Eintrag weiter verarbeiten
Type I Collagen Promotes the Malignant Phenotype of Pancreatic Ductal Adenocarcinoma
Gespeichert in:
| Zeitschriftentitel: | Clinical Cancer Research |
|---|---|
| Personen und Körperschaften: | , , , , , , , , |
| In: | Clinical Cancer Research, 10, 2004, 21, S. 7427-7437 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Association for Cancer Research (AACR)
|
| Schlagwörter: |
| author_facet |
Armstrong, Thomas Packham, Graham Murphy, Lindsay B. Bateman, Adrian C. Conti, John A. Fine, David R. Johnson, Colin D. Benyon, R. Christopher Iredale, John P. Armstrong, Thomas Packham, Graham Murphy, Lindsay B. Bateman, Adrian C. Conti, John A. Fine, David R. Johnson, Colin D. Benyon, R. Christopher Iredale, John P. |
|---|---|
| author |
Armstrong, Thomas Packham, Graham Murphy, Lindsay B. Bateman, Adrian C. Conti, John A. Fine, David R. Johnson, Colin D. Benyon, R. Christopher Iredale, John P. |
| spellingShingle |
Armstrong, Thomas Packham, Graham Murphy, Lindsay B. Bateman, Adrian C. Conti, John A. Fine, David R. Johnson, Colin D. Benyon, R. Christopher Iredale, John P. Clinical Cancer Research Type I Collagen Promotes the Malignant Phenotype of Pancreatic Ductal Adenocarcinoma Cancer Research Oncology |
| author_sort |
armstrong, thomas |
| spelling |
Armstrong, Thomas Packham, Graham Murphy, Lindsay B. Bateman, Adrian C. Conti, John A. Fine, David R. Johnson, Colin D. Benyon, R. Christopher Iredale, John P. 1078-0432 1557-3265 American Association for Cancer Research (AACR) Cancer Research Oncology http://dx.doi.org/10.1158/1078-0432.ccr-03-0825 <jats:title>Abstract</jats:title> <jats:p>Purpose: The purpose of this study was to determine the role of functional interactions between pancreatic cancer cells and pancreatic stellate cells (PSCs) in the formation of the desmoplastic reaction (DR) in pancreatic cancer and to characterize the effect of type I collagen (the predominant component of the DR) on pancreatic cancer cell phenotype.</jats:p> <jats:p>Experimental Design: PSCs and type I collagen were identified in sections of pancreatic cancer using immunohistochemistry, and their anatomic relationship was studied. Interactions among pancreatic cancer cell lines (MIA PaCa-2, Panc-1, and AsPC-1), primary cultures of human PSCs, and type I collagen were investigated in a series of tissue culture models.</jats:p> <jats:p>Results: In vivo, the DR causes gross distortion of normal pancreas, bringing cancer cells into close contact with numerous PSCs and abundant type I collagen. In tissue culture models of pancreatic cancer, conditioned media from each cell line increased PSC [3H]thymidine incorporation up to 6.3-fold that of controls, and AsPC-1 cells also increased PSC collagen synthesis 1.3-fold. Type I collagen was observed to increase long-term survival of pancreatic cancer cells treated with 5-fluorouracil, by up to 62% in clonogenic assays. This was because type I collagen increased the proliferation of cancer cells ([3H]thymidine incorporation was up to 2.8-fold that of cells cultured on tissue culture plastic) and reduced apoptosis of AsPC-1 cells in response to 5-fluorouracil (by regulating mcl-1).</jats:p> <jats:p>Conclusions: These experiments elucidate a mechanism by which the DR in pancreatic cancer may form and, via the collagen within it, promote the malignant phenotype of pancreatic cancer cells, suggesting significant detriment to the host.</jats:p> Type I Collagen Promotes the Malignant Phenotype of Pancreatic Ductal Adenocarcinoma Clinical Cancer Research |
| doi_str_mv |
10.1158/1078-0432.ccr-03-0825 |
| facet_avail |
Online Free |
| finc_class_facet |
Medizin |
| format |
ElectronicArticle |
| fullrecord |
blob:ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTE1OC8xMDc4LTA0MzIuY2NyLTAzLTA4MjU |
| id |
ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTE1OC8xMDc4LTA0MzIuY2NyLTAzLTA4MjU |
| institution |
DE-Gla1 DE-Zi4 DE-15 DE-Pl11 DE-Rs1 DE-105 DE-14 DE-Ch1 DE-L229 DE-D275 DE-Bn3 DE-Brt1 DE-Zwi2 DE-D161 |
| imprint |
American Association for Cancer Research (AACR), 2004 |
