Behavior of mild cervical dysplasia during long‐term follow‐up

Nasiell, K; Roger, V.; Nasiell, M

doi:10.1016/0020-7292(87)90258-x

Cited by 142 publications

(102 citation statements)

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“…First, there appears to be an increased incidence of HPV-associated genital cancer amongst immunosuppressed patients, whilst only a minority of genital HPV infections result in the development of cancer amongst otherwise healthy individuals. [2][3][4] Second, infiltrating CD4 + (T helper cells; Th1) and CD8 + (cytotoxic or suppressor T cells) T cells have been observed within spontaneously regressing HPV-associated warts. 4 Third, studies have demonstrated that immunized animals are protected from papillomavirus infections and from transplanted tumour cells expressing HPV E6 or E7 oncoproteins.…”

mentioning

confidence: 99%

Induction of human papillomavirus type 16‐specific immunologic responses in a normal and an human papillomavirus‐infected populations

Cheng

Lee²,

et al. 2005

Immunology

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Human papillomavirus (HPV) infection represents the most important risk factor for developing cervical cancer. Although there are over 20 oncogenic HPV genotypes, HPV16 is the most prevalent type in cervical cancer compared with other HPV genotypes regardless of geographical origin. SummaryHuman papillomavirus (HPV) infection, especially with the oncogenic genotypes, is the most important risk factor for developing cervical cancer. We focused on generating HPV16 E7-specific cytotoxic CD8 + T lymphocytes and evaluating HPV16 E7-specific immune responses in HPV16-infected and uninfected populations. Peripheral blood mononuclear cells (PBMCs) were first collected from an uninfected group with an human lymphocyte antigen (HLA) A2 haplotype (four volunteers). Mature monocyte-derived dendritic cells (DCs) were generated from the PBMCs and pulsed with one of two HLA-A2-restricted E7 peptides, aa 11-20 [YMLDLQPETT] and aa 86-93 [TLGIVCPI], as antigen presenting cells. The autologous naïve or cultured PBMCs were then cultured with peptide-pulsed DCs to detect the HPV16 E7-specific immune responses by a variety of techniques such as enzyme-linked immunosorbent assay (ELISA), enzyme-linked immunospot (ELISPOT) assay and cytotoxic T lymphocyte assay. Interferon-c (IFN-c) from E7-specific cytotoxic CD8 + T lymphocytes stimulated with the respective peptide was detected by ELISA. Using ELISPOT analysis, a marked increase in the number of IFN-c-secreting CD8 + E7-specific lymphocytes was observed following peptide stimulation. Cultured CD8 + T lymphocytes were highly cytotoxic against the CaSki cells. PBMCs were then colleted from an HPV16-infected population of the HLA-A2 haplotype, including four persons of HPV16 infection only, four with cervical intraepithelial neoplasia (CIN) lesions, and four cervical cancer patients. We then compared the immunologic responses to E7 between HPV16-infected and uninfected populations by ELISA and ELISPOT assay. The E7-specific immunologic responses of the HPV16-infected populations were significantly higher than those of the uninfected population. In addition, persons with an HPV16 infection only or those with CIN lesions generated higher E7-specific immunologic responses than cervical cancer patients. Our results demonstrate methods for evaluating E7-sepcific immunologic responses and reflect the biological responses of HPV16-infected people during different periods of cervical disease.

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confidence: 99%

Induction of human papillomavirus type 16‐specific immunologic responses in a normal and an human papillomavirus‐infected populations

Cheng

Lee²,

et al. 2005

Immunology

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“…21 Among 16,740 women with LSIL cytology, Melnikow et al estimated the rate of invasive cancer over a 24-month period to be 0.15% (95% CI, 0.0 -0.7%). However, in at least 2 of the original publications, 22,23 some of the cancers were diagnosed 6 -12 years after the low-grade cytology report. In these studies, the women were lost to follow-up for lengthy intervening periods.…”

Section: Discussionmentioning

confidence: 99%

Outcome after a cervical cytology report of low-grade squamous abnormality in Australia

Mitchell

2005

Cancer

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“…These lesions can often be identified in regions surrounding an invasive tumor, in biopsies taken from patients undergoing diagnostic evaluation for suspicion of cancer, or in samples acquired during preventive screening. Currently, limited metrics exist to identify lesions that will likely progress to carcinoma and require intervention from those that will naturally regress or remain stable (3,4). As imaging modalities and screening guidelines advance, the number of lesions identified will grow resulting in a need for more precise risk stratification methods and effective early intervention.…”

Section: The Bottleneck For Cancer Prevention and Early Detectionmentioning

confidence: 99%

The Case for a Pre-Cancer Genome Atlas (PCGA)

Campbell

Mazzilli

Reid

et al. 2016

Cancer Prevention Research

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Understanding the earliest molecular and cellular events associated with cancer initiation remains a key bottleneck to transforming our approach to cancer prevention and detection. While TCGA has provided unprecedented insights into the genomic events associated with advanced stage cancer, there have been few studies comprehensively profiling premalignant and early-stage disease or elucidating the role of the microenvironment in premalignancy and tumor initiation. In this article, we make a call for development of a "Pre-Cancer Genome Atlas (PCGA)," a concerted initiative to characterize the molecular alterations in premalignant lesions and the corresponding changes in the microenvironment associated with progression to invasive carcinoma. This initiative will require a multicenter coordinated effort to comprehensively profile (cellular and molecular) premalignant lesions and their corresponding "field of injury" collected longitudinally as the lesion progresses towards or regresses from frank malignancy across multiple tumor types. Genomic characterization of alterations in premalignant lesions and their microenvironment, for both bulk tissue and single cells, will enable development of biomarkers for early detection and risk stratification as well as allow for the development of novel targeted cancer interception strategies. The multi-institutional and multidisciplinary collaborative "big-data" effort underlying the PCGA will help usher in a new era of precision medicine for cancer detection and prevention. Cancer Prev Res; 9(2); 119-24. Ó2016 AACR. The Bottleneck for Cancer Prevention and Early DetectionOne of the critical barriers to developing new approaches for cancer detection and prevention is the lack of understanding of the key molecular and cellular changes that cause cancer initiation and progression. Unlike the extensive work that has been done profiling advanced stage tumors, few studies have comprehensively profiled the genomic alterations found in precancerous tissues. Premalignant lesions are currently characterized by histologic changes that precede the development of invasive carcinoma (1, 2). These lesions can often be identified in regions surrounding an invasive tumor, in biopsies taken from patients undergoing diagnostic evaluation for suspicion of cancer, or in samples acquired during preventive screening. Currently, limited metrics exist to identify lesions that will likely progress to carcinoma and require intervention from those that will naturally regress or remain stable (3, 4). As imaging modalities and screening guidelines advance, the number of lesions identified will grow resulting in a need for more precise risk stratification methods and effective early intervention. Characterization of the molecular alterations in premalignant lesions and the corresponding

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Behavior of mild cervical dysplasia during long‐term follow‐up

Cited by 142 publications

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Induction of human papillomavirus type 16‐specific immunologic responses in a normal and an human papillomavirus‐infected populations

Induction of human papillomavirus type 16‐specific immunologic responses in a normal and an human papillomavirus‐infected populations

Outcome after a cervical cytology report of low-grade squamous abnormality in Australia

The Case for a Pre-Cancer Genome Atlas (PCGA)

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