carcinomas, we examined 15 prostate tumors, four normal prostate tissue specimens and RNA from a pool of 62 normal human prostate tissues (Clontech) for the integrity of FHIT transcripts, using a robust singlestage PCR and a nested PCR method. In each case a major FHIT-speci®c full-length product was observed. Additional aberrantly sized products, which were more numerous in the nested PCR strategy, were present at a far lower level than the full-length transcripts in 14 of 15 tumors, three of four normal human prostate tissues and in the pooled normal prostate RNA. Sequence analysis revealed that these aberrant products corresponded to alternatively spliced FHIT transcripts, which were neither more numerous nor more prominent in the tumors than in the normal prostate specimens. Deletion at the FHIT locus was also evaluated by using three intragenic polymorphic markers (D13S1481, D3S1300, and D3S1234). Allelic loss was observed in two tumors, but these genomic alterations did not correspond to the aberrant FHIT transcripts. DNA analysis, furthermore, suggested that the tumor heterogeneity was not a likely explanation for presence of normal and alternatively spliced FHIT transcripts in the prostate tumors. In conclusion, we detected neither frequent loss of heterozygosity nor tumor speci®c transcripts of the FHIT gene in human prostate cancer.

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Section: Discussionsupporting

confidence: 88%

Molecular analysis of the FHIT gene in human prostate cancer

et al. 1998

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“…Recently the FHIT gene has been identified within the chromosome region 3p14.2, which is altered in several types of tumours, such as lung (Sozzi et al, 1996), breast (Hayashi et al, 1997) and oesophageal carcinomas (Zou et al, 1997), but not in others, such as colon carcinoma (Thiagalingam et al, 1996). These alterations are detected at the cDNA level in the form of exon losses.…”

Section: Loh At 3p and The Fhit Gene In CCmentioning

confidence: 99%

The molecular genetics of cervical carcinoma

1999

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In the pathogenesis of cervical carcinoma there are three major components, two of them related to the role of human papillomaviruses (HPV). First, the effect of viral E6 and E7 proteins. Second, the integration of viral DNA in chromosomal regions associated with well known tumour phenotypes. Some of these viral integrations occur recurrently at specific chromosomal locations, such as 8q24 and 12q15, both harbouring HPV18 and HPV16. And third, there are other recurrent genetic alterations not linked to HPV. Recurrent losses of heterozygosity (LOH) have been detected in chromosome regions 3p14–22, 4p16, 5p15, 6p21–22, 11q23, 17p13.3 without effect on p53, 18q12–22 and 19q13, all of them suggesting the alteration of putative tumour suppressor genes not yet identified. Recurrent amplification has been mapped to 3q+ arm, with the common region in 3q24–28 in 90% of invasive carcinomas. The mutator phenotype, microsatellite instability, plays a minor role and is detected in only 7% of cervical carcinomas. The development of cervical carcinoma requires the sequential occurrence and selection of several genetic alterations. The identification of the specific genes involved, and their correlation with specific tumour properties and stages could improve the understanding and perhaps the management of cervical carcinoma. © 1999 Cancer Research Campaign

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“…69 Another study found low rates of alterations in the FHIT open reading frame in primary esophageal cancers, although lack of expression of FHIT transcripts was common in esophageal cancer cell lines. 70 However, aberrant FHIT transcripts have…”

Section: Chromosome 3pmentioning

confidence: 99%

Molecular Biology of Barrett’s Adenocarcinoma

Wijnhoven

Tilanus²,

Dinjens³

2001

Annals of Surgery

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ObjectiveTo review the current knowledge on the genetic alterations involved in the development and progression of Barrett's esophagus-associated neoplastic lesions. Summary Background DataBarrett's esophagus (BE) is a premalignant condition in which the normal squamous epithelium of the esophagus is replaced by metaplastic columnar epithelium. BE predisposes patients to the development of esophageal adenocarcinoma. Endoscopic surveillance can detect esophageal adenocarcinomas when they are early and curable, but most of the adenocarcinomas are detected at an advanced stage. Despite advances in multimodal therapy, the prognosis for invasive esophageal adenocarcinoma is poor. A better understanding of the molecular evolution of the Barrett's metaplasia to dysplasia to adenocarcinoma sequence may allow improved diagnosis, therapy, and prognosis. MethodsThe authors reviewed data from the published literature to address what is known about the molecular changes thought to be important in the pathogenesis of BE-associated neoplastic lesions. ResultsThe progression of Barrett's metaplasia to adenocarcinoma is associated with several changes in gene structure, gene expression, and protein structure. Some of the molecular alterations already showed promise as markers for early cancer detection or prognostication. Among these, alterations in the p53 and p16 genes and cell cycle abnormalities or aneuploidy appear to be the most important and well-characterized molecular changes. However, the exact sequence of events is not known, and probably multiple molecular pathways interact and are involved in the progression of BE to adenocarcinoma. ConclusionsFurther research into the molecular biology of BE-associated adenocarcinoma will enhance our understanding of the genetic events critical for the initiation and progression of Barrett's adenocarcinoma, leading to more effective surveillance and treatment.Since 1970, the incidence of adenocarcinomas of the esophagus has increased in many countries at a rate that exceeds that of any other malignancy.

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FHIT gene alterations in esophageal cancer and ulcerative colitis (UC)

Cited by 34 publications

References 13 publications

Molecular analysis of the FHIT gene in human prostate cancer

Molecular analysis of the FHIT gene in human prostate cancer

The molecular genetics of cervical carcinoma

Molecular Biology of Barrett’s Adenocarcinoma

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