{"id":{"repo_id":"lund","oai_identifier":"oai:lup.lub.lu.se:f51bcf9a-5bd4-4c62-a91d-d703efa9ccb4"},"canonical_url":"https://search.dev.ndltd.org/etd/lund/oai:lup.lub.lu.se:f51bcf9a-5bd4-4c62-a91d-d703efa9ccb4","repository":{"repo_id":"lund","name":"University of Lund","base_url":"https://lup.lub.lu.se/oai"},"display":{"title":"Invasion and Proliferation in Malignant Cells","abstract":"Two key events in the oncogenic process of tumor cells are to acquire uncontrolled proliferation and invasive properties. This allows the tumor to grow and invade beyond the tissue from which the tumor cells originate. We here specifically studied p16 and ERK1/2 with special focus on and the relation to proliferation and invasion in non-melanoma skin cancer and in breast cancer. In a model system of basal cell carcinoma, we observed that tumor cells changed phenotype from a highly proliferative type in the centre of the tumor to an invasive type with low proliferation and a marked upregulation of p16 at the invasive front. The expression of p16 was transcriptionally regulated and possible p16 activators such as ERK1/2 or Ets were not the sole contributors. Similar findings were observed in squamous cell carcinoma of the skin, despite a non functional Rb pathway, which might indicate a proliferation independent role for p16 in invasive behaviors. In primary breast cancer, a signaling cascade from VEGFR2 via ERK1/2 phosphorylation to Ets2 phosphorylation and cyclin D1, could be outlined and ERK1/2 phosphorylation was linked to small tumors with good prognosis. We also observed a Notch1 independent activation of Hes1 in breast cancer. Further, postmenopausal patients with ERK1/2 phosphorylated tumors had an impaired tamoxifen response, but ERK1/2 phosphorylation was not linked to tamoxifen resistance in premenopausal women. Taken together, our results implicate that there is a general inverse association between invasion and proliferation in some malignancies and this novel finding could be important when designing new treatment strategies for cancer patients.","abstract_html":"Two key events in the oncogenic process of tumor cells are to acquire uncontrolled proliferation and invasive properties. This allows the tumor to grow and invade beyond the tissue from which the tumor cells originate. We here specifically studied p16 and ERK1/2 with special focus on and the relation to proliferation and invasion in non-melanoma skin cancer and in breast cancer. In a model system of basal cell carcinoma, we observed that tumor cells changed phenotype from a highly proliferative type in the centre of the tumor to an invasive type with low proliferation and a marked upregulation of p16 at the invasive front. The expression of p16 was transcriptionally regulated and possible p16 activators such as ERK1/2 or Ets were not the sole contributors. Similar findings were observed in squamous cell carcinoma of the skin, despite a non functional Rb pathway, which might indicate a proliferation independent role for p16 in invasive behaviors. In primary breast cancer, a signaling cascade from VEGFR2 via ERK1/2 phosphorylation to Ets2 phosphorylation and cyclin D1, could be outlined and ERK1/2 phosphorylation was linked to small tumors with good prognosis. We also observed a Notch1 independent activation of Hes1 in breast cancer. Further, postmenopausal patients with ERK1/2 phosphorylated tumors had an impaired tamoxifen response, but ERK1/2 phosphorylation was not linked to tamoxifen resistance in premenopausal women. Taken together, our results implicate that there is a general inverse association between invasion and proliferation in some malignancies and this novel finding could be important when designing new treatment strategies for cancer patients.","abstract_has_math":false,"creators":["Svensson Månsson, Sofie"],"institution":"Department of Laboratory Medicine, Lund University","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2006,"date_issued":"2006","date_published":"2006","updated_at":"2026-07-24T03:00:02Z","subjects":["Cancer and Oncology","Cell and Molecular Biology","cancerology","oncology","Cytology","breast cancer","squamous cell carcinoma","basal cell carcinoma","p16","proliferation","invasion","Cytologi","onkologi","cancer"],"languages":["eng"],"rights":["info:eu-repo/semantics/openAccess"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["urn:isbn:91-85559-35-0"],"render_values":[{"text":"urn:isbn:91-85559-35-0","href":null,"code":true}]}]},"links":{"outbound_url":"https://lup.lub.lu.se/record/547334","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Svensson Månsson, Sofie"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2006"]},{"key":"dc:publisher","label":"Institution","values":["Department of Laboratory Medicine, Lund University"]},{"key":"dc:type","label":"Dc Type","values":["thesis/doccomp","info:eu-repo/semantics/doctoralThesis","text"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Cancer and Oncology","Cell and Molecular Biology","cancerology","oncology","Cytology","breast cancer","squamous