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{{Infobox_gene}}
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{{GNF_Protein_box
| image = 
| image_source = 
| PDB =
| Name = Tumor necrosis factor receptor superfamily, member 8
| HGNCid = 11923
| Symbol = TNFRSF8
| AltSymbols =; CD30; D1S166E; KI-1
| OMIM = 153243
| ECnumber = 
| Homologene = 949
| MGIid = 99908
| GeneAtlas_image1 = PBB_GE_TNFRSF8_206729_at_tn.png
| Function = {{GNF_GO|id=GO:0004888 |text = transmembrane receptor activity}} {{GNF_GO|id=GO:0005515 |text = protein binding}}
| Component = {{GNF_GO|id=GO:0016020 |text = membrane}} {{GNF_GO|id=GO:0016021 |text = integral to membrane}}  
| Process = {{GNF_GO|id=GO:0007165 |text = signal transduction}} {{GNF_GO|id=GO:0008285 |text = negative regulation of cell proliferation}}
| Orthologs = {{GNF_Ortholog_box
    | Hs_EntrezGene = 943
    | Hs_Ensembl = ENSG00000120949
    | Hs_RefseqProtein = NP_001234
    | Hs_RefseqmRNA = NM_001243
    | Hs_GenLoc_db = 
    | Hs_GenLoc_chr = 1
    | Hs_GenLoc_start = 12046021
    | Hs_GenLoc_end = 12126851
    | Hs_Uniprot = P28908
    | Mm_EntrezGene = 21941
    | Mm_Ensembl = ENSMUSG00000028602
    | Mm_RefseqmRNA = NM_009401
    | Mm_RefseqProtein = NP_033427
    | Mm_GenLoc_db = 
    | Mm_GenLoc_chr = 4
    | Mm_GenLoc_start = 144535663
    | Mm_GenLoc_end = 144581834
    | Mm_Uniprot = Q60846
  }}
}}
'''CD30''', also known as '''TNFRSF8''', is a cell membrane [[protein]] of  the [[tumor necrosis factor receptor]] family and [[tumor marker]].
'''CD30''', also known as '''TNFRSF8''', is a cell membrane [[protein]] of  the [[tumor necrosis factor receptor]] family and [[tumor marker]].


This receptor is expressed by activated, but not by resting, [[T cell|T]] and [[B cell]]s. [[TRAF2]] and [[TRAF5]] can interact with this receptor, and mediate the signal transduction that leads to the activation of [[NF-kappaB]]. It is a positive regulator of [[apoptosis]], and also has been shown to limit the proliferative potential of autoreactive CD8 effector T cells and protect the body against autoimmunity. Two [[alternative splicing|alternatively spliced]] transcript variants of this gene encoding distinct isoforms have been reported.<ref name="entrez">{{cite web | title = Entrez Gene: TNFRSF8 tumor necrosis factor receptor superfamily, member 8| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=943| accessdate = }}</ref>
== Function ==


CD30 is associated with [[anaplastic large cell lymphoma]]. It is expressed in [[embryonal carcinoma]] but not in [[seminoma]] and is thus is a useful marker in distinguishing between these [[germ cell tumors]].<ref>{{cite journal |author=Teng LH, Lu DH, Xu QZ, Fu YJ, Yang H, He ZL |title=[Expression and diagnostic significance of OCT4, CD117 and CD30 in germ cell tumors] |language=Chinese |journal=Zhonghua Bing Li Xue Za Zhi |volume=34 |issue=11 |pages=711-5 |year=2005 |pmid=16536313 |doi=}}</ref>
This receptor is expressed by activated, but not by resting, [[T cell|T]] and [[B cell]]s. [[TRAF2]] and [[TRAF5]] can interact with this receptor, and mediate the signal transduction that leads to the activation of [[NF-kappaB]]. It is a positive regulator of [[apoptosis]], and also has been shown to limit the proliferative potential of autoreactive CD8 effector T cells and protect the body against autoimmunity. Two [[alternative splicing|alternatively spliced]] transcript variants of this gene encoding distinct isoforms have been reported.<ref name="entrez">{{cite web | title = Entrez Gene: TNFRSF8 tumor necrosis factor receptor superfamily, member 8| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=943| accessdate = }}</ref>


