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We began analyzing https://link.springer.com/article/10.1007/s00262-009-0806-4, but it redirected us to https://link.springer.com/article/10.1007/s00262-009-0806-4. The analysis below is for the second page.

Title[redir]:
Naturally occurring systemic immune responses to HPV antigens do not predict regression of CIN2/3 | Cancer Immunology, Immunotherapy
Description:
Essentially all squamous cervical cancers and their precursor lesions, high grade cervical intraepithelial neoplasia (CIN2/3), are caused by persistent human papillomavirus (HPV) infection. However, not all CIN2/3 lesions progress to cancer. In a brief, observational study window monitoring subjects with CIN2/3 from protocol entry (biopsy diagnosis) to definitive therapy (cervical conization) at week 15, in a cohort of 50 subjects, we found that 26% of CIN2/3 lesions associated with HPV16, the genotype most commonly associated with disease, underwent complete histologic regression. Nonetheless, HPV16-specific T cell responses measured in peripheral blood obtained at the time of study entry and at the time of conization were marginally detectable directly ex vivo, and did not correlate with lesion regression. This finding suggests that, in the setting of natural infection, immune responses which are involved in elimination of cervical dysplastic epithelium are not represented to any great extent in the systemic circulation.

Matching Content Categories {πŸ“š}

  • Health & Fitness
  • Education
  • Science

Content Management System {πŸ“}

What CMS is doi.org built with?

Custom-built

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Traffic Estimate {πŸ“ˆ}

What is the average monthly size of doi.org audience?

πŸ™οΈ Massive Traffic: 50M - 100M visitors per month


Based on our best estimate, this website will receive around 80,904,851 visitors per month in the current month.

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We're unsure if the website is profiting.

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Keywords {πŸ”}

article, cancer, cervical, human, pubmed, google, scholar, cas, hpv, papillomavirus, regression, cin, privacy, cookies, trimble, lesions, content, publish, search, systemic, immune, responses, intraepithelial, study, subjects, access, usa, data, information, log, journal, research, immunology, immunotherapy, december, cornelia, peng, thoburn, squamous, neoplasia, infection, time, discover, immunol, download, author, department, johns, hopkins, university,

Topics {βœ’οΈ}

month download article/chapter high-grade cervical dysplasia article cancer immunology squamous cervical cancers human papillomavirus-induced lesions cervical intraepithelial neoplasia full article pdf privacy choices/manage cookies peripheral blood obtained cell responses measured cervical dysplastic epithelium persistent human papillomavirus human papillomavirus type immune responses restricted viral peptides european economic area marginally detectable directly international biological study da silva dm human papillomavirus infection conditions privacy policy accepting optional cookies ferdynand kos cin2/3 lesions progress author information authors article trimble cervical cancer article log journal finder publish systemic circulation christopher thoburn human papillomavirus article cite check access pathology instant access related subjects trimble department human keratinocytes cervical conization privacy policy personal data hpv antigens books a immunotherapy aims affiliations department usa cornelia optional cookies manage preferences precursor lesions

Schema {πŸ—ΊοΈ}

WebPage:
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         headline:Naturally occurring systemic immune responses to HPV antigens do not predict regression of CIN2/3
         description:Essentially all squamous cervical cancers and their precursor lesions, high grade cervical intraepithelial neoplasia (CIN2/3), are caused by persistent human papillomavirus (HPV) infection. However, not all CIN2/3 lesions progress to cancer. In a brief, observational study window monitoring subjects with CIN2/3 from protocol entry (biopsy diagnosis) to definitive therapy (cervical conization) at week 15, in a cohort of 50 subjects, we found that 26% of CIN2/3 lesions associated with HPV16, the genotype most commonly associated with disease, underwent complete histologic regression. Nonetheless, HPV16-specific T cell responses measured in peripheral blood obtained at the time of study entry and at the time of conization were marginally detectable directly ex vivo, and did not correlate with lesion regression. This finding suggests that, in the setting of natural infection, immune responses which are involved in elimination of cervical dysplastic epithelium are not represented to any great extent in the systemic circulation.
         datePublished:2009-12-13T00:00:00Z
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            Cervical dysplasia
            Regression
            Systemic immune response
            Oncology
            Immunology
            Cancer Research
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      headline:Naturally occurring systemic immune responses to HPV antigens do not predict regression of CIN2/3
      description:Essentially all squamous cervical cancers and their precursor lesions, high grade cervical intraepithelial neoplasia (CIN2/3), are caused by persistent human papillomavirus (HPV) infection. However, not all CIN2/3 lesions progress to cancer. In a brief, observational study window monitoring subjects with CIN2/3 from protocol entry (biopsy diagnosis) to definitive therapy (cervical conization) at week 15, in a cohort of 50 subjects, we found that 26% of CIN2/3 lesions associated with HPV16, the genotype most commonly associated with disease, underwent complete histologic regression. Nonetheless, HPV16-specific T cell responses measured in peripheral blood obtained at the time of study entry and at the time of conization were marginally detectable directly ex vivo, and did not correlate with lesion regression. This finding suggests that, in the setting of natural infection, immune responses which are involved in elimination of cervical dysplastic epithelium are not represented to any great extent in the systemic circulation.
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         Cervical dysplasia
         Regression
         Systemic immune response
         Oncology
         Immunology
         Cancer Research
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      name:Ferdynand Kos
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