cell carcinoma","basal cell carcinoma","p16","proliferation","invasion","Cytologi","onkologi","cancer"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]},{"key":"dc:rights","label":"Dc Rights","values":["info:eu-repo/semantics/openAccess"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://lup.lub.lu.se/record/547334","urn:isbn:91-85559-35-0","https://portal.research.lu.se/files/4479044/547337.pdf"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Two key events in the oncogenic process of tumor cells are to acquire uncontrolled proliferation and invasive properties. This allows the tumor to grow and invade beyond the tissue from which the tumor cells originate. We here specifically studied p16 and ERK1/2 with special focus on and the relation to proliferation and invasion in non-melanoma skin cancer and in breast cancer. In a model system of basal cell carcinoma, we observed that tumor cells changed phenotype from a highly proliferative type in the centre of the tumor to an invasive type with low proliferation and a marked upregulation of p16 at the invasive front. The expression of p16 was transcriptionally regulated and possible p16 activators such as ERK1/2 or Ets were not the sole contributors. Similar findings were observed in squamous cell carcinoma of the skin, despite a non functional Rb pathway, which might indicate a proliferation independent role for p16 in invasive behaviors. In primary breast cancer, a signaling cascade from VEGFR2 via ERK1/2 phosphorylation to Ets2 phosphorylation and cyclin D1, could be outlined and ERK1/2 phosphorylation was linked to small tumors with good prognosis. We also observed a Notch1 independent activation of Hes1 in breast cancer. Further, postmenopausal patients with ERK1/2 phosphorylated tumors had an impaired tamoxifen response, but ERK1/2 phosphorylation was not linked to tamoxifen resistance in premenopausal women. Taken together, our results implicate that there is a general inverse association between invasion and proliferation in some malignancies and this novel finding could be important when designing new treatment strategies for cancer patients."]},{"key":"dc:format","label":"Dc Format","values":["application/pdf"]},{"key":"dc:source","label":"Dc Source","values":["Lund University Faculty of Medicine Doctoral Dissertation Series; 2006:111 (2006)","ISSN: 1652-8220"]},{"key":"dc:title","label":"Title","values":["Invasion and Proliferation in Malignant Cells"]}]}],"canonical_facts":{"dc:creator":["Svensson Månsson, Sofie"],"dc:date":["2006"],"dc:description":["Two key events in the oncogenic process of tumor cells are to acquire uncontrolled proliferation and invasive properties. This allows the tumor to grow and invade beyond the tissue from which the tumor cells originate. We here specifically studied p16 and ERK1/2 with special focus on and the relation to proliferation and invasion in non-melanoma skin cancer and in breast cancer. In a model system of basal cell carcinoma, we observed that tumor cells changed phenotype from a highly proliferative type in the centre of the tumor to an invasive type with low proliferation and a marked upregulation of p16 at the invasive front. The expression of p16 was transcriptionally regulated and possible p16 activators such as ERK1/2 or Ets were not the sole contributors. Similar findings were observed in squamous cell carcinoma of the skin, despite a non functional Rb pathway, which might indicate a proliferation independent role for p16 in invasive behaviors. In primary breast cancer, a signaling cascade from VEGFR2 via ERK1/2 phosphorylation to Ets2 phosphorylation and cyclin D1, could be outlined and ERK1/2 phosphorylation was linked to small tumors with good prognosis. We also observed a Notch1 independent activation of Hes1 in breast cancer. Further, postmenopausal patients with ERK1/2 phosphorylated tumors had an impaired tamoxifen response, but ERK1/2 phosphorylation was not linked to tamoxifen resistance in premenopausal women. Taken together, our results implicate that there is a general inverse association between invasion and proliferation in some malignancies and this novel finding could be important when designing new treatment strategies for cancer patients."],"dc:format":["application/pdf"],"dc:identifier":["https://lup.lub.lu.se/record/547334","urn:isbn:91-85559-35-0","https://portal.research.lu.se/files/4479044/547337.pdf"],"dc:language":["eng"],"dc:publisher":["Department of Laboratory Medicine, Lund University"],"dc:rights":["info:eu-repo/semantics/openAccess"],"dc:source":["Lund University Faculty of Medicine Doctoral Dissertation Series; 2006:111 (2006)","ISSN: 1652-8220"],"dc:subject":["Cancer and Oncology","Cell and Molecular Biology","cancerology","oncology","Cytology","breast cancer","squamous cell carcinoma","basal cell carcinoma","p16","proliferation","invasion","Cytologi","onkologi","cancer"],"dc:title":["Invasion and Proliferation in Malignant Cells"],"dc:type":["thesis/doccomp","info:eu-repo/semantics/doctoralThesis","text"]},"updated_at":"2026-07-24T03:00:02Z"}