Therapeutic preferability of gemcitabine for ARID1A-deficient ovarian clear cell carcinoma
Ovarian clear cell carcinoma (OCCC) is often resistant to conventional, standard chemotherapy using cytotoxic drugs. OCCC harbors a unique genomic feature of frequent (approximately 50%) ARID1A deficiency. The present study was performed to investigate standard chemotherapeutic options suitable for...
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| Veröffentlicht in: | Gynecologic oncology 2019-12, Vol.155 (3), p.489-498 |
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| creator | Kuroda, Takafumi Ogiwara, Hideaki Sasaki, Mariko Takahashi, Kazuaki Yoshida, Hiroshi Kiyokawa, Takako Sudo, Kazuki Tamura, Kenji Kato, Tomoyasu Okamoto, Aikou Kohno, Takashi |
| description | Ovarian clear cell carcinoma (OCCC) is often resistant to conventional, standard chemotherapy using cytotoxic drugs. OCCC harbors a unique genomic feature of frequent (approximately 50%) ARID1A deficiency. The present study was performed to investigate standard chemotherapeutic options suitable for ARID1A-deficient OCCC patients.
Drugs with selective toxicity to ARID1A-deficient OCCC cells were identified among six cytotoxic drugs used in standard chemotherapy for OCCC by employing multiple ARID1A-knockout cell lines and an OCCC cell line panel. Anti-tumor effects of drug treatment were assessed using a xenograft model. To obtain proof of concept in patients, seven OCCC patients who received single-agent therapy with gemcitabine were identified in a retrospective cohort of 149 OCCC patients. Patient samples and cases were analyzed for association between therapeutic response and ARID1A deficiency.
ARID1A-knockout and ARID1A-deficient OCCC cells had selective sensitivity to gemcitabine. IC50 values for gemcitabine of ARID1A-deficient cells were significantly lower than those of ARID1A-proficient cells (p = 0.0001). Growth of OCCC xenografts with ARID1A deficiency was inhibited by administration of gemcitabine, and gemcitabine treatment effectively induced apoptosis in ARID1A-deficient OCCC cells. Three ARID1A-deficient OCCC patients had significantly longer progression-free survival after gemcitabine treatment than four ARID1A-proficient OCCC patients (p = 0.02). An ARID1A-deficient case that was resistant to multiple cytotoxic drugs, including paclitaxel plus carboplatin in the adjuvant and etoposide plus irinotecan in the first-line treatment, exhibited a dramatic response to gemcitabine in the second-line treatment.
ARID1A-deficient OCCC patients could benefit from gemcitabine treatment in clinical settings.
•ARID1A-Deficient Ovarian Clear Cell Carcinoma (OCCC) cells were selectively sensitivity to gemcitabine.•Growth of xenograft derived from ARID1A-Deficient OCCC cells was suppressed by treatment with gemcitabine.•Gemcitabine treatment induced apoptosis in ARID1A-deficient OCCC cells.•Response to gemcitabine in ARID1A-deficient OCCC patients got better than that in ARID1A-proficient OCCC patients. |
| doi_str_mv | 10.1016/j.ygyno.2019.10.002 |
| format | Article |
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Drugs with selective toxicity to ARID1A-deficient OCCC cells were identified among six cytotoxic drugs used in standard chemotherapy for OCCC by employing multiple ARID1A-knockout cell lines and an OCCC cell line panel. Anti-tumor effects of drug treatment were assessed using a xenograft model. To obtain proof of concept in patients, seven OCCC patients who received single-agent therapy with gemcitabine were identified in a retrospective cohort of 149 OCCC patients. Patient samples and cases were analyzed for association between therapeutic response and ARID1A deficiency.
ARID1A-knockout and ARID1A-deficient OCCC cells had selective sensitivity to gemcitabine. IC50 values for gemcitabine of ARID1A-deficient cells were significantly lower than those of ARID1A-proficient cells (p = 0.0001). Growth of OCCC xenografts with ARID1A deficiency was inhibited by administration of gemcitabine, and gemcitabine treatment effectively induced apoptosis in ARID1A-deficient OCCC cells. Three ARID1A-deficient OCCC patients had significantly longer progression-free survival after gemcitabine treatment than four ARID1A-proficient OCCC patients (p = 0.02). An ARID1A-deficient case that was resistant to multiple cytotoxic drugs, including paclitaxel plus carboplatin in the adjuvant and etoposide plus irinotecan in the first-line treatment, exhibited a dramatic response to gemcitabine in the second-line treatment.
