Expression of imatinib mesylate-targeted kinases in endometrial carcinoma
Imatinib mesylate is a tyrosine kinase inhibitor that specifically targets c-Kit, Abl, and platelet-derived growth factor receptor (PDGFR). It has been shown to be an effective treatment for patients with chronic myelogenous leukemia (CML) and gastrointestinal stromal tumors (GIST). These cancers ar...
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| Veröffentlicht in: | Gynecologic oncology 2004-10, Vol.95 (1), p.32-36 |
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| creator | Slomovitz, Brian M. Broaddus, Russell R. Schmandt, Rosemarie Wu, Weiguo Oh, Jonathan C. Ramondetta, Lois M. Burke, Thomas W. Gershenson, David M. Lu, Karen H. |
| description | Imatinib mesylate is a tyrosine kinase inhibitor that specifically targets c-Kit, Abl, and platelet-derived growth factor receptor (PDGFR). It has been shown to be an effective treatment for patients with chronic myelogenous leukemia (CML) and gastrointestinal stromal tumors (GIST). These cancers are characterized by activating mutations of the Abl and c-Kit tyrosine kinases, respectively. To determine whether imatinib mesylate could be a potentially useful agent in the treatment of endometrial cancer, we assessed the expressions of Abl, c-Kit, and PDGFR in both primary and recurrent endometrial carcinoma.
We performed immunohistochemical analysis on formalin-fixed, paraffin-embedded sections from 63 patients: 33 with endometrioid endometrial carcinoma (EEC), 11 with uterine papillary serous carcinoma (UPSC), 12 with recurrent EEC, and seven with recurrent UPSC. The sections were stained with commercially available antibodies for Abl, PDGFR, and c-Kit. The sections were also stained for phosphorylated Abl and phosphorylated PDGFR.
Among the primary EEC, 28/33 (85%) stained positively for Abl and 30/33 (91%) were positive for PDGFR. Of the primary UPSC, 8/11 (73%) were positive for Abl. In addition, 8/11 (73%) of the primary UPSC tumors were positive for PDGFR. Neither the primary EEC (0/33) nor the primary UPSC (0/11) expressed c-Kit. Of the recurrent EEC tumors, 11/12 (92%) were positive for Abl expression, 12/12 (100%) were positive for PDGFR, and 2/8 (25%) were positive for c-Kit. Of the recurrent UPSC, 6/7 (86%) were positive for Abl, 7/7 (100%) were positive for PDGFR, and 2/4 (50%) for c-Kit. In addition, the majority of primary and recurrent tumors were positive for phosphorylated Abl (primary EEC, 91%; primary UPSC, 64%; recurrent EEC, 83%; recurrent UPSC, 86%), and phosphorylated PDGFR (primary EEC, 46%; primary UPSC, 40%; recurrent EEC, 58%; recurrent UPSC, 100%). Within the EEC primary tumors, the differences in kinase expression by grade of tumor were not significant except for PDGFR kinase; the lower grade tumors (1 and 2) had more PDGFR expression than the grade 3 tumors (P < 0.05).
The majority of primary and recurrent EEC, as well as primary and recurrent UPSC express Abl and PDGFR. This preclinical data suggest that imatinib mesylate may be useful in the treatment of patients with endometrial carcinoma. |
| doi_str_mv | 10.1016/j.ygyno.2004.06.052 |
| format | Article |
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We performed immunohistochemical analysis on formalin-fixed, paraffin-embedded sections from 63 patients: 33 with endometrioid endometrial carcinoma (EEC), 11 with uterine papillary serous carcinoma (UPSC), 12 with recurrent EEC, and seven with recurrent UPSC. The sections were stained with commercially available antibodies for Abl, PDGFR, and c-Kit. The sections were also stained for phosphorylated Abl and phosphorylated PDGFR.