| imprint_str_mv |
American Association for Cancer Research (AACR), 2004 |
| issn |
1078-0432 1557-3265 |
| issn_str_mv |
1078-0432 1557-3265 |
| language |
English |
| mega_collection |
American Association for Cancer Research (AACR) (CrossRef) |
| match_str |
armstrong2004typeicollagenpromotesthemalignantphenotypeofpancreaticductaladenocarcinoma |
| publishDateSort |
2004 |
| publisher |
American Association for Cancer Research (AACR) |
| recordtype |
ai |
| record_format |
ai |
| series |
Clinical Cancer Research |
| source_id |
49 |
| title |
Type I Collagen Promotes the Malignant Phenotype of Pancreatic Ductal Adenocarcinoma |
| title_unstemmed |
Type I Collagen Promotes the Malignant Phenotype of Pancreatic Ductal Adenocarcinoma |
| title_full |
Type I Collagen Promotes the Malignant Phenotype of Pancreatic Ductal Adenocarcinoma |
| title_fullStr |
Type I Collagen Promotes the Malignant Phenotype of Pancreatic Ductal Adenocarcinoma |
| title_full_unstemmed |
Type I Collagen Promotes the Malignant Phenotype of Pancreatic Ductal Adenocarcinoma |
| title_short |
Type I Collagen Promotes the Malignant Phenotype of Pancreatic Ductal Adenocarcinoma |
| title_sort |
type i collagen promotes the malignant phenotype of pancreatic ductal adenocarcinoma |
| topic |
Cancer Research Oncology |
| url |
http://dx.doi.org/10.1158/1078-0432.ccr-03-0825 |
| publishDate |
2004 |
| physical |
7427-7437 |
| description |
<jats:title>Abstract</jats:title>
<jats:p>Purpose: The purpose of this study was to determine the role of functional interactions between pancreatic cancer cells and pancreatic stellate cells (PSCs) in the formation of the desmoplastic reaction (DR) in pancreatic cancer and to characterize the effect of type I collagen (the predominant component of the DR) on pancreatic cancer cell phenotype.</jats:p>
<jats:p>Experimental Design: PSCs and type I collagen were identified in sections of pancreatic cancer using immunohistochemistry, and their anatomic relationship was studied. Interactions among pancreatic cancer cell lines (MIA PaCa-2, Panc-1, and AsPC-1), primary cultures of human PSCs, and type I collagen were investigated in a series of tissue culture models.</jats:p>
<jats:p>Results: In vivo, the DR causes gross distortion of normal pancreas, bringing cancer cells into close contact with numerous PSCs and abundant type I collagen. In tissue culture models of pancreatic cancer, conditioned media from each cell line increased PSC [3H]thymidine incorporation up to 6.3-fold that of controls, and AsPC-1 cells also increased PSC collagen synthesis 1.3-fold. Type I collagen was observed to increase long-term survival of pancreatic cancer cells treated with 5-fluorouracil, by up to 62% in clonogenic assays. This was because type I collagen increased the proliferation of cancer cells ([3H]thymidine incorporation was up to 2.8-fold that of cells cultured on tissue culture plastic) and reduced apoptosis of AsPC-1 cells in response to 5-fluorouracil (by regulating mcl-1).</jats:p>
<jats:p>Conclusions: These experiments elucidate a mechanism by which the DR in pancreatic cancer may form and, via the collagen within it, promote the malignant phenotype of pancreatic cancer cells, suggesting significant detriment to the host.</jats:p> |
| container_issue |
21 |
| container_start_page |
7427 |
| container_title |
Clinical Cancer Research |
| container_volume |
10 |
| format_de105 |
Article, E-Article |
| format_de14 |
Article, E-Article |
| format_de15 |
Article, E-Article |
| format_de520 |
Article, E-Article |
| format_de540 |
Article, E-Article |
| format_dech1 |
Article, E-Article |
| format_ded117 |
Article, E-Article |
| format_degla1 |
E-Article |
| format_del152 |
Buch |
| format_del189 |
Article, E-Article |
| format_dezi4 |
Article |
| format_dezwi2 |
Article, E-Article |
| format_finc |
Article, E-Article |
| format_nrw |
Article, E-Article |
| _version_ |
1792346165872689164 |
| geogr_code |
not assigned |
| last_indexed |
2024-03-01T17:35:04.154Z |
| geogr_code_person |
not assigned |
| openURL |