==References==
== Clinical significance ==
{{reflist|2}}
 
==Further reading==
CD30 is associated with [[anaplastic large cell lymphoma]]. It is expressed in [[embryonal carcinoma]] but not in [[seminoma]] and is thus a useful marker in distinguishing between these [[germ cell tumors]].<ref>{{cite journal | vauthors = Teng LH, Lu DH, Xu QZ, Fu YJ, Yang H, He ZL | title = [Expression and diagnostic significance of OCT4, CD117 and CD30 in germ cell tumors] | language = Chinese | journal = Zhonghua Bing Li Xue Za Zhi Chinese Journal of Pathology | volume = 34 | issue = 11 | pages = 711–5 | date = Nov 2005 | pmid = 16536313 | doi = }}</ref> CD30 and CD15 are also expressed on [[Reed-Sternberg cells]] typical for [[Hodgkin's lymphoma]].<ref>{{cite journal | vauthors = Gorczyca W, Tsang P, Liu Z, Wu CD, Dong HY, Goldstein M, Cohen P, Gangi M, Weisberger J | title = CD30-positive T-cell lymphomas co-expressing CD15: an immunohistochemical analysis | journal = International Journal of Oncology | volume = 22 | issue = 2 | pages = 319–24 | date = Feb 2003 | pmid = 12527929 | doi = 10.3892/ijo.22.2.319 }}</ref>
{{refbegin | 2}}
 
{{PBB_Further_reading
== Cancer treatment ==
| citations =  
 
*{{cite journal  | author=Schneider C, Hübinger G |title=Pleiotropic signal transduction mediated by human CD30: a member of the tumor necrosis factor receptor (TNFR) family. |journal=Leuk. Lymphoma |volume=43 |issue= 7 |pages= 1355-66 |year= 2003 |pmid= 12389614 |doi=  }}
CD30 is the target of the FDA approved therapeutic [[brentuximab vedotin]] (Adcetris).  It is approved for use in:
*{{cite journal  | author=Horie R, Higashihara M, Watanabe T |title=Hodgkin's lymphoma and CD30 signal transduction. |journal=Int. J. Hematol. |volume=77 |issue= 1 |pages= 37-47 |year= 2003 |pmid= 12568298 |doi= }}
# [[Hodgkin lymphoma]] (HL) (brentuximab vedotin) after failure of autologous stem cell transplant (ASCT)
*{{cite journal  | author=Tarkowski M |title=Expression and a role of CD30 in regulation of T-cell activity. |journal=Curr. Opin. Hematol. |volume=10 |issue= 4 |pages= 267-71 |year= 2004 |pmid= 12799531 |doi= }}
# HL in patients who are not ASCT candidates after failure of at least 2 multiagent chemotherapy regimens
*{{cite journal  | author=Granados S, Hwang ST |title=Roles for CD30 in the biology and treatment of CD30 lymphoproliferative diseases. |journal=J. Invest. Dermatol. |volume=122 |issue= 6 |pages= 1345-7 |year= 2004 |pmid= 15175022 |doi= 10.1111/j.0022-202X.2004.22616.x }}
# Systemic anaplastic large cell lymphoma (s[[ALCL]]) after failure of at least 1 multiagent chemotherapy regimen<ref>{{cite journal | vauthors = Deng C, Pan B, O'Connor OA | title = Brentuximab vedotin | journal = Clinical Cancer Research | volume = 19 | issue = 1 | pages = 22–7 | date = Jan 2013 | pmid = 23155186 | doi = 10.1158/1078-0432.CCR-12-0290 }}</ref>
*{{cite journal  | author=Dürkop H, Latza U, Hummel M, ''et al.'' |title=Molecular cloning and expression of a new member of the nerve growth factor receptor family that is characteristic for Hodgkin's disease. |journal=Cell |volume=68 |issue= 3 |pages= 421-7 |year= 1992 |pmid= 1310894 |doi= }}
# Primary cutaneous anaplastic large cell lymphoma (pcALCL) or CD30-expressing [[mycosis fungoides]] (MF) who have received prior systemic therapy<ref>{{cite web | url = https://www.fda.gov/Drugs/InformationOnDrugs/ApprovedDrugs/ucm584543.htm | title = FDA approves Brentuximab vedotin for the treatment of adult patients with primary cutaneous anaplastic large cell lymphoma | website = FDA.gov | access-date = March 2, 2018}}</ref>
*{{cite journal | author=Fonatsch C, Latza U, Dürkop H, ''et al.'' |title=Assignment of the human CD30 (Ki-1) gene to 1p36. |journal=Genomics |volume=14 |issue= 3 |pages= 825-6 |year= 1992 |pmid= 1330892 |doi= }}
 