Among the primary EEC, 28/33 (85%) stained positively for Abl and 30/33 (91%) were positive for PDGFR. Of the primary UPSC, 8/11 (73%) were positive for Abl. In addition, 8/11 (73%) of the primary UPSC tumors were positive for PDGFR. Neither the primary EEC (0/33) nor the primary UPSC (0/11) expressed c-Kit. Of the recurrent EEC tumors, 11/12 (92%) were positive for Abl expression, 12/12 (100%) were positive for PDGFR, and 2/8 (25%) were positive for c-Kit. Of the recurrent UPSC, 6/7 (86%) were positive for Abl, 7/7 (100%) were positive for PDGFR, and 2/4 (50%) for c-Kit. In addition, the majority of primary and recurrent tumors were positive for phosphorylated Abl (primary EEC, 91%; primary UPSC, 64%; recurrent EEC, 83%; recurrent UPSC, 86%), and phosphorylated PDGFR (primary EEC, 46%; primary UPSC, 40%; recurrent EEC, 58%; recurrent UPSC, 100%). Within the EEC primary tumors, the differences in kinase expression by grade of tumor were not significant except for PDGFR kinase; the lower grade tumors (1 and 2) had more PDGFR expression than the grade 3 tumors (P < 0.05).
The majority of primary and recurrent EEC, as well as primary and recurrent UPSC express Abl and PDGFR. This preclinical data suggest that imatinib mesylate may be useful in the treatment of patients with endometrial carcinoma.</description><identifier>ISSN: 0090-8258</identifier><identifier>EISSN: 1095-6859</identifier><identifier>DOI: 10.1016/j.ygyno.2004.06.052</identifier><identifier>PMID: 15385107</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Abl ; Antineoplastic Agents - pharmacology ; Benzamides ; Carcinoma, Endometrioid - drug therapy ; Carcinoma, Endometrioid - enzymology ; Carcinoma, Endometrioid - pathology ; Endometrial carcinoma ; Endometrial Neoplasms - drug therapy ; Endometrial Neoplasms - enzymology ; Endometrial Neoplasms - pathology ; Enzyme Inhibitors - pharmacology ; Female ; Humans ; Imatinib Mesylate ; Immunohistochemistry ; Paraffin Embedding ; PDGFR ; Phosphorylation ; Piperazines - pharmacology ; Protein-Tyrosine Kinases - antagonists & inhibitors ; Protein-Tyrosine Kinases - biosynthesis ; Protein-Tyrosine Kinases - metabolism ; Proto-Oncogene Proteins c-abl - antagonists & inhibitors ; Proto-Oncogene Proteins c-abl - biosynthesis ; Proto-Oncogene Proteins c-abl - metabolism ; Proto-Oncogene Proteins c-kit - biosynthesis ; Proto-Oncogene Proteins c-kit - metabolism ; Pyrimidines - pharmacology ; Receptors, Platelet-Derived Growth Factor - antagonists & inhibitors ; Receptors, Platelet-Derived Growth Factor - biosynthesis ; Receptors, Platelet-Derived Growth Factor - metabolism ; Uterine papillary serous carcinoma</subject><ispartof>Gynecologic oncology, 2004-10, Vol.95 (1), p.32-36</ispartof><rights>2004 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c355t-58445c5a755a36080cf8548f2d90b61ef2fabc7af5f92f3a917bffd94b48df7f3</citedby><cites>FETCH-LOGICAL-c355t-58445c5a755a36080cf8548f2d90b61ef2fabc7af5f92f3a917bffd94b48df7f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0090825804004287$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15385107$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Slomovitz, Brian M.</creatorcontrib><creatorcontrib>Broaddus, Russell R.</creatorcontrib><creatorcontrib>Schmandt, Rosemarie</creatorcontrib><creatorcontrib>Wu, Weiguo</creatorcontrib><creatorcontrib>Oh, Jonathan C.</creatorcontrib><creatorcontrib>Ramondetta, Lois M.</creatorcontrib><creatorcontrib>Burke, Thomas W.</creatorcontrib><creatorcontrib>Gershenson, David M.</creatorcontrib><creatorcontrib>Lu, Karen H.</creatorcontrib><title>Expression of imatinib mesylate-targeted kinases in endometrial carcinoma</title><title>Gynecologic oncology</title><addtitle>Gynecol Oncol</addtitle><description>Imatinib mesylate is a tyrosine kinase inhibitor that specifically targets c-Kit, Abl, and platelet-derived growth factor receptor (PDGFR). It has been shown to be an effective treatment for patients with chronic myelogenous leukemia (CML) and gastrointestinal stromal tumors (GIST). These cancers are characterized by activating mutations of the Abl and c-Kit tyrosine kinases, respectively. To determine whether imatinib mesylate could be a potentially useful agent in the treatment of endometrial cancer, we assessed the expressions of Abl, c-Kit, and PDGFR in both primary and recurrent endometrial carcinoma.