ARID1A-deficient OCCC patients could benefit from gemcitabine treatment in clinical settings.
•ARID1A-Deficient Ovarian Clear Cell Carcinoma (OCCC) cells were selectively sensitivity to gemcitabine.•Growth of xenograft derived from ARID1A-Deficient OCCC cells was suppressed by treatment with gemcitabine.•Gemcitabine treatment induced apoptosis in ARID1A-deficient OCCC cells.•Response to gemcitabine in ARID1A-deficient OCCC patients got better than that in ARID1A-proficient OCCC patients.</description><identifier>ISSN: 0090-8258</identifier><identifier>EISSN: 1095-6859</identifier><identifier>DOI: 10.1016/j.ygyno.2019.10.002</identifier><identifier>PMID: 31604667</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adenocarcinoma, Clear Cell - drug therapy ; Adenocarcinoma, Clear Cell - genetics ; Adenocarcinoma, Clear Cell - metabolism ; Adenocarcinoma, Clear Cell - pathology ; Adult ; Aged ; Animals ; Antimetabolites, Antineoplastic - administration & dosage ; Antimetabolites, Antineoplastic - pharmacology ; Apoptosis - drug effects ; ARID1A ; Cell Line, Tumor ; Deoxycytidine - administration & dosage ; Deoxycytidine - analogs & derivatives ; Deoxycytidine - pharmacology ; Female ; Gemcitabine ; Gene Knockout Techniques ; HCT116 Cells ; HEK293 Cells ; Humans ; Immunohistochemistry ; Mice ; Mice, Inbred BALB C ; Middle Aged ; Nuclear Proteins - deficiency ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Ovarian clear cell carcinoma (OCCC) ; Ovarian Neoplasms - drug therapy ; Ovarian Neoplasms - genetics ; Ovarian Neoplasms - metabolism ; Ovarian Neoplasms - pathology ; Precision medicine ; Predictive biomarker ; Random Allocation ; Transcription Factors - deficiency ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Xenograft Model Antitumor Assays</subject><ispartof>Gynecologic oncology, 2019-12, Vol.155 (3), p.489-498</ispartof><rights>2019 Elsevier Inc.</rights><rights>Copyright © 2019 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c425t-ad89949790d16c6ab3b6d84bbed12c24839a0ccb6ce0e53ac09c96fa55f7e633</citedby><cites>FETCH-LOGICAL-c425t-ad89949790d16c6ab3b6d84bbed12c24839a0ccb6ce0e53ac09c96fa55f7e633</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0090825819315598$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31604667$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kuroda, Takafumi</creatorcontrib><creatorcontrib>Ogiwara, Hideaki</creatorcontrib><creatorcontrib>Sasaki, Mariko</creatorcontrib><creatorcontrib>Takahashi, Kazuaki</creatorcontrib><creatorcontrib>Yoshida, Hiroshi</creatorcontrib><creatorcontrib>Kiyokawa, Takako</creatorcontrib><creatorcontrib>Sudo, Kazuki</creatorcontrib><creatorcontrib>Tamura, Kenji</creatorcontrib><creatorcontrib>Kato, Tomoyasu</creatorcontrib><creatorcontrib>Okamoto, Aikou</creatorcontrib><creatorcontrib>Kohno, Takashi</creatorcontrib><title>Therapeutic preferability of gemcitabine for ARID1A-deficient ovarian clear cell carcinoma</title><title>Gynecologic oncology</title><addtitle>Gynecol Oncol</addtitle><description>Ovarian clear cell carcinoma (OCCC) is often resistant to conventional, standard chemotherapy using cytotoxic drugs. OCCC harbors a unique genomic feature of frequent (approximately 50%) ARID1A deficiency. The present study was performed to investigate standard chemotherapeutic options suitable for ARID1A-deficient OCCC patients.