url_ver=Z39.88-2004&ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fvufind.svn.sourceforge.net%3Agenerator&rft.title=Type+I+Collagen+Promotes+the+Malignant+Phenotype+of+Pancreatic+Ductal+Adenocarcinoma&rft.date=2004-11-01&genre=article&issn=1557-3265&volume=10&issue=21&spage=7427&epage=7437&pages=7427-7437&jtitle=Clinical+Cancer+Research&atitle=Type+I+Collagen+Promotes+the+Malignant+Phenotype+of+Pancreatic+Ductal+Adenocarcinoma&aulast=Iredale&aufirst=John+P.&rft_id=info%3Adoi%2F10.1158%2F1078-0432.ccr-03-0825&rft.language%5B0%5D=eng |
| SOLR | |
| _version_ | 1792346165872689164 |
| author | Armstrong, Thomas, Packham, Graham, Murphy, Lindsay B., Bateman, Adrian C., Conti, John A., Fine, David R., Johnson, Colin D., Benyon, R. Christopher, Iredale, John P. |
| author_facet | Armstrong, Thomas, Packham, Graham, Murphy, Lindsay B., Bateman, Adrian C., Conti, John A., Fine, David R., Johnson, Colin D., Benyon, R. Christopher, Iredale, John P., Armstrong, Thomas, Packham, Graham, Murphy, Lindsay B., Bateman, Adrian C., Conti, John A., Fine, David R., Johnson, Colin D., Benyon, R. Christopher, Iredale, John P. |
| author_sort | armstrong, thomas |
| container_issue | 21 |
| container_start_page | 7427 |
| container_title | Clinical Cancer Research |
| container_volume | 10 |
| description | <jats:title>Abstract</jats:title> <jats:p>Purpose: The purpose of this study was to determine the role of functional interactions between pancreatic cancer cells and pancreatic stellate cells (PSCs) in the formation of the desmoplastic reaction (DR) in pancreatic cancer and to characterize the effect of type I collagen (the predominant component of the DR) on pancreatic cancer cell phenotype.</jats:p> <jats:p>Experimental Design: PSCs and type I collagen were identified in sections of pancreatic cancer using immunohistochemistry, and their anatomic relationship was studied. Interactions among pancreatic cancer cell lines (MIA PaCa-2, Panc-1, and AsPC-1), primary cultures of human PSCs, and type I collagen were investigated in a series of tissue culture models.</jats:p> <jats:p>Results: In vivo, the DR causes gross distortion of normal pancreas, bringing cancer cells into close contact with numerous PSCs and abundant type I collagen. In tissue culture models of pancreatic cancer, conditioned media from each cell line increased PSC [3H]thymidine incorporation up to 6.3-fold that of controls, and AsPC-1 cells also increased PSC collagen synthesis 1.3-fold. Type I collagen was observed to increase long-term survival of pancreatic cancer cells treated with 5-fluorouracil, by up to 62% in clonogenic assays. This was because type I collagen increased the proliferation of cancer cells ([3H]thymidine incorporation was up to 2.8-fold that of cells cultured on tissue culture plastic) and reduced apoptosis of AsPC-1 cells in response to 5-fluorouracil (by regulating mcl-1).</jats:p> <jats:p>Conclusions: These experiments elucidate a mechanism by which the DR in pancreatic cancer may form and, via the collagen within it, promote the malignant phenotype of pancreatic cancer cells, suggesting significant detriment to the host.</jats:p> |
| doi_str_mv | 10.1158/1078-0432.ccr-03-0825 |
| facet_avail | Online, Free |
| finc_class_facet | Medizin |
| format | ElectronicArticle |
| format_de105 | Article, E-Article |
| format_de14 | Article, E-Article |
| format_de15 | Article, E-Article |
| format_de520 | Article, E-Article |
| format_de540 | Article, E-Article |
| format_dech1 | Article, E-Article |
| format_ded117 | Article, E-Article |
| format_degla1 | E-Article |
| format_del152 | Buch |
| format_del189 | Article, E-Article |
| format_dezi4 | Article |
| format_dezwi2 | Article, E-Article |
| format_finc | Article, E-Article |
| format_nrw | Article, E-Article |
| geogr_code | not assigned |
| geogr_code_person | not assigned |
| id | ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTE1OC8xMDc4LTA0MzIuY2NyLTAzLTA4MjU |
| imprint | American Association for Cancer Research (AACR), 2004 |
| imprint_str_mv | American Association for Cancer Research (AACR), 2004 |
