CD30

TNFRSF8
Available structures
PDBOrtholog search: PDBe RCSB
Identifiers
Aliases TNFRSF8, CD30, D1S166E, Ki-1, tumor necrosis factor receptor superfamily member 8
External IDs OMIM: 153243 MGI: 99908 HomoloGene: 949 GeneCards: TNFRSF8
RNA expression pattern
More reference expression data
Orthologs
Species Human Mouse
Entrez

943

21941

Ensembl

ENSG00000120949

ENSMUSG00000028602

UniProt

P28908

Q60846

RefSeq (mRNA)

NM_001243
NM_001281430
NM_152942

NM_009401

RefSeq (protein)

NP_001234.3
NP_001268359.2

NP_033427.1

Location (UCSC) Chr 1: 12.06 – 12.14 Mb Chr 4: 145.27 – 145.32 Mb
PubMed search [1] [2]
Wikidata
View/Edit HumanView/Edit Mouse

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.[3]

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.[4] CD30 and CD15 are also expressed on classical Hodgkin Lymphoma Reed-Sternberg cells.[5]

Cancer treatment

CD30 is the target of the FDA approved therapeutic brentuximab Vedotin (Adcetris), designed and developed by Seattle Genetics. 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[6]

Interactions

CD30 has been shown to interact with TRAF5,[7] TRAF1,[8] TRAF2[7][8] and TRAF3.[8]

References

  1. ↑ "Human PubMed Reference:".
  2. ↑ "Mouse PubMed Reference:".
  3. ↑ "Entrez Gene: TNFRSF8 tumor necrosis factor receptor superfamily, member 8".
  4. ↑ 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.
  5. ↑ 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.
  6. ↑ 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.
  7. 1 2 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.
  8. 1 2 3 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 19493Freely accessible. PMID 8943059. (Retracted. If this is intentional, 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.

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