Drugs with selective toxicity to ARID1A-deficient OCCC cells were identified among six cytotoxic drugs used in standard chemotherapy for OCCC by employing multiple ARID1A-knockout cell lines and an OCCC cell line panel. Anti-tumor effects of drug treatment were assessed using a xenograft model. To obtain proof of concept in patients, seven OCCC patients who received single-agent therapy with gemcitabine were identified in a retrospective cohort of 149 OCCC patients. Patient samples and cases were analyzed for association between therapeutic response and ARID1A deficiency.
ARID1A-knockout and ARID1A-deficient OCCC cells had selective sensitivity to gemcitabine. IC50 values for gemcitabine of ARID1A-deficient cells were significantly lower than those of ARID1A-proficient cells (p = 0.0001). Growth of OCCC xenografts with ARID1A deficiency was inhibited by administration of gemcitabine, and gemcitabine treatment effectively induced apoptosis in ARID1A-deficient OCCC cells. Three ARID1A-deficient OCCC patients had significantly longer progression-free survival after gemcitabine treatment than four ARID1A-proficient OCCC patients (p = 0.02). An ARID1A-deficient case that was resistant to multiple cytotoxic drugs, including paclitaxel plus carboplatin in the adjuvant and etoposide plus irinotecan in the first-line treatment, exhibited a dramatic response to gemcitabine in the second-line treatment.
ARID1A-deficient OCCC patients could benefit from gemcitabine treatment in clinical settings.
•ARID1A-Deficient Ovarian Clear Cell Carcinoma (OCCC) cells were selectively sensitivity to gemcitabine.•Growth of xenograft derived from ARID1A-Deficient OCCC cells was suppressed by treatment with gemcitabine.•Gemcitabine treatment induced apoptosis in ARID1A-deficient OCCC cells.•Response to gemcitabine in ARID1A-deficient OCCC patients got better than that in ARID1A-proficient OCCC patients.</description><subject>Adenocarcinoma, Clear Cell - drug therapy</subject><subject>Adenocarcinoma, Clear Cell - genetics</subject><subject>Adenocarcinoma, Clear Cell - metabolism</subject><subject>Adenocarcinoma, Clear Cell - pathology</subject><subject>Adult</subject><subject>Aged</subject><subject>Animals</subject><subject>Antimetabolites, Antineoplastic - administration & dosage</subject><subject>Antimetabolites, Antineoplastic - pharmacology</subject><subject>Apoptosis - drug effects</subject><subject>ARID1A</subject><subject>Cell Line, Tumor</subject><subject>Deoxycytidine - administration & dosage</subject><subject>Deoxycytidine - analogs & derivatives</subject><subject>Deoxycytidine - pharmacology</subject><subject>Female</subject><subject>Gemcitabine</subject><subject>Gene Knockout Techniques</subject><subject>HCT116 Cells</subject><subject>HEK293 Cells</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Middle Aged</subject><subject>Nuclear Proteins - deficiency</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>Ovarian clear cell carcinoma (OCCC)</subject><subject>Ovarian Neoplasms - drug therapy</subject><subject>Ovarian Neoplasms - genetics</subject><subject>Ovarian Neoplasms - metabolism</subject><subject>Ovarian Neoplasms - pathology</subject><subject>Precision medicine</subject><subject>Predictive biomarker</subject><subject>Random Allocation</subject><subject>Transcription Factors - deficiency</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Xenograft Model Antitumor