We performed immunohistochemical analysis on formalin-fixed, paraffin-embedded sections from 63 patients: 33 with endometrioid endometrial carcinoma (EEC), 11 with uterine papillary serous carcinoma (UPSC), 12 with recurrent EEC, and seven with recurrent UPSC. The sections were stained with commercially available antibodies for Abl, PDGFR, and c-Kit. The sections were also stained for phosphorylated Abl and phosphorylated PDGFR.
Among the primary EEC, 28/33 (85%) stained positively for Abl and 30/33 (91%) were positive for PDGFR. Of the primary UPSC, 8/11 (73%) were positive for Abl. In addition, 8/11 (73%) of the primary UPSC tumors were positive for PDGFR. Neither the primary EEC (0/33) nor the primary UPSC (0/11) expressed c-Kit. Of the recurrent EEC tumors, 11/12 (92%) were positive for Abl expression, 12/12 (100%) were positive for PDGFR, and 2/8 (25%) were positive for c-Kit. Of the recurrent UPSC, 6/7 (86%) were positive for Abl, 7/7 (100%) were positive for PDGFR, and 2/4 (50%) for c-Kit. In addition, the majority of primary and recurrent tumors were positive for phosphorylated Abl (primary EEC, 91%; primary UPSC, 64%; recurrent EEC, 83%; recurrent UPSC, 86%), and phosphorylated PDGFR (primary EEC, 46%; primary UPSC, 40%; recurrent EEC, 58%; recurrent UPSC, 100%). Within the EEC primary tumors, the differences in kinase expression by grade of tumor were not significant except for PDGFR kinase; the lower grade tumors (1 and 2) had more PDGFR expression than the grade 3 tumors (P < 0.05).
The majority of primary and recurrent EEC, as well as primary and recurrent UPSC express Abl and PDGFR. This preclinical data suggest that imatinib mesylate may be useful in the treatment of patients with endometrial carcinoma.</description><subject>Abl</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Benzamides</subject><subject>Carcinoma, Endometrioid - drug therapy</subject><subject>Carcinoma, Endometrioid - enzymology</subject><subject>Carcinoma, Endometrioid - pathology</subject><subject>Endometrial carcinoma</subject><subject>Endometrial Neoplasms - drug therapy</subject><subject>Endometrial Neoplasms - enzymology</subject><subject>Endometrial Neoplasms - pathology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Female</subject><subject>Humans</subject><subject>Imatinib Mesylate</subject><subject>Immunohistochemistry</subject><subject>Paraffin Embedding</subject><subject>PDGFR</subject><subject>Phosphorylation</subject><subject>Piperazines - pharmacology</subject><subject>Protein-Tyrosine Kinases - antagonists & inhibitors</subject><subject>Protein-Tyrosine Kinases - biosynthesis</subject><subject>Protein-Tyrosine Kinases - metabolism</subject><subject>Proto-Oncogene Proteins c-abl - antagonists & inhibitors</subject><subject>Proto-Oncogene Proteins c-abl - biosynthesis</subject><subject>Proto-Oncogene Proteins c-abl - metabolism</subject><subject>Proto-Oncogene Proteins c-kit - biosynthesis</subject><subject>Proto-Oncogene Proteins c-kit - metabolism</subject><subject>Pyrimidines - pharmacology</subject><subject>Receptors, Platelet-Derived Growth Factor - antagonists & inhibitors</subject><subject>Receptors, Platelet-Derived Growth Factor - biosynthesis</subject><subject>Receptors, Platelet-Derived Growth Factor - metabolism</subject><subject>Uterine papillary serous carcinoma</subject><issn>0090-8258</issn><issn>1095-6859</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kLFOwzAURS0EoqXwBUgoE1vCcxIn9sCAUIFKlVhgthznuXJJ7GKniP49Ka3ExvSWc-_TPYRcU8go0Opune1WO-ezHKDMoMqA5SdkSkGwtOJMnJIpgICU54xPyEWMawAogObnZEJZwRmFekoW8-9NwBitd4k3ie3VYJ1tkh7jrlMDpoMKKxywTT6sUxFjYl2CrvU9DsGqLtEqaOt8ry7JmVFdxKvjnZH3p_nb40u6fH1ePD4sU10wNqSMlyXTTNWMqaICDtpwVnKTtwKaiqLJjWp0rQwzIjeFErRujGlF2ZS8NbUpZuT20LsJ_nOLcZC9jRq7Tjn02yirSoyzczGCxQHUwccY0MhNGPeFnaQg9wblWv4alHuDEio5GhxTN8f6bdNj-5c5KhuB-wOA48gvi0FGbdFpbG1APcjW238f_ADmh4St</recordid><startdate>200410</startdate><enddate>200410</enddate><creator>Slomovitz, Brian M.</creator><creator>Broaddus, Russell R.