*{{cite journal  | author=Josimovic-Alasevic O, Dürkop H, Schwarting R, ''et al.'' |title=Ki-1 (CD30) antigen is released by Ki-1-positive tumor cells ''in vitro'' and ''in vivo''. I. Partial characterization of soluble Ki-1 antigen and detection of the antigen in cell culture supernatants and in serum by an enzyme-linked immunosorbent assay. |journal=Eur. J. Immunol. |volume=19 |issue= 1 |pages= 157-62 |year= 1989 |pmid= 2537734 |doi=  }}
== Interactions ==
*{{cite journal | author=Stein H, Gerdes J, Schwab U, ''et al.'' |title=Identification of Hodgkin and Sternberg-reed cells as a unique cell type derived from a newly-detected small-cell population. |journal=Int. J. Cancer |volume=30 |issue= 4 |pages= 445-59 |year= 1983 |pmid= 6754630 |doi= }}
 
*{{cite journal | author=Jung W, Krueger S, Renner C, ''et al.'' |title=Opposite effects of the CD30 ligand are not due to CD30 mutations: results from cDNA cloning and sequence comparison of the CD30 antigen from different sources. |journal=Mol. Immunol. |volume=31 |issue= 17 |pages= 1329-34 |year= 1995 |pmid= 7527901 |doi= }}
CD30 has been shown to [[Protein-protein interaction|interact]] with [[TRAF5]],<ref name=pmid8999898>{{cite journal | vauthors = Aizawa S, Nakano H, Ishida T, Horie R, Nagai M, Ito K, Yagita H, Okumura K, Inoue J, Watanabe T | title = Tumor necrosis factor receptor-associated factor (TRAF) 5 and TRAF2 are involved in CD30-mediated NFkappaB activation | journal = The Journal of Biological Chemistry | volume = 272 | issue = 4 | pages = 2042–5 | date = Jan 1997 | pmid = 8999898 | doi = 10.1074/jbc.272.4.2042 }}</ref> [[TRAF1]],<ref name=pmid8943059>{{cite journal | vauthors = Ansieau S, Scheffrahn I, Mosialos G, Brand H, Duyster J, Kaye K, Harada J, Dougall B, Hübinger G, Kieff E, Herrmann F, Leutz A, Gruss HJ | title = Tumor necrosis factor receptor-associated factor (TRAF)-1, TRAF-2, and TRAF-3 interact in vivo with the CD30 cytoplasmic domain; TRAF-2 mediates CD30-induced nuclear factor kappa B activation | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 93 | issue = 24 | pages = 14053–8 | date = Nov 1996 | pmid = 8943059 | pmc = 19493 | doi = 10.1073/pnas.93.24.14053 }}{{Retracted paper}}</ref> [[TRAF2]]<ref name=pmid8999898/><ref name=pmid8943059/> and [[TRAF3]].<ref name=pmid8943059/>
*{{cite journal | author=Shiota M, Fujimoto J, Semba T, ''et al.'' |title=Hyperphosphorylation of a novel 80 kDa protein-tyrosine kinase similar to Ltk in a human Ki-1 lymphoma cell line, AMS3. |journal=Oncogene |volume=9 |issue= 6 |pages= 1567-74 |year= 1994 |pmid= 8183550 |doi= }}
{{Clear}}
*{{cite journal | author=Lee SY, Park CG, Choi Y |title=T cell receptor-dependent cell death of T cell hybridomas mediated by the CD30 cytoplasmic domain in association with tumor necrosis factor receptor-associated factors. |journal=J. Exp. Med. |volume=183 |issue= 2 |pages= 669-74 |year= 1996 |pmid= 8627180 |doi= }}
 
