Eintrag weiter verarbeiten
CHFR silencing or microsatellite instability is associated with increased antitumor activity of docetaxel or gemcitabine in colorectal cancer
Gespeichert in:
| Zeitschriftentitel: | International Journal of Cancer |
|---|---|
| Personen und Körperschaften: | , , , , , , |
| In: | International Journal of Cancer, 134, 2014, 3, S. 596-605 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
|
| Schlagwörter: |
| author_facet |
Pelosof, Lorraine Yerram, Sashidhar R. Ahuja, Nita Delmas, Andrew Danilova, Ludmila Herman, James G. Azad, Nilofer S. Pelosof, Lorraine Yerram, Sashidhar R. Ahuja, Nita Delmas, Andrew Danilova, Ludmila Herman, James G. Azad, Nilofer S. |
|---|---|
| author |
Pelosof, Lorraine Yerram, Sashidhar R. Ahuja, Nita Delmas, Andrew Danilova, Ludmila Herman, James G. Azad, Nilofer S. |
| spellingShingle |
Pelosof, Lorraine Yerram, Sashidhar R. Ahuja, Nita Delmas, Andrew Danilova, Ludmila Herman, James G. Azad, Nilofer S. International Journal of Cancer CHFR silencing or microsatellite instability is associated with increased antitumor activity of docetaxel or gemcitabine in colorectal cancer Cancer Research Oncology |
| author_sort |
pelosof, lorraine |
| spelling |
Pelosof, Lorraine Yerram, Sashidhar R. Ahuja, Nita Delmas, Andrew Danilova, Ludmila Herman, James G. Azad, Nilofer S. 0020-7136 1097-0215 Wiley Cancer Research Oncology http://dx.doi.org/10.1002/ijc.28390 <jats:p>Phenotypic differences among cancers with the same origin may be associated with chemotherapy response. <jats:italic>CHFR</jats:italic> silencing associated with DNA methylation has been suggested to be predictive of taxane sensitivity in diverse tumor types. However, the use of microsatellite instability (MSI:unstable–MSS:stable) as a predictive marker for therapeutic effect has had conflicting results. We examined these molecular alterations as predictors of chemotherapy sensitivity in colorectal cancer (CRC). Differential sensitivity to docetaxel and gemcitabine was compared to potential predictive biomarkers <jats:italic>CHFR</jats:italic> methylation and MSI status. Cell lines that were MSI‐H/<jats:italic>CHFR</jats:italic>‐methylated, MSS/<jats:italic>CHFR</jats:italic>‐methylated and MSS/<jats:italic>CHFR</jats:italic>‐unmethylated were assessed for <jats:italic>in vivo</jats:italic> sensitivity of CRC cell line xenografts to docetaxel and/or gemcitabine. We observed increased sensitivity <jats:italic>in vitro</jats:italic> to gemcitabine in cell lines with MSI and docetaxel in cell lines with <jats:italic>CHFR</jats:italic> inactivation <jats:italic>via</jats:italic> DNA methylation. <jats:italic>In vivo</jats:italic> treatment of human xenografts confirmed differential sensitivity, with the MSI‐H/<jats:italic>CHFR</jats:italic>‐methylated line RKO having tumor growth inhibition to each agent, and at least additive tumor growth inhibition with combination therapy. The MSS‐<jats:italic>CHFR</jats:italic>‐unmethylated line, CACO<jats:sub>2</jats:sub>, was resistant to single and combination therapy, while COLO205, the MSS/<jats:italic>CHFR</jats:italic>‐methylated line, showed tumor growth inhibition with docetaxel, but not gemcitabine, therapy. <jats:italic>CHFR</jats:italic> methylation in CRC cell lines predicted for sensitivity <jats:italic>in vitro</jats:italic> and <jats:italic>in vivo</jats:italic> to docetaxel, while MSI‐H cell lines were more sensitive to gemcitabine. These data suggest that a subset of CRC patients would be selectively sensitive to a novel combination of gemcitabine and docetaxel, and are the basis for an ongoing clinical trial of this combination in a biomarker‐selected patient population.</jats:p> <i>CHFR</i> silencing or microsatellite instability is associated with increased antitumor activity of docetaxel or gemcitabine in colorectal cancer International Journal of Cancer |
| doi_str_mv |
10.1002/ijc.28390 |
| facet_avail |
Online Free |
| finc_class_facet |
Medizin |
| format |
ElectronicArticle |
| fullrecord |
blob:ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTAwMi9pamMuMjgzOTA |
| id |
ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTAwMi9pamMuMjgzOTA |
| 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 |
Wiley, 2014 |
| imprint_str_mv |
