Autologous hematopoietic stem cell transplantation for efficient treatment of multisystem, high-risk, BRAF V600E-negative Langerhans cell histiocytosis
Langerhans cell histiocytosis (LCH) is a disorder caused by clonal proliferation of CD1a+/CD207+ cells and characterized by varying degrees of organ involvement. Treatment of LCH is risk adapted; patients with multisystem disease and risk-organ involvement require more intensive therapy. Optimal the...
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| Veröffentlicht in: | Journal of international medical research 2019-09, Vol.47 (9), p.4522-4529 |
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| creator | Pan, Yaozhu Xi, Rui Wang, Cunbang Fang, Lei Bai, Jiaofeng Cai, Yonggang Guo, Min Qiao, Ruiyun Lan, Xu Yin, Jiaojiao Yang, Ke Bai, Hai |
| description | Langerhans cell histiocytosis (LCH) is a disorder caused by clonal proliferation of CD1a+/CD207+ cells and characterized by varying degrees of organ involvement. Treatment of LCH is risk adapted; patients with multisystem disease and risk-organ involvement require more intensive therapy. Optimal therapies for multisystem, high-risk LCH remain uncertain. Recently, targeted therapy using inhibitors of mutated BRAF (the gene encoding serine/threonine-protein kinase B-Raf) has proven very effective in patients with multisystem refractory LCH. Herein, we report a case of LCH with involvement of the bones, liver, and lymph nodes. Using next-generation sequencing of the patient’s pathological sample, we identified a mutation in MAP2K1 in exon 3 (c.362G>C, p.Cys121Ser) and no mutation in BRAF; thus, high-risk, multisystem LCH with MAP2K1 mutation and wild-type BRAF was diagnosed. After four chemotherapy treatments (COEP regimen), the patient received autologous hematopoietic stem cell transplantation (auto-HSCT). Complete remission was confirmed by follow-up positron emission tomography–computed tomography, which showed no lesions in liver, lymph nodes, or bones compared with the pretreatment period. To date, the patient has sustained good health for 24 months. In conclusion, auto-HSCT may be an effective treatment option for high-risk, multisystem BRAF V600E-negative LCH. |
| doi_str_mv | 10.1177/0300060519864807 |
| format | Article |
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Treatment of LCH is risk adapted; patients with multisystem disease and risk-organ involvement require more intensive therapy. Optimal therapies for multisystem, high-risk LCH remain uncertain. Recently, targeted therapy using inhibitors of mutated BRAF (the gene encoding serine/threonine-protein kinase B-Raf) has proven very effective in patients with multisystem refractory LCH. Herein, we report a case of LCH with involvement of the bones, liver, and lymph nodes. Using next-generation sequencing of the patient’s pathological sample, we identified a mutation in MAP2K1 in exon 3 (c.362G>C, p.Cys121Ser) and no mutation in BRAF; thus, high-risk, multisystem LCH with MAP2K1 mutation and wild-type BRAF was diagnosed. After four chemotherapy treatments (COEP regimen), the patient received autologous hematopoietic stem cell transplantation (auto-HSCT). Complete remission was confirmed by follow-up positron emission tomography–computed tomography, which showed no lesions in liver, lymph nodes, or bones compared with the pretreatment period. To date, the patient has sustained good health for 24 months. In conclusion, auto-HSCT may be an effective treatment option for high-risk, multisystem BRAF V600E-negative LCH.