*{{cite journal | author=Gedrich RW, Gilfillan MC, Duckett CS, ''et al.'' |title=CD30 contains two binding sites with different specificities for members of the tumor necrosis factor receptor-associated factor family of signal transducing proteins. |journal=J. Biol. Chem. |volume=271 |issue= 22 |pages= 12852-8 |year= 1996 |pmid= 8662842 |doi= }}
== References ==
*{{cite journal | author=Horie R, Ito K, Tatewaki M, ''et al.'' |title=A variant CD30 protein lacking extracellular and transmembrane domains is induced in HL-60 by tetradecanoylphorbol acetate and is expressed in alveolar macrophages. |journal=Blood |volume=88 |issue= 7 |pages= 2422-32 |year= 1996 |pmid= 8839832 |doi= }}
{{reflist|33em}}
*{{cite journal | author=Ansieau S, Scheffrahn I, Mosialos G, ''et al.'' |title=Tumor necrosis factor receptor-associated factor (TRAF)-1, TRAF-2, and TRAF-3 interact ''in vivo'' with the CD30 cytoplasmic domain; TRAF-2 mediates CD30-induced nuclear factor kappa B activation. |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=93 |issue= 24 |pages= 14053-8 |year= 1997 |pmid= 8943059 |doi= }}
 