Wiley, 2014 |
| issn |
1097-0215 0020-7136 |
| issn_str_mv |
1097-0215 0020-7136 |
| language |
English |
| mega_collection |
Wiley (CrossRef) |
| match_str |
pelosof2014chfrsilencingormicrosatelliteinstabilityisassociatedwithincreasedantitumoractivityofdocetaxelorgemcitabineincolorectalcancer |
| publishDateSort |
2014 |
| publisher |
Wiley |
| recordtype |
ai |
| record_format |
ai |
| series |
International Journal of Cancer |
| source_id |
49 |
| title |
CHFR silencing or microsatellite instability is associated with increased antitumor activity of docetaxel or gemcitabine in colorectal cancer |
| title_unstemmed |
CHFR silencing or microsatellite instability is associated with increased antitumor activity of docetaxel or gemcitabine in colorectal cancer |
| title_full |
CHFR silencing or microsatellite instability is associated with increased antitumor activity of docetaxel or gemcitabine in colorectal cancer |
| title_fullStr |
CHFR silencing or microsatellite instability is associated with increased antitumor activity of docetaxel or gemcitabine in colorectal cancer |
| title_full_unstemmed |
CHFR silencing or microsatellite instability is associated with increased antitumor activity of docetaxel or gemcitabine in colorectal cancer |
| title_short |
CHFR silencing or microsatellite instability is associated with increased antitumor activity of docetaxel or gemcitabine in colorectal cancer |
| title_sort |
<i>chfr</i> silencing or microsatellite instability is associated with increased antitumor activity of docetaxel or gemcitabine in colorectal cancer |
| topic |
Cancer Research Oncology |
| url |
http://dx.doi.org/10.1002/ijc.28390 |
| publishDate |
2014 |
| physical |
596-605 |
| description |
<jats:p>Phenotypic differences among cancers with the same origin may be associated with chemotherapy response. <jats:italic>CHFR</jats:italic> silencing associated with DNA methylation has been suggested to be predictive of taxane sensitivity in diverse tumor types. However, the use of microsatellite instability (MSI:unstable–MSS:stable) as a predictive marker for therapeutic effect has had conflicting results. We examined these molecular alterations as predictors of chemotherapy sensitivity in colorectal cancer (CRC). Differential sensitivity to docetaxel and gemcitabine was compared to potential predictive biomarkers <jats:italic>CHFR</jats:italic> methylation and MSI status. Cell lines that were MSI‐H/<jats:italic>CHFR</jats:italic>‐methylated, MSS/<jats:italic>CHFR</jats:italic>‐methylated and MSS/<jats:italic>CHFR</jats:italic>‐unmethylated were assessed for <jats:italic>in vivo</jats:italic> sensitivity of CRC cell line xenografts to docetaxel and/or gemcitabine. We observed increased sensitivity <jats:italic>in vitro</jats:italic> to gemcitabine in cell lines with MSI and docetaxel in cell lines with <jats:italic>CHFR</jats:italic> inactivation <jats:italic>via</jats:italic> DNA methylation. <jats:italic>In vivo</jats:italic> treatment of human xenografts confirmed differential sensitivity, with the MSI‐H/<jats:italic>CHFR</jats:italic>‐methylated line RKO having tumor growth inhibition to each agent, and at least additive tumor growth inhibition with combination therapy. The MSS‐<jats:italic>CHFR</jats:italic>‐unmethylated line, CACO<jats:sub>2</jats:sub>, was resistant to single and combination therapy, while COLO205, the MSS/<jats:italic>CHFR</jats:italic>‐methylated line, showed tumor growth inhibition with docetaxel, but not gemcitabine, therapy. <jats:italic>CHFR</jats:italic> methylation in CRC cell lines predicted for sensitivity <jats:italic>in vitro</jats:italic> and <jats:italic>in vivo</jats:italic> to docetaxel, while MSI‐H cell lines were more sensitive to gemcitabine. These data suggest that a subset of CRC patients would be selectively sensitive to a novel combination of gemcitabine and docetaxel, and are the basis for an ongoing clinical trial of this combination in a biomarker‐selected patient population.</jats:p> |
| container_issue |
3 |
| container_start_page |
596 |
| container_title |
International Journal of Cancer |
| container_volume |
134 |
| 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_ |
1792335222860152840 |
| geogr_code |
not assigned |
| last_indexed |
2024-03-01T14:41:03.333Z |