</description><identifier>ISSN: 0300-0605</identifier><identifier>EISSN: 1473-2300</identifier><identifier>DOI: 10.1177/0300060519864807</identifier><identifier>PMID: 31426694</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Adult ; Autoimmune diseases ; Biopsy ; Case Reports ; Hematopoietic Stem Cell Transplantation ; Histiocytosis, Langerhans-Cell - diagnostic imaging ; Histiocytosis, Langerhans-Cell - pathology ; Histiocytosis, Langerhans-Cell - therapy ; Humans ; Kinases ; Liver - diagnostic imaging ; Liver - pathology ; Lymph Nodes - diagnostic imaging ; Lymph Nodes - pathology ; Lymphatic system ; Male ; Mutation ; Positron Emission Tomography Computed Tomography ; Proto-Oncogene Proteins B-raf - genetics ; Risk Factors ; Stem cell transplantation ; Stem cells ; Transplantation, Autologous</subject><ispartof>Journal of international medical research, 2019-09, Vol.47 (9), p.4522-4529</ispartof><rights>The Author(s) 2019</rights><rights>The Author(s) 2019. This work is licensed under the Creative Commons Attribution – Non-Commercial License http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s) 2019 2019 SAGE Publications</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c462t-8e4823d0a43bb0608796f74a496455fc635452c7da8cd31b230196366dada42a3</citedby><cites>FETCH-LOGICAL-c462t-8e4823d0a43bb0608796f74a496455fc635452c7da8cd31b230196366dada42a3</cites><orcidid>0000-0003-2752-8342 ; 0000-0002-3111-6933</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6753533/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6753533/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,21945,27830,27901,27902,44921,45309,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31426694$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pan, Yaozhu</creatorcontrib><creatorcontrib>Xi, Rui</creatorcontrib><creatorcontrib>Wang, Cunbang</creatorcontrib><creatorcontrib>Fang, Lei</creatorcontrib><creatorcontrib>Bai, Jiaofeng</creatorcontrib><creatorcontrib>Cai, Yonggang</creatorcontrib><creatorcontrib>Guo, Min</creatorcontrib><creatorcontrib>Qiao, Ruiyun</creatorcontrib><creatorcontrib>Lan, Xu</creatorcontrib><creatorcontrib>Yin, Jiaojiao</creatorcontrib><creatorcontrib>Yang, Ke</creatorcontrib><creatorcontrib>Bai, Hai</creatorcontrib><title>Autologous hematopoietic stem cell transplantation for efficient treatment of multisystem, high-risk, BRAF V600E-negative Langerhans cell histiocytosis</title><title>Journal of international medical research</title><addtitle>J Int Med Res</addtitle><description>Langerhans cell histiocytosis (LCH) is a disorder caused by clonal proliferation of CD1a+/CD207+ cells and characterized by varying degrees of organ involvement. Treatment of LCH is risk adapted; patients with multisystem disease and risk-organ involvement require more intensive therapy. Optimal therapies for multisystem, high-risk LCH remain uncertain. Recently, targeted therapy using inhibitors of mutated BRAF (the gene encoding serine/threonine-protein kinase B-Raf) has proven very effective in patients with multisystem refractory LCH. Herein, we report a case of LCH with involvement of the bones, liver, and lymph nodes. Using next-generation sequencing of the patient’s pathological sample, we identified a mutation in MAP2K1 in exon 3 (c.362G>C, p.Cys121Ser) and no mutation in BRAF; thus, high-risk, multisystem LCH with MAP2K1 mutation and wild-type BRAF was diagnosed. After four chemotherapy treatments (COEP regimen), the patient received autologous hematopoietic stem cell transplantation (auto-HSCT). Complete remission was confirmed by follow-up positron emission tomography–computed tomography, which showed no lesions in liver, lymph nodes, or bones compared with the pretreatment period. To date, the patient has sustained good health for 24 months. In conclusion, auto-HSCT may be an effective treatment option for high-risk, multisystem BRAF V600E-negative LCH.</description><subject>Adult</subject><subject>Autoimmune diseases</subject><subject>Biopsy</subject><subject>Case Reports</subject><subject>Hematopoietic Stem Cell Transplantation</subject><subject>Histiocytosis, Langerhans-Cell - diagnostic imaging</subject><subject>Histiocytosis, Langerhans-Cell - pathology</subject><subject>Histiocytosis, Langerhans-Cell - therapy</subject><subject>Humans</subject><subject>Kinases</subject><subject>Liver - diagnostic imaging</subject><subject>Liver - pathology</subject><subject>Lymph Nodes - diagnostic imaging</subject><subject>Lymph Nodes - pathology</subject><subject>Lymphatic system</subject><subject>Male</subject><subject>Mutation</subject><subject>Positron Emission Tomography Computed Tomography</subject><subject>Proto-Oncogene Proteins B-raf - genetics</subject><subject>Risk Factors</subject><subject>Stem cell transplantation</subject><subject>Stem cells</subject><subject>Transplantation, Autologous</subject><issn>0300-0605</issn><issn>1473-2300</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>AFRWT</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kU1v1DAQhi0EotvCnROyxIVD0_o7zgVpqdpSaaVKCLhaXsdJXBJ7sZ1K-0v4uzjaUqASJ4887zwz7wwAbzA6w7iuzxFFCAnEcSMFk6h-BlaY1bQi5f85WC3paskfgeOU7hBiRHDyEhxRXCLRsBX4uZ5zGEMf5gQHO-kcdsHZ7AxM2U7Q2HGEOWqfdqP2WWcXPOxChLbrnHHW55K1Ok9LFDo4zWN2ab_UnsLB9UMVXfp-Cj9-Xl_BbwKhy8rbvmDuLdxo39s4FPahzeBSwZt9DsmlV-BFp8dkXz-8J-Dr1eWXi0_V5vb65mK9qQwTJFfSMkloizSj221xKutGdDXTrBGM884Iyhknpm61NC3F27IY3AgqRKtbzYimJ-DDgbubt5NtTfER9ah20U067lXQTv2b8W5QfbhXouaUU1oA7x8AMfyYbcpqcmnxo70tS1WENKRpuKR1kb57Ir0Lc_TFniKFxKUs4xYVOqhMDClF2z0Og5Farq6eXr2UvP3bxGPB7zMXQXUQJN3bP13_C_wF8-a29w</recordid><startdate>20190901</startdate><enddate>20190901</enddate><creator>Pan, Yaozhu</creator><creator>Xi, Rui</creator><creator>Wang, Cunbang</creator><creator>Fang, Lei</creator><creator>Bai, Jiaofeng</creator><creator>Cai, Yonggang</creator><creator>Guo, Min</creator><creator>Qiao, Ruiyun</creator><creator>Lan, Xu</creator><creator>Yin, Jiaojiao</creator><creator>Yang, Ke</creator><creator>Bai, Hai</creator><general>SAGE Publications</general><general>Sage Publications Ltd</general><scope>AFRWT</scope><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>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><orcidid>https://orcid.org/0000-0003-2752-8342</orcidid><orcidid>https://orcid.org/0000-0002-3111-6933</orcidid></search><sort><creationdate>20190901</creationdate><title>Autologous hematopoietic stem cell transplantation for efficient treatment of multisystem, high-risk, BRAF V600E-negative Langerhans cell histiocytosis</title><author>Pan, Yaozhu ; 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Treatment of LCH is risk adapted; patients with multisystem disease and risk-organ involvement require more intensive therapy. Optimal therapies for multisystem, high-risk LCH remain uncertain. Recently, targeted therapy using inhibitors of mutated BRAF (the gene encoding serine/threonine-protein kinase B-Raf) has proven very effective in patients with multisystem refractory LCH. Herein, we report a case of LCH with involvement of the bones, liver, and lymph nodes. Using next-generation sequencing of the patient’s pathological sample, we identified a mutation in MAP2K1 in exon 3 (c.362G>C, p.Cys121Ser) and no mutation in BRAF; thus, high-risk, multisystem LCH with MAP2K1 mutation and wild-type BRAF was diagnosed. After four chemotherapy treatments (COEP regimen), the patient received autologous hematopoietic stem cell transplantation (auto-HSCT). Complete remission was confirmed by follow-up positron emission tomography–computed tomography, which showed no lesions in liver, lymph nodes, or bones compared with the pretreatment period. To date, the patient has sustained good health for 24 months. In conclusion, auto-HSCT may be an effective treatment option for high-risk, multisystem BRAF V600E-negative LCH.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>31426694</pmid><doi>10.1177/0300060519864807</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0003-2752-8342</orcidid><orcidid>https://orcid.org/0000-0002-3111-6933</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Autoimmune diseases Biopsy Case Reports Hematopoietic Stem Cell Transplantation Histiocytosis, Langerhans-Cell - diagnostic imaging Histiocytosis, Langerhans-Cell - pathology Histiocytosis, Langerhans-Cell - therapy Humans Kinases Liver - diagnostic imaging Liver - pathology Lymph Nodes - diagnostic imaging Lymph Nodes - pathology Lymphatic system Male Mutation Positron Emission Tomography Computed Tomography Proto-Oncogene Proteins B-raf - genetics Risk Factors Stem cell transplantation Stem cells Transplantation, Autologous |
| title | Autologous hematopoietic stem cell transplantation for efficient treatment of multisystem, high-risk, BRAF V600E-negative Langerhans cell histiocytosis |
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