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We are analyzing https://link.springer.com/article/10.1186/bcr306.

Title:
In vivo cell kinetics in breast carcinogenesis | Breast Cancer Research
Description:
Background Disruption of the balance between apoptosis and proliferation is considered to be an important factor in the development and progression of tumours. In the present study we determined the in vivo cell kinetics along the spectrum of apparently normal epithelium, hyperplasia, preinvasive lesions and invasive carcinoma, in breast tissues affected by fibrocystic changes in which preinvasive and/or invasive lesions developed, as a model of breast carcinogenesis. Materials and methods A total of 32 areas of apparently normal epithelium and 135 ductal proliferative and neoplastic lesions were studied. More than one epithelial lesion per case were analyzed. The apoptotic index (AI) and the proliferative index (PI) were expressed as the percentage of TdT-mediated dUTP-nick end-labelling (TUNEL) and Ki-67-positive cells, respectively. The PI/AI (P/A index) was calculated for each case. Results The AIs and PIs were significantly higher in hyperplasia than in apparently normal epithelium (P = 0.04 and P = 0.0005, respectively), in atypical hyperplasia than in hyperplasia (P = 0.01 and P = 0.04, respectively) and in invasive carcinoma than in in situ carcinoma (P < 0.001 and P < 0.001, respectively). The two indices were similar in atypical hyperplasia and in in situ carcinoma. The P/A index increased significantly from normal epithelium to hyperplasia (P = 0.01) and from preinvasive lesions to invasive carcinoma (P = 0.04) whereas it was decreased (non-significantly) from hyperplasia to preinvasive lesions. A strong positive correlation between the AIs and the PIs was found (r = 0.83, P < 0.001). Conclusion These findings suggest accelerating cell turnover along the continuum of breast carcinogenesis. Atypical hyperplasias and in situ carcinomas might be kinetically similar lesions. In the transition from normal epithelium to hyperplasia and from preinvasive lesions to invasive carcinoma the net growth of epithelial cells results from a growth imbalance in favour of proliferation. In the transition from hyperplasia to preinvasive lesions there is an imbalance in favour of apoptosis.
Website Age:
28 years and 1 months (reg. 1997-05-29).

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Custom-built

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🌠 Phenomenal Traffic: 5M - 10M visitors per month


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Keywords {πŸ”}

breast, apoptosis, carcinoma, hyperplasia, cell, google, scholar, situ, invasive, article, pubmed, lesions, cells, cas, cancer, carcinomas, apoptotic, ductal, proliferation, epithelium, normal, preinvasive, proliferative, index, study, atypical, tissue, positive, slides, tunel, activity, progression, antibody, sections, epithelial, growth, pathol, carcinogenesis, ais, pis, present, higher, apparently, lesion, found, criteria, negative, results, indices, correlation,

Topics {βœ’οΈ}

terminal-deoxynucleotidyl-transferase-mediated dutp-fitc nick tdt-mediated dutp-nick end-labelling poly-l-lysine-coated glass slides apoptosis avidin-biotin-peroxidase complex avidin-biotin-peroxidase complex ibm-compatible personal computer contained dutp-digoxigenin pre-menopausal human breast cyclin b1/cdc2 kinase mann-whitney tests demonstrated mann-whitney tests showed situ end-labelling proliferating-cell nuclear antigen full size image maria bai md metaplasia-dysplasia-carcinoma sequence fitc-conjugated antidigoxigenin antibody breast cancers determined breast cancer research low-grade intraepithelial neoplasia paraffin-embedded tissue samples avoid false-positive results privacy choices/manage cookies polyclonal rabbit antibody human breast cancer poorly differentiated models accelerating cell turnover steady-state condition tdt reaction step normal rabbit serum tunel-positive apoptotic cells tumor suppressor genes human ki-67 protein article bai lelle rj laryngeal carcinomas showed human hepatocellular carcinomas tunel assay showed reactive lymph nodes van diest ps adding peroxidase-conjugated cell proliferation suggest mann-whitney test static-cell population increasing cell turnover multicolor immunofluorescence reveals potent mechanisms exist eosin-stained slides phosphate-buffered saline conjugated antidigoxigenin antibody