| 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=CHFR+silencing+or+microsatellite+instability+is+associated+with+increased+antitumor+activity+of+docetaxel+or+gemcitabine+in+colorectal+cancer&rft.date=2014-02-01&genre=article&issn=1097-0215&volume=134&issue=3&spage=596&epage=605&pages=596-605&jtitle=International+Journal+of+Cancer&atitle=%3Ci%3ECHFR%3C%2Fi%3E+silencing+or+microsatellite+instability+is+associated+with+increased+antitumor+activity+of+docetaxel+or+gemcitabine+in+colorectal+cancer&aulast=Azad&aufirst=Nilofer+S.&rft_id=info%3Adoi%2F10.1002%2Fijc.28390&rft.language%5B0%5D=eng |
| SOLR | |
| _version_ | 1792335222860152840 |
| author | Pelosof, Lorraine, Yerram, Sashidhar R., Ahuja, Nita, Delmas, Andrew, Danilova, Ludmila, Herman, James G., Azad, Nilofer S. |
| author_facet | Pelosof, Lorraine, Yerram, Sashidhar R., Ahuja, Nita, Delmas, Andrew, Danilova, Ludmila, Herman, James G., Azad, Nilofer S., Pelosof, Lorraine, Yerram, Sashidhar R., Ahuja, Nita, Delmas, Andrew, Danilova, Ludmila, Herman, James G., Azad, Nilofer S. |
| author_sort | pelosof, lorraine |
| container_issue | 3 |
| container_start_page | 596 |
| container_title | International Journal of Cancer |
| container_volume | 134 |
| description | <jats:p>Phenotypic differences among cancers with the same origin may be associated with chemotherapy response. <jats:italic>CHFR</jats:italic> silencing associated with DNA methylation has been suggested to be predictive of taxane sensitivity in diverse tumor types. However, the use of microsatellite instability (MSI:unstable–MSS:stable) as a predictive marker for therapeutic effect has had conflicting results. We examined these molecular alterations as predictors of chemotherapy sensitivity in colorectal cancer (CRC). Differential sensitivity to docetaxel and gemcitabine was compared to potential predictive biomarkers <jats:italic>CHFR</jats:italic> methylation and MSI status. Cell lines that were MSI‐H/<jats:italic>CHFR</jats:italic>‐methylated, MSS/<jats:italic>CHFR</jats:italic>‐methylated and MSS/<jats:italic>CHFR</jats:italic>‐unmethylated were assessed for <jats:italic>in vivo</jats:italic> sensitivity of CRC cell line xenografts to docetaxel and/or gemcitabine. We observed increased sensitivity <jats:italic>in vitro</jats:italic> to gemcitabine in cell lines with MSI and docetaxel in cell lines with <jats:italic>CHFR</jats:italic> inactivation <jats:italic>via</jats:italic> DNA methylation. <jats:italic>In vivo</jats:italic> treatment of human xenografts confirmed differential sensitivity, with the MSI‐H/<jats:italic>CHFR</jats:italic>‐methylated line RKO having tumor growth inhibition to each agent, and at least additive tumor growth inhibition with combination therapy. The MSS‐<jats:italic>CHFR</jats:italic>‐unmethylated line, CACO<jats:sub>2</jats:sub>, was resistant to single and combination therapy, while COLO205, the MSS/<jats:italic>CHFR</jats:italic>‐methylated line, showed tumor growth inhibition with docetaxel, but not gemcitabine, therapy. <jats:italic>CHFR</jats:italic> methylation in CRC cell lines predicted for sensitivity <jats:italic>in vitro</jats:italic> and <jats:italic>in vivo</jats:italic> to docetaxel, while MSI‐H cell lines were more sensitive to gemcitabine. These data suggest that a subset of CRC patients would be selectively sensitive to a novel combination of gemcitabine and docetaxel, and are the basis for an ongoing clinical trial of this combination in a biomarker‐selected patient population.</jats:p> |
| doi_str_mv | 10.1002/ijc.28390 |
| 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-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTAwMi9pamMuMjgzOTA |
| imprint | Wiley, 2014 |
| imprint_str_mv | Wiley, 2014 |
| 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 | 1097-0215, 0020-7136 |
| issn_str_mv | 1097-0215, 0020-7136 |
| language | English |
| last_indexed | 2024-03-01T14:41:03.333Z |
| match_str | pelosof2014chfrsilencingormicrosatelliteinstabilityisassociatedwithincreasedantitumoractivityofdocetaxelorgemcitabineincolorectalcancer |
| mega_collection | Wiley (CrossRef) |
| physical | 596-605 |
| publishDate | 2014 |
| publishDateSort | 2014 |
| publisher | Wiley |
| record_format | ai |
| recordtype | ai |
