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Therapeutic efficacy of lenvatinib in nonviral unresectable hepatocellular carcinoma
Aim To investigate the therapeutic effect of lenvatinib (LEN) in liver disease etiology, especially nonviral hepatocellular carcinoma (HCC). Methods and Results Sixty‐seven patients with unresectable advanced HCC (u‐HCC) treated with LEN and consisting of 26 hepatitis C virus (HCV), 19 hepatitis B v...
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| Published in: | JGH open 2021-11, Vol.5 (11), p.1275-1283 |
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| creator | Tomonari, Tetsu Sato, Yasushi Tanaka, Hironori Mitsuhashi, Takeshi Hirao, Akihiro Tanaka, Takahiro Taniguchi, Tatsuya Okamoto, Koichi Sogabe, Masahiro Miyamoto, Hiroshi Muguruma, Naoki Takayama, Tetsuji |
| description | Aim
To investigate the therapeutic effect of lenvatinib (LEN) in liver disease etiology, especially nonviral hepatocellular carcinoma (HCC).
Methods and Results
Sixty‐seven patients with unresectable advanced HCC (u‐HCC) treated with LEN and consisting of 26 hepatitis C virus (HCV), 19 hepatitis B virus (HBV), 11 alcohol, and 11 nonalcoholic steatohepatitis (NASH) cases were retrospectively recruited. Univariate and multivariate Cox proportional hazard models were used to determine predictive factors for survival. The objective response rate in the nonviral (alcohol and NASH) group was higher than that in the viral group (59.1% [13/22] vs. 46.7% [21/45]). Progression‐free survival was significantly longer in the nonviral group than in the viral group (13.7 vs. 6.6 months; hazard ratio [HR] 0.324; 95% confidence interval [CI] 0.174–0.602; P |
| doi_str_mv | 10.1002/jgh3.12663 |
| format | article |
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To investigate the therapeutic effect of lenvatinib (LEN) in liver disease etiology, especially nonviral hepatocellular carcinoma (HCC).
Methods and Results
Sixty‐seven patients with unresectable advanced HCC (u‐HCC) treated with LEN and consisting of 26 hepatitis C virus (HCV), 19 hepatitis B virus (HBV), 11 alcohol, and 11 nonalcoholic steatohepatitis (NASH) cases were retrospectively recruited. Univariate and multivariate Cox proportional hazard models were used to determine predictive factors for survival. The objective response rate in the nonviral (alcohol and NASH) group was higher than that in the viral group (59.1% [13/22] vs. 46.7% [21/45]). Progression‐free survival was significantly longer in the nonviral group than in the viral group (13.7 vs. 6.6 months; hazard ratio [HR] 0.324; 95% confidence interval [CI] 0.174–0.602; P < 0.01). Similarly, median overall survival (OS) was significantly longer in the nonviral group than in the viral group (not evaluable vs. 15.9 months; HR = 0.277; 95% CI = 0.116–0.662; P < 0.01). Multivariate analysis revealed that portal vein invasion (HR = 5.327, P = 0.0025), treatment line (HR = 0.455, P = 0.023), and etiology (HR = 0.180, P = 0.00055) were significant independent factors associated with OS in u‐HCC patients treated with LEN.
Conclusion
Our results suggest that LEN is more effective against nonviral u‐HCC than against viral u‐HCC.