Schema {πŸ—ΊοΈ}

WebPage:
      mainEntity:
         headline:In vivo cell kinetics in breast carcinogenesis
         description:Disruption of the balance between apoptosis and proliferation is considered to be an important factor in the development and progression of tumours. In the present study we determined the in vivo cell kinetics along the spectrum of apparently normal epithelium, hyperplasia, preinvasive lesions and invasive carcinoma, in breast tissues affected by fibrocystic changes in which preinvasive and/or invasive lesions developed, as a model of breast carcinogenesis. A total of 32 areas of apparently normal epithelium and 135 ductal proliferative and neoplastic lesions were studied. More than one epithelial lesion per case were analyzed. The apoptotic index (AI) and the proliferative index (PI) were expressed as the percentage of TdT-mediated dUTP-nick end-labelling (TUNEL) and Ki-67-positive cells, respectively. The PI/AI (P/A index) was calculated for each case. The AIs and PIs were significantly higher in hyperplasia than in apparently normal epithelium (P = 0.04 and P = 0.0005, respectively), in atypical hyperplasia than in hyperplasia (P = 0.01 and P = 0.04, respectively) and in invasive carcinoma than in in situ carcinoma (P &lt; 0.001 and P &lt; 0.001, respectively). The two indices were similar in atypical hyperplasia and in in situ carcinoma. The P/A index increased significantly from normal epithelium to hyperplasia (P = 0.01) and from preinvasive lesions to invasive carcinoma (P = 0.04) whereas it was decreased (non-significantly) from hyperplasia to preinvasive lesions. A strong positive correlation between the AIs and the PIs was found (r = 0.83, P &lt; 0.001). These findings suggest accelerating cell turnover along the continuum of breast carcinogenesis. Atypical hyperplasias and in situ carcinomas might be kinetically similar lesions. In the transition from normal epithelium to hyperplasia and from preinvasive lesions to invasive carcinoma the net growth of epithelial cells results from a growth imbalance in favour of proliferation. In the transition from hyperplasia to preinvasive lesions there is an imbalance in favour of apoptosis.
         datePublished:2001-06-05T00:00:00Z
         dateModified:2001-06-05T00:00:00Z
         pageStart:1
         pageEnd:8
         sameAs:https://doi.org/10.1186/bcr306
         keywords:
            apoptosis
            breast carcinoma
            hyperplasia
            proliferation
            Cancer Research
            Oncology
            Surgical Oncology
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                     name:University of Thessalia
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ScholarlyArticle:
      headline:In vivo cell kinetics in breast carcinogenesis
      description:Disruption of the balance between apoptosis and proliferation is considered to be an important factor in the development and progression of tumours. In the present study we determined the in vivo cell kinetics along the spectrum of apparently normal epithelium, hyperplasia, preinvasive lesions and invasive carcinoma, in breast tissues affected by fibrocystic changes in which preinvasive and/or invasive lesions developed, as a model of breast carcinogenesis. A total of 32 areas of apparently normal epithelium and 135 ductal proliferative and neoplastic lesions were studied. More than one epithelial lesion per case were analyzed. The apoptotic index (AI) and the proliferative index (PI) were expressed as the percentage of TdT-mediated dUTP-nick end-labelling (TUNEL) and Ki-67-positive cells, respectively. The PI/AI (P/A index) was calculated for each case. The AIs and PIs were significantly higher in hyperplasia than in apparently normal epithelium (P = 0.04 and P = 0.0005, respectively), in atypical hyperplasia than in hyperplasia (P = 0.01 and P = 0.04, respectively) and in invasive carcinoma than in in situ carcinoma (P &lt; 0.001 and P &lt; 0.001, respectively). The two indices were similar in atypical hyperplasia and in in situ carcinoma. The P/A index increased significantly from normal epithelium to hyperplasia (P = 0.01) and from preinvasive lesions to invasive carcinoma (P = 0.04) whereas it was decreased (non-significantly) from hyperplasia to preinvasive lesions. A strong positive correlation between the AIs and the PIs was found (r = 0.83, P &lt; 0.001). These findings suggest accelerating cell turnover along the continuum of breast carcinogenesis. Atypical hyperplasias and in situ carcinomas might be kinetically similar lesions. In the transition from normal epithelium to hyperplasia and from preinvasive lesions to invasive carcinoma the net growth of epithelial cells results from a growth imbalance in favour of proliferation. In the transition from hyperplasia to preinvasive lesions there is an imbalance in favour of apoptosis.
      datePublished:2001-06-05T00:00:00Z
      dateModified:2001-06-05T00:00:00Z
      pageStart:1
      pageEnd:8
      sameAs:https://doi.org/10.1186/bcr306
      keywords:
         apoptosis
         breast carcinoma
         hyperplasia
         proliferation
         Cancer Research
         Oncology
         Surgical Oncology
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         name:Assistant Professor of Pathology, Department of Pathology, Medical School, University of Ioannina, Ioannina, Greece
         type:PostalAddress
      name:University Hospital of Ioannina
      address:
         name:Statistics, University Hospital of Ioannina, Ioannina, Greece
         type:PostalAddress
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      name:Maria Bai
      affiliation:
            name:University of Ioannina
            address:
               name:Assistant Professor of Pathology, Department of Pathology, Medical School, University of Ioannina, Ioannina, Greece
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            name:University of Ioannina
            address:
               name:Assistant Professor of Pathology, Department of Pathology, Medical School, University of Ioannina, Ioannina, Greece
               type:PostalAddress
            type:Organization
      name:Sevasti Kamina
      affiliation:
            name:University of Ioannina
            address:
               name:Assistant Professor of Pathology, Department of Pathology, Medical School, University of Ioannina, Ioannina, Greece
               type:PostalAddress
            type:Organization
      name:Asimina Demou
      affiliation:
            name:University of Ioannina
            address:
               name:Assistant Professor of Pathology, Department of Pathology, Medical School, University of Ioannina, Ioannina, Greece
               type:PostalAddress
            type:Organization
      name:Panayiota Zagorianakou
      affiliation:
            name:University of Ioannina
            address:
               name:Assistant Professor of Pathology, Department of Pathology, Medical School, University of Ioannina, Ioannina, Greece
               type:PostalAddress
            type:Organization
      name:Aphroditi Katsaraki
      affiliation:
            name:University Hospital of Ioannina
            address:
               name:Statistics, University Hospital of Ioannina, Ioannina, Greece
               type:PostalAddress
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      name:Panayiotis Kanavaros
      affiliation:
            name:University of Thessalia
            address:
               name:Department of Histology, Medical School, University of Thessalia, Larissa, Greece
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Assistant Professor of Pathology, Department of Pathology, Medical School, University of Ioannina, Ioannina, Greece
      name:Assistant Professor of Pathology, Department of Pathology, Medical School, University of Ioannina, Ioannina, Greece
      name:Assistant Professor of Pathology, Department of Pathology, Medical School, University of Ioannina, Ioannina, Greece
      name:Assistant Professor of Pathology, Department of Pathology, Medical School, University of Ioannina, Ioannina, Greece
      name:Assistant Professor of Pathology, Department of Pathology, Medical School, University of Ioannina, Ioannina, Greece
      name:Statistics, University Hospital of Ioannina, Ioannina, Greece
      name:Department of Histology, Medical School, University of Thessalia, Larissa, Greece

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