| series | International Journal of Cancer |
| source_id | 49 |
| spelling | Pelosof, Lorraine Yerram, Sashidhar R. Ahuja, Nita Delmas, Andrew Danilova, Ludmila Herman, James G. Azad, Nilofer S. 0020-7136 1097-0215 Wiley Cancer Research Oncology http://dx.doi.org/10.1002/ijc.28390 <jats:p>Phenotypic differences among cancers with the same origin may be associated with chemotherapy response. <jats:italic>CHFR</jats:italic> silencing associated with DNA methylation has been suggested to be predictive of taxane sensitivity in diverse tumor types. However, the use of microsatellite instability (MSI:unstable–MSS:stable) as a predictive marker for therapeutic effect has had conflicting results. We examined these molecular alterations as predictors of chemotherapy sensitivity in colorectal cancer (CRC). Differential sensitivity to docetaxel and gemcitabine was compared to potential predictive biomarkers <jats:italic>CHFR</jats:italic> methylation and MSI status. Cell lines that were MSI‐H/<jats:italic>CHFR</jats:italic>‐methylated, MSS/<jats:italic>CHFR</jats:italic>‐methylated and MSS/<jats:italic>CHFR</jats:italic>‐unmethylated were assessed for <jats:italic>in vivo</jats:italic> sensitivity of CRC cell line xenografts to docetaxel and/or gemcitabine. We observed increased sensitivity <jats:italic>in vitro</jats:italic> to gemcitabine in cell lines with MSI and docetaxel in cell lines with <jats:italic>CHFR</jats:italic> inactivation <jats:italic>via</jats:italic> DNA methylation. <jats:italic>In vivo</jats:italic> treatment of human xenografts confirmed differential sensitivity, with the MSI‐H/<jats:italic>CHFR</jats:italic>‐methylated line RKO having tumor growth inhibition to each agent, and at least additive tumor growth inhibition with combination therapy. The MSS‐<jats:italic>CHFR</jats:italic>‐unmethylated line, CACO<jats:sub>2</jats:sub>, was resistant to single and combination therapy, while COLO205, the MSS/<jats:italic>CHFR</jats:italic>‐methylated line, showed tumor growth inhibition with docetaxel, but not gemcitabine, therapy. <jats:italic>CHFR</jats:italic> methylation in CRC cell lines predicted for sensitivity <jats:italic>in vitro</jats:italic> and <jats:italic>in vivo</jats:italic> to docetaxel, while MSI‐H cell lines were more sensitive to gemcitabine. These data suggest that a subset of CRC patients would be selectively sensitive to a novel combination of gemcitabine and docetaxel, and are the basis for an ongoing clinical trial of this combination in a biomarker‐selected patient population.</jats:p> <i>CHFR</i> silencing or microsatellite instability is associated with increased antitumor activity of docetaxel or gemcitabine in colorectal cancer International Journal of Cancer |
| spellingShingle | Pelosof, Lorraine, Yerram, Sashidhar R., Ahuja, Nita, Delmas, Andrew, Danilova, Ludmila, Herman, James G., Azad, Nilofer S., International Journal of Cancer, CHFR silencing or microsatellite instability is associated with increased antitumor activity of docetaxel or gemcitabine in colorectal cancer, Cancer Research, Oncology |
| title | CHFR silencing or microsatellite instability is associated with increased antitumor activity of docetaxel or gemcitabine in colorectal cancer |
| title_full | CHFR silencing or microsatellite instability is associated with increased antitumor activity of docetaxel or gemcitabine in colorectal cancer |
| title_fullStr | CHFR silencing or microsatellite instability is associated with increased antitumor activity of docetaxel or gemcitabine in colorectal cancer |
| title_full_unstemmed | CHFR silencing or microsatellite instability is associated with increased antitumor activity of docetaxel or gemcitabine in colorectal cancer |
| title_short | CHFR silencing or microsatellite instability is associated with increased antitumor activity of docetaxel or gemcitabine in colorectal cancer |
| title_sort | <i>chfr</i> silencing or microsatellite instability is associated with increased antitumor activity of docetaxel or gemcitabine in colorectal cancer |
| title_unstemmed | CHFR silencing or microsatellite instability is associated with increased antitumor activity of docetaxel or gemcitabine in colorectal cancer |
| topic | Cancer Research, Oncology |
| url | http://dx.doi.org/10.1002/ijc.28390 |