Assays</subject><issn>0090-8258</issn><issn>1095-6859</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE9r3DAQxUVJaLZJPkGh6JiLtyPL0lqHHJYkbQOBQNlTL0Iej1MttrWVvAv77SN30xx7Gubx5s_7MfZZwFKA0F-3y-PLcQzLEoTJyhKg_MAWAowqdK3MGVsAGCjqUtUX7FNKWwCQIMqP7EIKDZXWqwX7tflN0e1oP3nku0hd7hrf--nIQ8dfaEA_ZWEk3oXI1z8f78W6aKnz6GmceDi46N3IsScXOVLfc3QR_RgGd8XOO9cnun6rl2zz7WFz96N4ev7-eLd-KrAq1VS4tjamMisDrdCoXSMb3dZV01ArSiyrWhoHiI1GAlLSIRg0unNKdSvSUl6ym9PaXQx_9pQmO_g0f-JGCvtkSwkKlK6kyVZ5smIMKeWwdhf94OLRCrAzU7u1f5nameksZqZ56svbgX0zUPs-8w9iNtyeDJRTHjxFm2Y6SK2PhJNtg__vgVd0GIoE</recordid><startdate>201912</startdate><enddate>201912</enddate><creator>Kuroda, Takafumi</creator><creator>Ogiwara, Hideaki</creator><creator>Sasaki, Mariko</creator><creator>Takahashi, Kazuaki</creator><creator>Yoshida, Hiroshi</creator><creator>Kiyokawa, Takako</creator><creator>Sudo, Kazuki</creator><creator>Tamura, Kenji</creator><creator>Kato, Tomoyasu</creator><creator>Okamoto, Aikou</creator><creator>Kohno, Takashi</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>201912</creationdate><title>Therapeutic preferability of gemcitabine for ARID1A-deficient ovarian clear cell carcinoma</title><author>Kuroda, Takafumi ; Ogiwara, Hideaki ; Sasaki, Mariko ; Takahashi, Kazuaki ; Yoshida, Hiroshi ; Kiyokawa, Takako ; Sudo, Kazuki ; Tamura, Kenji ; Kato, Tomoyasu ; Okamoto, Aikou ; Kohno, Takashi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c425t-ad89949790d16c6ab3b6d84bbed12c24839a0ccb6ce0e53ac09c96fa55f7e633</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adenocarcinoma, Clear Cell - drug therapy</topic><topic>Adenocarcinoma, Clear Cell - genetics</topic><topic>Adenocarcinoma, Clear Cell - metabolism</topic><topic>Adenocarcinoma, Clear Cell - pathology</topic><topic>Adult</topic><topic>Aged</topic><topic>Animals</topic><topic>Antimetabolites, Antineoplastic - administration & dosage</topic><topic>Antimetabolites, Antineoplastic - pharmacology</topic><topic>Apoptosis - drug effects</topic><topic>ARID1A</topic><topic>Cell Line, Tumor</topic><topic>Deoxycytidine - administration & dosage</topic><topic>Deoxycytidine - analogs & derivatives</topic><topic>Deoxycytidine - pharmacology</topic><topic>Female</topic><topic>Gemcitabine</topic><topic>Gene Knockout Techniques</topic><topic>HCT116 Cells</topic><topic>HEK293 Cells</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Middle Aged</topic><topic>Nuclear Proteins - deficiency</topic><topic>Nuclear Proteins - genetics</topic><topic>Nuclear Proteins - metabolism</topic><topic>Ovarian clear cell carcinoma (OCCC)</topic><topic>Ovarian Neoplasms - drug therapy</topic><topic>Ovarian Neoplasms - genetics</topic><topic>Ovarian Neoplasms - metabolism</topic><topic>Ovarian Neoplasms - pathology</topic><topic>Precision medicine</topic><topic>Predictive biomarker</topic><topic>Random Allocation</topic><topic>Transcription Factors - deficiency</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kuroda, Takafumi</creatorcontrib><creatorcontrib>Ogiwara, Hideaki</creatorcontrib><creatorcontrib>Sasaki, Mariko</creatorcontrib><creatorcontrib>Takahashi, Kazuaki</creatorcontrib><creatorcontrib>Yoshida, Hiroshi</creatorcontrib><creatorcontrib>Kiyokawa, Takako</creatorcontrib><creatorcontrib>Sudo, Kazuki</creatorcontrib><creatorcontrib>Tamura, Kenji</creatorcontrib><creatorcontrib>Kato, Tomoyasu</creatorcontrib><creatorcontrib>Okamoto, Aikou</creatorcontrib><creatorcontrib>Kohno, Takashi</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>Kuroda, Takafumi</au><au>Ogiwara, Hideaki</au><au>Sasaki, Mariko</au><au>Takahashi, Kazuaki</au><au>Yoshida, Hiroshi</au><au>Kiyokawa, Takako</au><au>Sudo, Kazuki</au><au>Tamura, Kenji</au><au>Kato, Tomoyasu</au><au>Okamoto, Aikou</au><au>Kohno, Takashi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Therapeutic preferability of gemcitabine for ARID1A-deficient ovarian clear cell carcinoma</atitle><jtitle>Gynecologic oncology</jtitle><addtitle>Gynecol Oncol</addtitle><date>2019-12</date><risdate>2019</risdate><volume>155</volume><issue>3</issue><spage>489</spage><epage>498</epage><pages>489-498</pages><issn>0090-8258</issn><eissn>1095-6859</eissn><abstract>Ovarian clear cell carcinoma (OCCC) is often resistant to conventional, standard chemotherapy using cytotoxic drugs. OCCC harbors a unique genomic feature of frequent (approximately 50%) ARID1A deficiency. The present study was performed to investigate standard chemotherapeutic options suitable for ARID1A-deficient OCCC patients.