</creator><creator>Schmandt, Rosemarie</creator><creator>Wu, Weiguo</creator><creator>Oh, Jonathan C.</creator><creator>Ramondetta, Lois M.</creator><creator>Burke, Thomas W.</creator><creator>Gershenson, David M.</creator><creator>Lu, Karen H.</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>200410</creationdate><title>Expression of imatinib mesylate-targeted kinases in endometrial carcinoma</title><author>Slomovitz, Brian M. ; Broaddus, Russell R. ; Schmandt, Rosemarie ; Wu, Weiguo ; Oh, Jonathan C. ; Ramondetta, Lois M. ; Burke, Thomas W. ; Gershenson, David M. ; Lu, Karen H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c355t-58445c5a755a36080cf8548f2d90b61ef2fabc7af5f92f3a917bffd94b48df7f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Abl</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Benzamides</topic><topic>Carcinoma, Endometrioid - drug therapy</topic><topic>Carcinoma, Endometrioid - enzymology</topic><topic>Carcinoma, Endometrioid - pathology</topic><topic>Endometrial carcinoma</topic><topic>Endometrial Neoplasms - drug therapy</topic><topic>Endometrial Neoplasms - enzymology</topic><topic>Endometrial Neoplasms - pathology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Female</topic><topic>Humans</topic><topic>Imatinib Mesylate</topic><topic>Immunohistochemistry</topic><topic>Paraffin Embedding</topic><topic>PDGFR</topic><topic>Phosphorylation</topic><topic>Piperazines - pharmacology</topic><topic>Protein-Tyrosine Kinases - antagonists & inhibitors</topic><topic>Protein-Tyrosine Kinases - biosynthesis</topic><topic>Protein-Tyrosine Kinases - metabolism</topic><topic>Proto-Oncogene Proteins c-abl - antagonists & inhibitors</topic><topic>Proto-Oncogene Proteins c-abl - biosynthesis</topic><topic>Proto-Oncogene Proteins c-abl - metabolism</topic><topic>Proto-Oncogene Proteins c-kit - biosynthesis</topic><topic>Proto-Oncogene Proteins c-kit - metabolism</topic><topic>Pyrimidines - pharmacology</topic><topic>Receptors, Platelet-Derived Growth Factor - antagonists & inhibitors</topic><topic>Receptors, Platelet-Derived Growth Factor - biosynthesis</topic><topic>Receptors, Platelet-Derived Growth Factor - metabolism</topic><topic>Uterine papillary serous carcinoma</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Slomovitz, Brian M.</creatorcontrib><creatorcontrib>Broaddus, Russell R.</creatorcontrib><creatorcontrib>Schmandt, Rosemarie</creatorcontrib><creatorcontrib>Wu, Weiguo</creatorcontrib><creatorcontrib>Oh, Jonathan C.</creatorcontrib><creatorcontrib>Ramondetta, Lois M.</creatorcontrib><creatorcontrib>Burke, Thomas W.</creatorcontrib><creatorcontrib>Gershenson, David M.</creatorcontrib><creatorcontrib>Lu, Karen H.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Gynecologic oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Slomovitz, Brian M.</au><au>Broaddus, Russell R.</au><au>Schmandt, Rosemarie</au><au>Wu, Weiguo</au><au>Oh, Jonathan C.</au><au>Ramondetta, Lois M.</au><au>Burke, Thomas W.</au><au>Gershenson, David M.</au><au>Lu, Karen H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression of imatinib mesylate-targeted kinases in endometrial carcinoma</atitle><jtitle>Gynecologic oncology</jtitle><addtitle>Gynecol Oncol</addtitle><date>2004-10</date><risdate>2004</risdate><volume>95</volume><issue>1</issue><spage>32</spage><epage>36</epage><pages>32-36</pages><issn>0090-8258</issn><eissn>1095-6859</eissn><abstract>Imatinib mesylate is a tyrosine kinase inhibitor that specifically targets c-Kit, Abl, and platelet-derived growth factor receptor (PDGFR). It has been shown to be an effective treatment for patients with chronic myelogenous leukemia (CML) and gastrointestinal stromal tumors (GIST). These cancers are characterized by activating mutations of the Abl and c-Kit tyrosine kinases, respectively. To determine whether imatinib mesylate could be a potentially useful agent in the treatment of endometrial cancer, we assessed the expressions of Abl, c-Kit, and PDGFR in both primary and recurrent endometrial carcinoma.