*{{cite journal | author=Aizawa S, Nakano H, Ishida T, ''et al.'' |title=Tumor necrosis factor receptor-associated factor (TRAF) 5 and TRAF2 are involved in CD30-mediated NFkappaB activation. |journal=J. Biol. Chem. |volume=272 |issue= 4 |pages= 2042-5 |year= 1997 |pmid= 8999898 |doi= }}
== Further reading ==
*{{cite journal | author=Lee SY, Lee SY, Choi Y |title=TRAF-interacting protein (TRIP): a novel component of the tumor necrosis factor receptor (TNFR)- and CD30-TRAF signaling complexes that inhibits TRAF2-mediated NF-kappaB activation. |journal=J. Exp. Med. |volume=185 |issue= 7 |pages= 1275-85 |year= 1997 |pmid= 9104814 |doi= }}
{{refbegin|33em}}
*{{cite journal | author=Boucher LM, Marengère LE, Lu Y, ''et al.'' |title=Binding sites of cytoplasmic effectors TRAF1, 2, and 3 on CD30 and other members of the TNF receptor superfamily. |journal=Biochem. Biophys. Res. Commun. |volume=233 |issue= 3 |pages= 592-600 |year= 1997 |pmid= 9168896 |doi= 10.1006/bbrc.1997.6509 }}
* {{cite journal | vauthors = Schneider C, Hübinger G | title = Pleiotropic signal transduction mediated by human CD30: a member of the tumor necrosis factor receptor (TNFR) family | journal = Leukemia & Lymphoma | volume = 43 | issue = 7 | pages = 1355–66 | date = Jul 2002 | pmid = 12389614 | doi = 10.1080/10428190290033288 }}
*{{cite journal | author=Duckett CS, Thompson CB |title=CD30-dependent degradation of TRAF2: implications for negative regulation of TRAF signaling and the control of cell survival. |journal=Genes Dev. |volume=11 |issue= 21 |pages= 2810-21 |year= 1997 |pmid= 9353251 |doi= }}
* {{cite journal | vauthors = Horie R, Higashihara M, Watanabe T | title = Hodgkin's lymphoma and CD30 signal transduction | journal = International Journal of Hematology | volume = 77 | issue = 1 | pages = 37–47 | date = Jan 2003 | pmid = 12568298 | doi = 10.1007/BF02982601 }}
*{{cite journal | author=Mizushima S, Fujita M, Ishida T, ''et al.'' |title=Cloning and characterization of a cDNA encoding the human homolog of tumor necrosis factor receptor-associated factor 5 (TRAF5). |journal=Gene |volume=207 |issue= 2 |pages= 135-40 |year= 1998 |pmid= 9511754 |doi=  }}
* {{cite journal | vauthors = Tarkowski M | title = Expression and a role of CD30 in regulation of T-cell activity | journal = Current Opinion in Hematology | volume = 10 | issue = 4 | pages = 267–71 | date = Jul 2003 | pmid = 12799531 | doi = 10.1097/00062752-200307000-00003 }}
*{{cite journal  | author=Kurts C, Carbone FR, Krummel MF, ''et al.'' |title=Signalling through CD30 protects against autoimmune diabetes mediated by CD8 T cells. |journal=Nature |volume=398 |issue= 6725 |pages= 341-4 |year= 1999 |pmid= 10192335 |doi= 10.1038/18692 }}
* {{cite journal | vauthors = Granados S, Hwang ST | title = Roles for CD30 in the biology and treatment of CD30 lymphoproliferative diseases | journal = The Journal of Investigative Dermatology | volume = 122 | issue = 6 | pages = 1345–7 | date = Jun 2004 | pmid = 15175022 | doi = 10.1111/j.0022-202X.2004.22616.x }}
}}
* {{cite journal | vauthors = Dürkop H, Latza U, Hummel M, Eitelbach F, Seed B, Stein H | title = Molecular cloning and expression of a new member of the nerve growth factor receptor family that is characteristic for Hodgkin's disease | journal = Cell | volume = 68 | issue = 3 | pages = 421–7 | date = Feb 1992 | pmid = 1310894 | doi = 10.1016/0092-8674(92)90180-K }}
* {{cite journal | vauthors = Fonatsch C, Latza U, Dürkop H, Rieder H, Stein H | title = Assignment of the human CD30 (Ki-1) gene to 1p36 | journal = Genomics | volume = 14 | issue = 3 | pages = 825–6 | date = Nov 1992 | pmid = 1330892 | doi = 10.1016/S0888-7543(05)80203-4 }}
* {{cite journal | vauthors = Josimovic-Alasevic O, Dürkop H, Schwarting R, Backé E, Stein H, Diamantstein T | title = Ki-1 (CD30) antigen is released by Ki-1-positive tumor cells in vitro and in vivo. I. Partial characterization of soluble Ki-1 antigen and detection of the antigen in cell culture supernatants and in serum by an enzyme-linked immunosorbent assay | journal = European Journal of Immunology | volume = 19 | issue = 1 | pages = 157–62 | date = Jan 1989 | pmid = 2537734 | doi = 10.1002/eji.1830190125 }}
* {{cite journal | vauthors = Stein H, Gerdes J, Schwab U, Lemke H, Mason DY, Ziegler A, Schienle W, Diehl V | title = Identification of Hodgkin and Sternberg-reed cells as a unique cell type derived from a newly-detected small-cell population | journal = International Journal of Cancer | volume = 30 | issue = 4 | pages = 445–59 | date = Oct 1982 | pmid = 6754630 | doi = 10.1002/ijc.2910300411 }}
