Cervical intraepithelial neoplasia.

Buckley, C. H.; Butler, E B; Fox, H.

doi:10.1136/jcp.35.1.1

Cited by 201 publications

(71 citation statements)

References 25 publications

(1 reference statement)

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“…In the cervix, squamous cell carcinoma develops from an initially low grade and later high grade squamous dysplasia before developing into in-situ and then invasive malignancy (Buckley et al, 1982). Evidence for comparable disease progression in the breast is largely based on epidemiological studies.…”

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Increasing chromosome 1 copy number parallels histological progression in breast carcinogenesis

Cummings

Aubele²,

Mattis

et al. 2000

Br J Cancer

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Summary Chromosome 1 copy number in the benign breast lesions hyperplasia and atypical duct hyperplasia (ADH) was investigated using fluorescence in situ hybridization on paraffin sections. Progression of chromosome 1 changes occurring in parallel with histological progression from normal through hyperplasia and ADH to ductal carcinoma in situ (DCIS) and invasive carcinoma was also assessed, both overall and within individual patients. The mean signal number for normal cells was 1.14, while that for hyperplasia was 1.56 and ADH was 1.5, while values for DCIS of 1.95 and invasive duct carcinoma of 1.79, were higher (P < 0.001). Six of the seven cases also showed a significant trend towards an increasing proportion of cells with greater than 2 signals per nucleus occurring with histological progression (P < 0.001). These results support the concept that benign proliferative breast disease is a biological precursor of in-situ and invasive ductal carcinoma, the early histological changes possibly indicating a field effect with further genetic changes required for the development of a malignant phenotype.

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“…Many adenocarcinomas of the endometrium arise on a background of endometrial hyperplasia with and without atypia (Fox and Buckley, 1982). In the cervix, squamous cell carcinoma develops from an initially low grade and later high grade squamous dysplasia before developing into in-situ and then invasive malignancy (Buckley et al, 1982).…”

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confidence: 99%

Increasing chromosome 1 copy number parallels histological progression in breast carcinogenesis

Cummings

Aubele²,

Mattis

et al. 2000

Br J Cancer

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“…Biopsies were taken at the time of serum sampling. Histological diagnosis was undertaken by the Pathology Department of St Mary's Hospital, according to published criteria (Buckley et al, 1982). The histological diagnosis was used to classify the 'COL' population into 18 borderline cytology, eight CIN 1, 20 CIN 2 and 26 CIN 3.…”

Section: Elisamentioning

confidence: 99%

Differences in serological IgA responses to recombinant baculovirus-derived human papillomavirus E2 protein in the natural history of cervical neoplasia

Rocha‐Zavaleta

Jordan²,

Pepper³

et al. 1997

Br J Cancer

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Summary Infection with certain types of human papillomavirus (HPV) presents a high risk for the subsequent development of cervical intraepithelial neoplasia (CIN) and cervical carcinoma. Immunological mechanisms are likely to play a role in control of cervical HPV lesions.The HPV E2 protein has roles in virus replication and transcription, and loss of E2 functions may be associated with progression of cervical neoplasia. Accordingly, it is of interest to monitor immune responses to the E2 protein, and previous studies have reported associations between serological reactivity to E2 peptide antigens and cervical neoplasia. In order to investigate serological responses to native, full-length E2 protein, we expressed HPV-1 6 E2 proteins with and without an N-terminal polyhistidine tag using the baculovirus system. Purified HPV-1 6 E2 protein was used to develop enzyme-linked immunosorbent assays to detect serological IgG and IgA responses in cervical neoplasia patients and controls. We found that serum IgA levels against the E2 protein were elevated in CIN patients relative to normal control subjects but were not elevated in cervical cancer patients. Moreover, there appeared to be a gradient of response within cervical neoplasia such that the highest antibody levels were seen in lower grades of neoplasia up to CIN 2, whereas lower levels were observed in CIN 3 and still lower levels in cervical carcinoma. These findings suggest that the IgA antiboay response to E2 may associate with stage and progression in cervical neoplasia.Keywords: human papillomavirus; serology; E2 protein; cervical neoplasia; baculovirus Human papillomaviruses comprise a large group of DNA viruses that exclusively infect epithelium. Certain types of HPV are capable of infecting genital mucosal epithelium, which can result in cervical intraepithelial neoplasia (CIN). CIN is classified by histopathology into stages 1, 2 and 3, which are thought to represent progressively advanced precursor lesions of cervical carcinoma (CaCx). HPV infection is a prerequisite for the genesis of almost all CIN and cervical carcinomas Schiffman et al, 1993). Most CIN contains detectable HPV DNA. HPV-16, -18 and related types have been classed as 'high-risk' genital HPV types because of their associations with high-grade CIN and CaCx (reviewed in Walboomers et al, 1994).Genital-type HPV genomes are approximately 8 kbp in length and comprise six open reading frames (ORFs) encoding early functions (E1-E7) and two late ORFs encoding the capsid proteins. The E2 ORF encodes an approximately 45-kDa nuclear phosphoprotein that binds to specific sequence elements within the HPV long control region (LCR). Binding of the E2 protein to these elements functions in regulation of HPV transcription and replication. Binding of E2 to sites near the constitutive early promoter of HPV-16 or -18 can negatively regulate expression of the two major

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“…In most cases there appears to be a progression from mild cervical intra-epithelial neoplasia (CIN 1), through moderate (CIN 2), to severe dysplasia/carcinoma-in situ (CIN 3) before frank invasive carcinoma supervenes (Reagan et al, 1953;Richart, 1967;Buckley et al, 1982). In a small number of women, the diagnosis of invasive tumour is made soon after a previous negative smear, with no detectable transition stage (Ashley, 1966;Hakama & Penttinen, 1981;Peters et al, 1988).…”

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confidence: 99%

XH1 – a new cervical carcinoma cell line and xenograft model of tumour invasion, 'metastasis' and regression

Han

Lyle²,

Eustace³

et al. 1991

Br J Cancer

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Cervical intraepithelial neoplasia.

Cited by 201 publications

References 25 publications

Increasing chromosome 1 copy number parallels histological progression in breast carcinogenesis

Increasing chromosome 1 copy number parallels histological progression in breast carcinogenesis

Differences in serological IgA responses to recombinant baculovirus-derived human papillomavirus E2 protein in the natural history of cervical neoplasia

XH1 – a new cervical carcinoma cell line and xenograft model of tumour invasion, 'metastasis' and regression

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