We performed immunohistochemical analysis on formalin-fixed, paraffin-embedded sections from 63 patients: 33 with endometrioid endometrial carcinoma (EEC), 11 with uterine papillary serous carcinoma (UPSC), 12 with recurrent EEC, and seven with recurrent UPSC. The sections were stained with commercially available antibodies for Abl, PDGFR, and c-Kit. The sections were also stained for phosphorylated Abl and phosphorylated PDGFR.
Among the primary EEC, 28/33 (85%) stained positively for Abl and 30/33 (91%) were positive for PDGFR. Of the primary UPSC, 8/11 (73%) were positive for Abl. In addition, 8/11 (73%) of the primary UPSC tumors were positive for PDGFR. Neither the primary EEC (0/33) nor the primary UPSC (0/11) expressed c-Kit. Of the recurrent EEC tumors, 11/12 (92%) were positive for Abl expression, 12/12 (100%) were positive for PDGFR, and 2/8 (25%) were positive for c-Kit. Of the recurrent UPSC, 6/7 (86%) were positive for Abl, 7/7 (100%) were positive for PDGFR, and 2/4 (50%) for c-Kit. In addition, the majority of primary and recurrent tumors were positive for phosphorylated Abl (primary EEC, 91%; primary UPSC, 64%; recurrent EEC, 83%; recurrent UPSC, 86%), and phosphorylated PDGFR (primary EEC, 46%; primary UPSC, 40%; recurrent EEC, 58%; recurrent UPSC, 100%). Within the EEC primary tumors, the differences in kinase expression by grade of tumor were not significant except for PDGFR kinase; the lower grade tumors (1 and 2) had more PDGFR expression than the grade 3 tumors (P < 0.05).
The majority of primary and recurrent EEC, as well as primary and recurrent UPSC express Abl and PDGFR. This preclinical data suggest that imatinib mesylate may be useful in the treatment of patients with endometrial carcinoma.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>15385107</pmid><doi>10.1016/j.ygyno.2004.06.052</doi><tpages>5</tpages></addata></record> |
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| subjects | Abl Antineoplastic Agents - pharmacology Benzamides Carcinoma, Endometrioid - drug therapy Carcinoma, Endometrioid - enzymology Carcinoma, Endometrioid - pathology Endometrial carcinoma Endometrial Neoplasms - drug therapy Endometrial Neoplasms - enzymology Endometrial Neoplasms - pathology Enzyme Inhibitors - pharmacology Female Humans Imatinib Mesylate Immunohistochemistry Paraffin Embedding PDGFR Phosphorylation Piperazines - pharmacology Protein-Tyrosine Kinases - antagonists & inhibitors Protein-Tyrosine Kinases - biosynthesis Protein-Tyrosine Kinases - metabolism Proto-Oncogene Proteins c-abl - antagonists & inhibitors Proto-Oncogene Proteins c-abl - biosynthesis Proto-Oncogene Proteins c-abl - metabolism Proto-Oncogene Proteins c-kit - biosynthesis Proto-Oncogene Proteins c-kit - metabolism Pyrimidines - pharmacology Receptors, Platelet-Derived Growth Factor - antagonists & inhibitors Receptors, Platelet-Derived Growth Factor - biosynthesis Receptors, Platelet-Derived Growth Factor - metabolism Uterine papillary serous carcinoma |
| title | Expression of imatinib mesylate-targeted kinases in endometrial carcinoma |
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