* {{cite journal | vauthors = Jung W, Krueger S, Renner C, Gause A, Sahin U, Trümper L, Pfreundschuh M | title = Opposite effects of the CD30 ligand are not due to CD30 mutations: results from cDNA cloning and sequence comparison of the CD30 antigen from different sources | journal = Molecular Immunology | volume = 31 | issue = 17 | pages = 1329–34 | date = Dec 1994 | pmid = 7527901 | doi = 10.1016/0161-5890(94)90051-5 }}
* {{cite journal | vauthors = Shiota M, Fujimoto J, Semba T, Satoh H, Yamamoto T, Mori S | title = Hyperphosphorylation of a novel 80 kDa protein-tyrosine kinase similar to Ltk in a human Ki-1 lymphoma cell line, AMS3 | journal = Oncogene | volume = 9 | issue = 6 | pages = 1567–74 | date = Jun 1994 | pmid = 8183550 | doi = }}
* {{cite journal | vauthors = Lee SY, Park CG, Choi Y | title = T cell receptor-dependent cell death of T cell hybridomas mediated by the CD30 cytoplasmic domain in association with tumor necrosis factor receptor-associated factors | journal = The Journal of Experimental Medicine | volume = 183 | issue = 2 | pages = 669–74 | date = Feb 1996 | pmid = 8627180 | pmc = 2192463 | doi = 10.1084/jem.183.2.669 }}
* {{cite journal | vauthors = Gedrich RW, Gilfillan MC, Duckett CS, Van Dongen JL, Thompson CB | title = CD30 contains two binding sites with different specificities for members of the tumor necrosis factor receptor-associated factor family of signal transducing proteins | journal = The Journal of Biological Chemistry | volume = 271 | issue = 22 | pages = 12852–8 | date = May 1996 | pmid = 8662842 | doi = 10.1074/jbc.271.22.12852 }}
* {{cite journal | vauthors = Horie R, Ito K, Tatewaki M, Nagai M, Aizawa S, Higashihara M, Ishida T, Inoue J, Takizawa H, Watanabe T | title = A variant CD30 protein lacking extracellular and transmembrane domains is induced in HL-60 by tetradecanoylphorbol acetate and is expressed in alveolar macrophages | journal = Blood | volume = 88 | issue = 7 | pages = 2422–32 | date = Oct 1996 | pmid = 8839832 | doi =  }}
* {{cite journal | vauthors = Aizawa S, Nakano H, Ishida T, Horie R, Nagai M, Ito K, Yagita H, Okumura K, Inoue J, Watanabe T | title = Tumor necrosis factor receptor-associated factor (TRAF) 5 and TRAF2 are involved in CD30-mediated NFkappaB activation | journal = The Journal of Biological Chemistry | volume = 272 | issue = 4 | pages = 2042–5 | date = Jan 1997 | pmid = 8999898 | doi = 10.1074/jbc.272.4.2042 }}
* {{cite journal | vauthors = Lee SY, Lee SY, Choi Y | title = TRAF-interacting protein (TRIP): a novel component of the tumor necrosis factor receptor (TNFR)- and CD30-TRAF signaling complexes that inhibits TRAF2-mediated NF-kappaB activation | journal = The Journal of Experimental Medicine | volume = 185 | issue = 7 | pages = 1275–85 | date = Apr 1997 | pmid = 9104814 | pmc = 2196258 | doi = 10.1084/jem.185.7.1275 }}
* {{cite journal | vauthors = Boucher LM, Marengère LE, Lu Y, Thukral S, Mak TW | title = Binding sites of cytoplasmic effectors TRAF1, 2, and 3 on CD30 and other members of the TNF receptor superfamily | journal = Biochemical and Biophysical Research Communications | volume = 233 | issue = 3 | pages = 592–600 | date = Apr 1997 | pmid = 9168896 | doi = 10.1006/bbrc.1997.6509 }}
* {{cite journal | vauthors = Duckett CS, Thompson CB | title = CD30-dependent degradation of TRAF2: implications for negative regulation of TRAF signaling and the control of cell survival | journal = Genes & Development | volume = 11 | issue = 21 | pages = 2810–21 | date = Nov 1997 | pmid = 9353251 | pmc = 316646 | doi = 10.1101/gad.11.21.2810 }}
* {{cite journal | vauthors = Mizushima S, Fujita M, Ishida T, Azuma S, Kato K, Hirai M, Otsuka M, Yamamoto T, Inoue J | title = Cloning and characterization of a cDNA encoding the human homolog of tumor necrosis factor receptor-associated factor 5 (TRAF5) | journal = Gene | volume = 207 | issue = 2 | pages = 135–40 | date = Jan 1998 | pmid = 9511754 | doi = 10.1016/S0378-1119(97)00616-1 }}
* {{cite journal | vauthors = Kurts C, Carbone FR, Krummel MF, Koch KM, Miller JF, Heath WR | title = Signalling through CD30 protects against autoimmune diabetes mediated by CD8 T cells | journal = Nature | volume = 398 | issue = 6725 | pages = 341–4 | date = Mar 1999 | pmid = 10192335 | doi = 10.1038/18692 }}
{{refend}}
{{refend}}