Kaplan–Meier analysis of progression‐free survival among patients with unresectable advanced hepatocellular carcinoma treated with lenvatinib according to etiology. The PFS in the non‐viral group was significantly longer than that in the viral group. Our results suggest that LEN is more effective against non‐viral u‐HCC than against viral u‐HCC.</description><identifier>ISSN: 2397-9070</identifier><identifier>EISSN: 2397-9070</identifier><identifier>DOI: 10.1002/jgh3.12663</identifier><identifier>PMID: 34816013</identifier><language>eng</language><publisher>Melbourne: Wiley Publishing Asia Pty Ltd</publisher><subject>Alcohol ; atezolizumab ; bevacizumab ; Diabetes ; Drug dosages ; Etiology ; Hepatitis B ; Hepatitis C ; Immunotherapy ; Inflammation ; Laboratories ; lenvatinib ; Liver cancer ; Magnetic resonance imaging ; Monoclonal antibodies ; Original ; Patients ; Targeted cancer therapy ; Tumors</subject><ispartof>JGH open, 2021-11, Vol.5 (11), p.1275-1283</ispartof><rights>2021 The Authors. JGH Open published by Journal of Gastroenterology and Hepatology Foundation and John Wiley & Sons Australia, Ltd.</rights><rights>2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6243-8f125d0ce926fd6b13859aa0d26a3b470148177333f0b3f310e5a9d0931c3ee83</citedby><cites>FETCH-LOGICAL-c6243-8f125d0ce926fd6b13859aa0d26a3b470148177333f0b3f310e5a9d0931c3ee83</cites><orcidid>0000-0002-8484-9866 ; 0000-0003-4712-0192</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2597666703/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2597666703?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,11562,25753,27924,27925,37012,37013,44590,46052,46476,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34816013$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tomonari, Tetsu</creatorcontrib><creatorcontrib>Sato, Yasushi</creatorcontrib><creatorcontrib>Tanaka, Hironori</creatorcontrib><creatorcontrib>Mitsuhashi, Takeshi</creatorcontrib><creatorcontrib>Hirao, Akihiro</creatorcontrib><creatorcontrib>Tanaka, Takahiro</creatorcontrib><creatorcontrib>Taniguchi, Tatsuya</creatorcontrib><creatorcontrib>Okamoto, Koichi</creatorcontrib><creatorcontrib>Sogabe, Masahiro</creatorcontrib><creatorcontrib>Miyamoto, Hiroshi</creatorcontrib><creatorcontrib>Muguruma, Naoki</creatorcontrib><creatorcontrib>Takayama, Tetsuji</creatorcontrib><title>Therapeutic efficacy of lenvatinib in nonviral unresectable hepatocellular carcinoma</title><title>JGH open</title><addtitle>JGH Open</addtitle><description>Aim
To investigate the therapeutic effect of lenvatinib (LEN) in liver disease etiology, especially nonviral hepatocellular carcinoma (HCC).
Methods and Results
Sixty‐seven patients with unresectable advanced HCC (u‐HCC) treated with LEN and consisting of 26 hepatitis C virus (HCV), 19 hepatitis B virus (HBV), 11 alcohol, and 11 nonalcoholic steatohepatitis (NASH) cases were retrospectively recruited. Univariate and multivariate Cox proportional hazard models were used to determine predictive factors for survival. The objective response rate in the nonviral (alcohol and NASH) group was higher than that in the viral group (59.1% [13/22] vs. 46.7% [21/45]). Progression‐free survival was significantly longer in the nonviral group than in the viral group (13.7 vs. 6.6 months; hazard ratio [HR] 0.324; 95% confidence interval [CI] 0.174–0.602; P < 0.01). Similarly, median overall survival (OS) was significantly longer in the nonviral group than in the viral group (not evaluable vs. 15.9 months; HR = 0.277; 95% CI = 0.116–0.662; P < 0.01). Multivariate analysis revealed that portal vein invasion (HR = 5.327, P = 0.0025), treatment line (HR = 0.455, P = 0.023), and etiology (HR = 0.180, P = 0.00055) were significant independent factors associated with OS in u‐HCC patients treated with LEN.
Conclusion
Our results suggest that LEN is more effective against nonviral u‐HCC than against viral u‐HCC.
