CD30

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An Error has occurred retrieving Wikidata item for infobox 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]

Brentuximab vedotin is also currently being studied in and recommended for treating:

  1. Various types of CD30-positive B cell lymphomas[6]
  2. Various types of CD30-positive T cell lymphomas[7]
  3. CD30-positive cases of the NK cell lymphoma, extranodal NK/T-cell lymphoma, nasal type[8]


Interactions

CD30 has been shown to interact with TRAF5,[9] and TRAF2.[9]

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. ^ Berger GK, McBride A, Lawson S, Royball K, Yun S, Gee K, Bin Riaz I, Saleh AA, Puvvada S, Anwer F (January 2017). "Brentuximab vedotin for treatment of non-Hodgkin lymphomas: A systematic review". Critical Reviews in Oncology/Hematology. 109: 42–50. doi:10.1016/j.critrevonc.2016.11.009. PMC 5218629. PMID 28010897.
  7. ^ Scott LJ (March 2017). "Brentuximab Vedotin: A Review in CD30-Positive Hodgkin Lymphoma". Drugs. 77 (4): 435–445. doi:10.1007/s40265-017-0705-5. PMC 7102329. PMID 28190142.
  8. ^ Hu B, Oki Y (2018). "Novel Immunotherapy Options for Extranodal NK/T-Cell Lymphoma". Frontiers in Oncology. 8: 139. doi:10.3389/fonc.2018.00139. PMC 5937056. PMID 29761078.
  9. ^ a b 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.

Further reading

External links

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