==External links==
== External links ==
* {{MeshName|CD30+Antigens}}
* {{MeshName|CD30+Antigens}}
* {{UCSC gene info|TNFRSF8}}


{{NLM content}}
{{NLM content}}
{{membrane-protein-stub}}
 
{{Clusters of differentiation}}
{{Clusters of differentiation}}
{{Tumor necrosis factor receptor superfamily}}
{{Cytokine receptor}}
{{Tumor markers}}
{{Tumor markers}}
{{WikiDoc Sources}}
{{Cytokine receptor modulators}}

Latest revision as of 23:21, 9 January 2019

VALUE_ERROR (nil)
Identifiers
Aliases
External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

n/a

n/a

RefSeq (protein)

n/a

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Location (UCSC)n/an/a
PubMed searchn/an/a
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View/Edit Human

CD30, also known as TNFRSF8, is a cell membrane protein of the tumor necrosis factor receptor family and tumor marker.

Function

This receptor is expressed by activated, but not by resting, T and B cells. TRAF2 and TRAF5 can interact with this receptor, and mediate the signal transduction that leads to the activation of NF-kappaB. It is a positive regulator of apoptosis, and also has been shown to limit the proliferative potential of autoreactive CD8 effector T cells and protect the body against autoimmunity. Two alternatively spliced transcript variants of this gene encoding distinct isoforms have been reported.[1]

Clinical significance

CD30 is associated with anaplastic large cell lymphoma. It is expressed in embryonal carcinoma but not in seminoma and is thus a useful marker in distinguishing between these germ cell tumors.[2] CD30 and CD15 are also expressed on Reed-Sternberg cells typical for Hodgkin's lymphoma.[3]

Cancer treatment

CD30 is the target of the FDA approved therapeutic brentuximab vedotin (Adcetris). It is approved for use in:

  1. Hodgkin lymphoma (HL) (brentuximab vedotin) after failure of autologous stem cell transplant (ASCT)
  2. HL in patients who are not ASCT candidates after failure of at least 2 multiagent chemotherapy regimens
  3. Systemic anaplastic large cell lymphoma (sALCL) after failure of at least 1 multiagent chemotherapy regimen[4]
  4. Primary cutaneous anaplastic large cell lymphoma (pcALCL) or CD30-expressing mycosis fungoides (MF) who have received prior systemic therapy[5]

Interactions

CD30 has been shown to interact with TRAF5,[6] TRAF1,[7] TRAF2[6][7] and TRAF3.[7]

References

  1. "Entrez Gene: TNFRSF8 tumor necrosis factor receptor superfamily, member 8".
  2. Teng LH, Lu DH, Xu QZ, Fu YJ, Yang H, He ZL (Nov 2005). "[Expression and diagnostic significance of OCT4, CD117 and CD30 in germ cell tumors]". Zhonghua Bing Li Xue Za Zhi Chinese Journal of Pathology (in Chinese). 34 (11): 711–5. PMID 16536313.
  3. Gorczyca W, Tsang P, Liu Z, Wu CD, Dong HY, Goldstein M, Cohen P, Gangi M, Weisberger J (Feb 2003). "CD30-positive T-cell lymphomas co-expressing CD15: an immunohistochemical analysis". International Journal of Oncology. 22 (2): 319–24. doi:10.3892/ijo.22.2.319. PMID 12527929.
  4. Deng C, Pan B, O'Connor OA (Jan 2013). "Brentuximab vedotin". Clinical Cancer Research. 19 (1): 22–7. doi:10.1158/1078-0432.CCR-12-0290. PMID 23155186.
  5. "FDA approves Brentuximab vedotin for the treatment of adult patients with primary cutaneous anaplastic large cell lymphoma". FDA.gov. Retrieved March 2, 2018.
  6. 6.0 6.1 Aizawa S, Nakano H, Ishida T, Horie R, Nagai M, Ito K, Yagita H, Okumura K, Inoue J, Watanabe T (Jan 1997). "Tumor necrosis factor receptor-associated factor (TRAF) 5 and TRAF2 are involved in CD30-mediated NFkappaB activation". The Journal of Biological Chemistry. 272 (4): 2042–5. doi:10.1074/jbc.272.4.2042. PMID 8999898.
  7. 7.0 7.1 7.2 Ansieau S, Scheffrahn I, Mosialos G, Brand H, Duyster J, Kaye K, Harada J, Dougall B, Hübinger G, Kieff E, Herrmann F, Leutz A, Gruss HJ (Nov 1996). "Tumor necrosis factor receptor-associated factor (TRAF)-1, TRAF-2, and TRAF-3 interact in vivo with the CD30 cytoplasmic domain; TRAF-2 mediates CD30-induced nuclear factor kappa B activation". Proceedings of the National Academy of Sciences of the United States of America. 93 (24): 14053–8. doi:10.1073/pnas.93.24.14053. PMC 19493. PMID 8943059. (Retracted. If this is an intentional citation to a retracted paper, please replace {{Retracted}} with {{Retracted|intentional=yes}}.)

Further reading

External links

This article incorporates text from the United States National Library of Medicine, which is in the public domain.