Kaplan–Meier analysis of progression‐free survival among patients with unresectable advanced hepatocellular carcinoma treated with lenvatinib according to etiology. The PFS in the non‐viral group was significantly longer than that in the viral group. Our results suggest that LEN is more effective against non‐viral u‐HCC than against viral u‐HCC.</description><subject>Alcohol</subject><subject>atezolizumab</subject><subject>bevacizumab</subject><subject>Diabetes</subject><subject>Drug dosages</subject><subject>Etiology</subject><subject>Hepatitis B</subject><subject>Hepatitis C</subject><subject>Immunotherapy</subject><subject>Inflammation</subject><subject>Laboratories</subject><subject>lenvatinib</subject><subject>Liver cancer</subject><subject>Magnetic resonance imaging</subject><subject>Monoclonal antibodies</subject><subject>Original</subject><subject>Patients</subject><subject>Targeted cancer therapy</subject><subject>Tumors</subject><issn>2397-9070</issn><issn>2397-9070</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNp9kc1q3DAURk1paUKaTR-gGLophUklXVuyNoUSmp8S6Ga6Flfy9YwGjzSV7Snz9tXESUi66EpCOhx9ul9RvOfsgjMmvmxWa7jgQkp4VZwK0GqhmWKvn-1PivNh2DDGeKN0DfJtcQJVwyXjcFosl2tKuKNp9K6krvMO3aGMXdlT2OPog7elD2WIYe8T9uUUEg3kRrQ9lWva4Rgd9f3UYyodJudD3OK74k2H_UDnD-tZ8evq-_LyZnH38_r28tvdwklRwaLpuKhb5kgL2bXScmhqjchaIRFspRjPMZUCgI5Z6IAzqlG3TAN3QNTAWXE7e9uIG7NLfovpYCJ6c38Q08pgyh_rybSWCW5roRveVs6qpuJY26quuqNX2-z6Ort2k91S6yiM-b8vpC9vgl-bVdybnBlUo7Pg04Mgxd8TDaPZ-uE4GwwUp8GIPPD8OgeV0Y__oJs4pZBHZUStlZRSMcjU55lyKQ5Dou4pDGfm2L05dm_uu8_wh-fxn9DHpjPAZ-CP7-nwH5X5cX0Ds_Qvawu4rA</recordid><startdate>202111</startdate><enddate>202111</enddate><creator>Tomonari, Tetsu</creator><creator>Sato, Yasushi</creator><creator>Tanaka, Hironori</creator><creator>Mitsuhashi, Takeshi</creator><creator>Hirao, Akihiro</creator><creator>Tanaka, Takahiro</creator><creator>Taniguchi, Tatsuya</creator><creator>Okamoto, Koichi</creator><creator>Sogabe, Masahiro</creator><creator>Miyamoto, Hiroshi</creator><creator>Muguruma, Naoki</creator><creator>Takayama, Tetsuji</creator><general>Wiley Publishing Asia Pty Ltd</general><general>John Wiley & Sons, Inc</general><general>Wiley</general><scope>24P</scope><scope>WIN</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-8484-9866</orcidid><orcidid>https://orcid.org/0000-0003-4712-0192</orcidid></search><sort><creationdate>202111</creationdate><title>Therapeutic efficacy of lenvatinib in nonviral unresectable hepatocellular carcinoma</title><author>Tomonari, Tetsu ; Sato, Yasushi ; Tanaka, Hironori ; Mitsuhashi, Takeshi ; Hirao, Akihiro ; Tanaka, Takahiro ; Taniguchi, Tatsuya ; Okamoto, Koichi ; Sogabe, Masahiro ; Miyamoto, Hiroshi ; Muguruma, Naoki ; Takayama, Tetsuji</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6243-8f125d0ce926fd6b13859aa0d26a3b470148177333f0b3f310e5a9d0931c3ee83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Alcohol</topic><topic>atezolizumab</topic><topic>bevacizumab</topic><topic>Diabetes</topic><topic>Drug dosages</topic><topic>Etiology</topic><topic>Hepatitis B</topic><topic>Hepatitis C</topic><topic>Immunotherapy</topic><topic>Inflammation</topic><topic>Laboratories</topic><topic>lenvatinib</topic><topic>Liver cancer</topic><topic>Magnetic resonance imaging</topic><topic>Monoclonal antibodies</topic><topic>Original</topic><topic>Patients</topic><topic>Targeted cancer