Deletion of the FHIT gene in neoplastic and invasive cervical lesions is related to high‐risk HPV infection but is independent of histopathological features

Butler, David; Collins, Claire; Mabruk, Mohamed; Walsh, Caitriona Barry; Leader, M.; Kay, Elaine W.

doi:10.1002/1096-9896(2000)9999:9999<::aid-path718>3.3.co;2-8

Cited by 9 publications

(11 citation statements)

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“…It is suggested that high-risk HPV infection is related to the FHIT abnormalities [8,9,10,11]. A recent in vivo study discovered that HPV inserts its genes into the chromosome 3 fragile site FRA3B (located at 3p14.2), deleting a piece of DNA, and it was also postulated that viral induction of fragile sites involves a delay in DNA replication [31].…”

Section: Fig 2 Pcr Amplification Of Hpvmentioning

confidence: 99%

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Deletion of the FHIT gene in human colorectal cancer is independent of high-risk HPV infection

Shun

Luo

et al. 2002

Int J Colorectal Dis

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Section: Fig 2 Pcr Amplification Of Hpvmentioning

confidence: 99%

“…Recent studies suggest that human papillomavirus (HPV) infection is correlated with deletion of the FHIT gene [8,9,10,11]. HPVs belongs to a large family of viruses, the papova viridae, and more than a 100 different types have been identified in humans.…”

Section: Introductionmentioning

confidence: 99%

Deletion of the FHIT gene in human colorectal cancer is independent of high-risk HPV infection

Shun

Luo

et al. 2002

Int J Colorectal Dis

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“…There is a fragile site (FRA3B) adjacent to the FHIT gene. According to Butler et al (2000), there is a link between the integration of viral HPV DNA and FHIT gene deletion. The fragile site (FRA3B) is a site for the integration of HPV DNA (Thorland et al 2000).…”

Section: Fhit Lohmentioning

confidence: 99%

Human papillomavirus and lung cancinogenesis: an overview

Freitas

Gurgel

Lima

et al. 2016

J Cancer Res Clin Oncol

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Lung cancer is the most common cause of cancer deaths worldwide. Although tobacco smoking is considered to be the main risk factor and the most well-established risk factor for lung cancer, a number of patients who do not smoke have developed this disease. This number varies between 15 % to over one-half of lung cancer cases, and the deaths from lung cancer in non-smokers are increasing every year. There are many other agents that are thought to be etiological, including diesel exhaust exposure, metals, radiation, radon, hormonal factors, cooking oil, air pollution and infectious diseases, such as human papillomavirus (HPV). Studies in various parts of the world have detected HPV DNA at different rates in lung tumors. However, the role of HPV in lung cancer is still unclear. Thus, in this review, we investigated some molecular mechanisms of HPV protein activity in host cells, the entry of HPV into lung tissue and the possible route used by the virus to reach the lung cells.

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“…A ratio of ratios between the normal and tumour PCR products was calculated to give an overall allele ratio. The cut-off value for allelic imbalance/loss of heterozygosity (AI/LOH) was 0.74, as was previously published from studies in our laboratory [1,22,24]. Microsatellite instability (MSI) was defined as the presence of novel alleles or extra peaks in the tumour DNA sample not seen in the normal DNA.…”

Section: Tissue Samples and Pathological Analysismentioning

confidence: 99%

Leiomyosarcoma and malignant fibrous histiocytoma share similar allelic imbalance pattern at 9p

et al. 2005

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Formalin-fixed, paraffin-embedded tissue from 45 soft tissue sarcomas was analysed for allelic imbalance/loss of heterozygosity (AI/LOH) of chromosome 9. The specimens consisted of 17 cases of soft tissue leiomyosarcoma (LMS), 4 cases of cutaneous LMS, 22 cases of conventional malignant fibrous histiocytoma (MFH) and 2 cases of angiomatoid fibrous histiocytoma. All cases were categorised morphologically and immunohistochemically. DNA was microdissected from normal and neoplastic tissues. AI/LOH was performed using six microsatellite markers on the 9p region. The frequency of allelic imbalance at different loci on chromosome 9p was analysed in LMS and MFH and then compared with values previously examined in synovial sarcoma and malignant peripheral nerve sheath tumour. Although AI/LOH and microsatellite instability (MSI) were more frequent in MFH, LMS and MFH groups showed similar patterns of allelic imbalance at the 9p region. Alterations of chromosome 9p have been reported in many cell lines and tumours including LMS and MFH. 9p21 region encodes p16(INK4A) and p15(INK4B). Allelic imbalance observed at 9p 21 in this study suggests that alterations of the negative cell cycle regulators may be an important step in the pathogenesis of MFH and LMS. However, the most frequent allelic imbalance was observed at 9p24 at D9S230. Alterations of this locus were very rare in synovial sarcoma and malignant peripheral nerve sheath tumours and were absent in cutaneous LMS and angiomatoid fibrous histiocytoma. This locus may point to the existence of a genetically altered tumour suppressor gene involved in the pathogenesis of LMS and MFH. Our results support the hypothesis that MFHs may represent a morphological pathway in tumour progression of LMSs.

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Deletion of the FHIT gene in neoplastic and invasive cervical lesions is related to high‐risk HPV infection but is independent of histopathological features

Cited by 9 publications

References 0 publications

Deletion of the FHIT gene in human colorectal cancer is independent of high-risk HPV infection

Deletion of the FHIT gene in human colorectal cancer is independent of high-risk HPV infection

Human papillomavirus and lung cancinogenesis: an overview

Leiomyosarcoma and malignant fibrous histiocytoma share similar allelic imbalance pattern at 9p

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