Drugs with selective toxicity to ARID1A-deficient OCCC cells were identified among six cytotoxic drugs used in standard chemotherapy for OCCC by employing multiple ARID1A-knockout cell lines and an OCCC cell line panel. Anti-tumor effects of drug treatment were assessed using a xenograft model. To obtain proof of concept in patients, seven OCCC patients who received single-agent therapy with gemcitabine were identified in a retrospective cohort of 149 OCCC patients. Patient samples and cases were analyzed for association between therapeutic response and ARID1A deficiency.
ARID1A-knockout and ARID1A-deficient OCCC cells had selective sensitivity to gemcitabine. IC50 values for gemcitabine of ARID1A-deficient cells were significantly lower than those of ARID1A-proficient cells (p = 0.0001). Growth of OCCC xenografts with ARID1A deficiency was inhibited by administration of gemcitabine, and gemcitabine treatment effectively induced apoptosis in ARID1A-deficient OCCC cells. Three ARID1A-deficient OCCC patients had significantly longer progression-free survival after gemcitabine treatment than four ARID1A-proficient OCCC patients (p = 0.02). An ARID1A-deficient case that was resistant to multiple cytotoxic drugs, including paclitaxel plus carboplatin in the adjuvant and etoposide plus irinotecan in the first-line treatment, exhibited a dramatic response to gemcitabine in the second-line treatment.
ARID1A-deficient OCCC patients could benefit from gemcitabine treatment in clinical settings.
•ARID1A-Deficient Ovarian Clear Cell Carcinoma (OCCC) cells were selectively sensitivity to gemcitabine.•Growth of xenograft derived from ARID1A-Deficient OCCC cells was suppressed by treatment with gemcitabine.•Gemcitabine treatment induced apoptosis in ARID1A-deficient OCCC cells.•Response to gemcitabine in ARID1A-deficient OCCC patients got better than that in ARID1A-proficient OCCC patients.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>31604667</pmid><doi>10.1016/j.ygyno.2019.10.002</doi><tpages>10</tpages></addata></record> |
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| subjects | Adenocarcinoma, Clear Cell - drug therapy Adenocarcinoma, Clear Cell - genetics Adenocarcinoma, Clear Cell - metabolism Adenocarcinoma, Clear Cell - pathology Adult Aged Animals Antimetabolites, Antineoplastic - administration & dosage Antimetabolites, Antineoplastic - pharmacology Apoptosis - drug effects ARID1A Cell Line, Tumor Deoxycytidine - administration & dosage Deoxycytidine - analogs & derivatives Deoxycytidine - pharmacology Female Gemcitabine Gene Knockout Techniques HCT116 Cells HEK293 Cells Humans Immunohistochemistry Mice Mice, Inbred BALB C Middle Aged Nuclear Proteins - deficiency Nuclear Proteins - genetics Nuclear Proteins - metabolism Ovarian clear cell carcinoma (OCCC) Ovarian Neoplasms - drug therapy Ovarian Neoplasms - genetics Ovarian Neoplasms - metabolism Ovarian Neoplasms - pathology Precision medicine Predictive biomarker Random Allocation Transcription Factors - deficiency Transcription Factors - genetics Transcription Factors - metabolism Xenograft Model Antitumor Assays |
| title | Therapeutic preferability of gemcitabine for ARID1A-deficient ovarian clear cell carcinoma |
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