therapy</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tomonari, Tetsu</creatorcontrib><creatorcontrib>Sato, Yasushi</creatorcontrib><creatorcontrib>Tanaka, Hironori</creatorcontrib><creatorcontrib>Mitsuhashi, Takeshi</creatorcontrib><creatorcontrib>Hirao, Akihiro</creatorcontrib><creatorcontrib>Tanaka, Takahiro</creatorcontrib><creatorcontrib>Taniguchi, Tatsuya</creatorcontrib><creatorcontrib>Okamoto, Koichi</creatorcontrib><creatorcontrib>Sogabe, Masahiro</creatorcontrib><creatorcontrib>Miyamoto, Hiroshi</creatorcontrib><creatorcontrib>Muguruma, Naoki</creatorcontrib><creatorcontrib>Takayama, Tetsuji</creatorcontrib><collection>Open Access: Wiley-Blackwell Open Access Journals</collection><collection>Wiley Free Archive</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>JGH open</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tomonari, Tetsu</au><au>Sato, Yasushi</au><au>Tanaka, Hironori</au><au>Mitsuhashi, Takeshi</au><au>Hirao, Akihiro</au><au>Tanaka, Takahiro</au><au>Taniguchi, Tatsuya</au><au>Okamoto, Koichi</au><au>Sogabe, Masahiro</au><au>Miyamoto, Hiroshi</au><au>Muguruma, Naoki</au><au>Takayama, Tetsuji</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Therapeutic efficacy of lenvatinib in nonviral unresectable hepatocellular carcinoma</atitle><jtitle>JGH open</jtitle><addtitle>JGH Open</addtitle><date>2021-11</date><risdate>2021</risdate><volume>5</volume><issue>11</issue><spage>1275</spage><epage>1283</epage><pages>1275-1283</pages><issn>2397-9070</issn><eissn>2397-9070</eissn><abstract>Aim
To investigate the therapeutic effect of lenvatinib (LEN) in liver disease etiology, especially nonviral hepatocellular carcinoma (HCC).
Methods and Results
Sixty‐seven patients with unresectable advanced HCC (u‐HCC) treated with LEN and consisting of 26 hepatitis C virus (HCV), 19 hepatitis B virus (HBV), 11 alcohol, and 11 nonalcoholic steatohepatitis (NASH) cases were retrospectively recruited. Univariate and multivariate Cox proportional hazard models were used to determine predictive factors for survival. The objective response rate in the nonviral (alcohol and NASH) group was higher than that in the viral group (59.1% [13/22] vs. 46.7% [21/45]). Progression‐free survival was significantly longer in the nonviral group than in the viral group (13.7 vs. 6.6 months; hazard ratio [HR] 0.324; 95% confidence interval [CI] 0.174–0.602; P < 0.01). Similarly, median overall survival (OS) was significantly longer in the nonviral group than in the viral group (not evaluable vs. 15.9 months; HR = 0.277; 95% CI = 0.116–0.662; P < 0.01). Multivariate analysis revealed that portal vein invasion (HR = 5.327, P = 0.0025), treatment line (HR = 0.455, P = 0.023), and etiology (HR = 0.180, P = 0.00055) were significant independent factors associated with OS in u‐HCC patients treated with LEN.
Conclusion
Our results suggest that LEN is more effective against nonviral u‐HCC than against viral u‐HCC.
Kaplan–Meier analysis of progression‐free survival among patients with unresectable advanced hepatocellular carcinoma treated with lenvatinib according to etiology. The PFS in the non‐viral group was significantly longer than that in the viral group. Our results suggest that LEN is more effective against non‐viral u‐HCC than against viral u‐HCC.</abstract><cop>Melbourne</cop><pub>Wiley Publishing Asia Pty Ltd</pub><pmid>34816013</pmid><doi>10.1002/jgh3.12663</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-8484-9866</orcidid><orcidid>https://orcid.org/0000-0003-4712-0192</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Alcohol atezolizumab bevacizumab Diabetes Drug dosages Etiology Hepatitis B Hepatitis C Immunotherapy Inflammation Laboratories lenvatinib Liver cancer Magnetic resonance imaging Monoclonal antibodies Original Patients Targeted cancer therapy Tumors |
| title | Therapeutic efficacy of lenvatinib in nonviral unresectable hepatocellular carcinoma |
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