| institution | DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161 |
| issn | 1078-0432, 1557-3265 |
| issn_str_mv | 1078-0432, 1557-3265 |
| language | English |
| last_indexed | 2024-03-01T17:35:04.154Z |
| match_str | armstrong2004typeicollagenpromotesthemalignantphenotypeofpancreaticductaladenocarcinoma |
| mega_collection | American Association for Cancer Research (AACR) (CrossRef) |
| physical | 7427-7437 |
| publishDate | 2004 |
| publishDateSort | 2004 |
| publisher | American Association for Cancer Research (AACR) |
| record_format | ai |
| recordtype | ai |
| series | Clinical Cancer Research |
| source_id | 49 |
| spelling | Armstrong, Thomas Packham, Graham Murphy, Lindsay B. Bateman, Adrian C. Conti, John A. Fine, David R. Johnson, Colin D. Benyon, R. Christopher Iredale, John P. 1078-0432 1557-3265 American Association for Cancer Research (AACR) Cancer Research Oncology http://dx.doi.org/10.1158/1078-0432.ccr-03-0825 <jats:title>Abstract</jats:title> <jats:p>Purpose: The purpose of this study was to determine the role of functional interactions between pancreatic cancer cells and pancreatic stellate cells (PSCs) in the formation of the desmoplastic reaction (DR) in pancreatic cancer and to characterize the effect of type I collagen (the predominant component of the DR) on pancreatic cancer cell phenotype.</jats:p> <jats:p>Experimental Design: PSCs and type I collagen were identified in sections of pancreatic cancer using immunohistochemistry, and their anatomic relationship was studied. Interactions among pancreatic cancer cell lines (MIA PaCa-2, Panc-1, and AsPC-1), primary cultures of human PSCs, and type I collagen were investigated in a series of tissue culture models.</jats:p> <jats:p>Results: In vivo, the DR causes gross distortion of normal pancreas, bringing cancer cells into close contact with numerous PSCs and abundant type I collagen. In tissue culture models of pancreatic cancer, conditioned media from each cell line increased PSC [3H]thymidine incorporation up to 6.3-fold that of controls, and AsPC-1 cells also increased PSC collagen synthesis 1.3-fold. Type I collagen was observed to increase long-term survival of pancreatic cancer cells treated with 5-fluorouracil, by up to 62% in clonogenic assays. This was because type I collagen increased the proliferation of cancer cells ([3H]thymidine incorporation was up to 2.8-fold that of cells cultured on tissue culture plastic) and reduced apoptosis of AsPC-1 cells in response to 5-fluorouracil (by regulating mcl-1).</jats:p> <jats:p>Conclusions: These experiments elucidate a mechanism by which the DR in pancreatic cancer may form and, via the collagen within it, promote the malignant phenotype of pancreatic cancer cells, suggesting significant detriment to the host.</jats:p> Type I Collagen Promotes the Malignant Phenotype of Pancreatic Ductal Adenocarcinoma Clinical Cancer Research |
| spellingShingle | Armstrong, Thomas, Packham, Graham, Murphy, Lindsay B., Bateman, Adrian C., Conti, John A., Fine, David R., Johnson, Colin D., Benyon, R. Christopher, Iredale, John P., Clinical Cancer Research, Type I Collagen Promotes the Malignant Phenotype of Pancreatic Ductal Adenocarcinoma, Cancer Research, Oncology |
| title | Type I Collagen Promotes the Malignant Phenotype of Pancreatic Ductal Adenocarcinoma |
| title_full | Type I Collagen Promotes the Malignant Phenotype of Pancreatic Ductal Adenocarcinoma |
| title_fullStr | Type I Collagen Promotes the Malignant Phenotype of Pancreatic Ductal Adenocarcinoma |
| title_full_unstemmed | Type I Collagen Promotes the Malignant Phenotype of Pancreatic Ductal Adenocarcinoma |
| title_short | Type I Collagen Promotes the Malignant Phenotype of Pancreatic Ductal Adenocarcinoma |
| title_sort | type i collagen promotes the malignant phenotype of pancreatic ductal adenocarcinoma |
| title_unstemmed | Type I Collagen Promotes the Malignant Phenotype of Pancreatic Ductal Adenocarcinoma |
| topic | Cancer Research, Oncology |
| url | http://dx.doi.org/10.1158/1078-0432.ccr-03-0825 |