# CD30

Source: https://onco.cc/targets/cd30/  
OnCo record `cd30` (Target). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)"; commercial use needs a licence.

## TL;DR

CD30 is a protein on the malignant Reed-Sternberg cells of Hodgkin lymphoma and on some T-cell lymphomas, and the address for the ADC brentuximab vedotin.

## Summary

TNF-receptor family member expressed on activated lymphocytes and near-universally on Hodgkin Reed-Sternberg cells, anaplastic large-cell lymphoma, and subsets of peripheral T-cell lymphoma and DLBCL. Brentuximab vedotin (2011) validated it; CD30 CAR-T (phase 1/2, ~60-70% ORR in relapsed Hodgkin) and CD30 bispecifics are in trials. Expression level does not predict brentuximab response well.

## Fields

- Kind: Target
- Last checked: 2026-09-07
- Tags: adc-target
- Symbol: TNFRSF8
- Class: surface-antigen
- Biology: Signals via TRAF proteins to NF-κB; shed soluble CD30 is a serum marker. Sparse normal expression outside activated T and B cells.
- Where found: Classical Hodgkin lymphoma (~100%); Anaplastic large-cell lymphoma; Peripheral T-cell lymphoma (subset); Primary mediastinal B-cell lymphoma; Embryonal carcinoma

## Notes

- Lymphoma: Essentially every Reed-Sternberg cell of classical Hodgkin lymphoma, anaplastic large cell lymphoma, a subset of peripheral T-cell lymphoma and of primary mediastinal B-cell lymphoma, and lymphomatoid papulosis. Also on healthy cells: Activated T and B cells, and monocytes: the Human Protein Atlas reads TNFRSF8 as lineage enriched in monocytes (97 nTPM). Resting lymphocytes do not carry it, which is why CD30 is the closest thing in lymphoma to a tumour-restricted antigen in an adult. What the medicine does: CD30 signals to NF-kB through TRAF proteins and internalises, so it carries the conjugate brentuximab vedotin. The free antigen is also shed into serum, which complicates attempts to use it as a blood marker. How tumours lose it: Loss of CD30 at relapse after brentuximab vedotin has been reported but is not the dominant mechanism; failure is more often payload-related or driven by the microenvironment. What that costs the patient: Peripheral neuropathy, cumulative and dose-limiting, from the auristatin payload; neutropenia; and, rarely, progressive multifocal leukoencephalopathy. Unlike the B-cell antigens, CD30 blockade does not empty a whole normal compartment, so there is no equivalent of B-cell aplasia.
- Lymphoma, The Hodgkin microenvironment, where the cancer cell is a minority: A classical Hodgkin lymph node is mostly not cancer. The Hodgkin and Reed-Sternberg cells are a small minority of the tissue, surrounded by T cells, eosinophils, plasma cells, macrophages and fibrosis that the tumour recruits and then uses. Their identity was only settled by picking single cells off a histological section with a micromanipulator and amplifying the immunoglobulin genes: each case gave a single clonal heavy-chain rearrangement, proving that the scattered giant cells are one clone of B-lineage origin even though they have lost almost every B-cell marker (Kuppers 1994). Because the malignant cells are so rare, bulk genomic assays on a Hodgkin biopsy mostly measure the infiltrate, which is why the 9p24.1 work needed laser capture and fluorescence in situ hybridisation rather than sequencing. Frequency: An increased number of CD68-positive macrophages, measured by immunohistochemistry in an independent cohort of 166 patients, tracked shorter progression-free survival, a higher chance of relapse after autologous transplant and shorter disease-specific survival, and outperformed the International Prognostic Score in multivariable analysis (Steidl 2010). What it changes about treatment: No test on the infiltrate is used to choose treatment. The practical consequences are methodological: a Hodgkin biopsy needs enough tissue for architecture, a core needle sample is often not enough, and interim PET rather than a molecular marker is what the treatment is adapted to.
- Lymphoma, Epstein-Barr virus and its latency programmes: Epstein-Barr virus persists for life in the memory B-cell pool of almost everyone, and what it expresses while it is there decides what it can cause. In latency I only EBNA1 is made, which is enough to keep the episome but gives the immune system almost nothing to see; this is the Burkitt pattern, where the virus coexists with a MYC translocation. In latency II, EBNA1 with LMP1 and LMP2, LMP1 mimics a permanently engaged CD40 receptor and drives NF-kB; this is the Hodgkin and NK/T-cell pattern. In latency III the full set of nuclear antigens and membrane proteins is expressed and will immortalise a resting B cell outright, which is what happens when T-cell surveillance is removed, as in post-transplant lymphoproliferative disorder and HIV-associated lymphoma. The virus was found in the first place by electron microscopy of cells cultured from Burkitt lymphoma, whose geographic distribution matching holoendemic malaria had suggested a viral cause (Young and Rickinson 2004). Frequency: The share of each disease that is EBV-positive varies by subtype, by geography and by age, and this layer does not state a single figure because the published ranges are wide and cohort-dependent. What is consistent is the direction: the proportion rises with immunosuppression and with age, and endemic Burkitt lymphoma in equatorial Africa is almost uniformly positive while sporadic Burkitt lymphoma usually is not. What it changes about treatment: Reducing immunosuppression is the first treatment of post-transplant lymphoproliferative disorder, which is the only place where acting on the virus changes the plan. Plasma EBV DNA is used to monitor response in NK/T-cell lymphoma and in post-transplant disease. EBV-specific T cells are licensed for post-transplant disease after transplant failure.

## Sources

- Wikipedia: https://en.wikipedia.org/wiki/CD30
- Wikipedia: https://en.wikipedia.org/wiki/CD30
- Kuppers, Nat Rev Cancer 2009: the biology of Hodgkin's lymphoma: https://doi.org/10.1038/nrc2542
- Kuppers et al., PNAS 1994: micromanipulated Hodgkin and Reed-Sternberg cells carry clonal immunoglobulin rearrangements: https://doi.org/10.1073/pnas.91.23.10962
- Steidl et al., N Engl J Med 2010: tumour-associated macrophages and survival in classical Hodgkin lymphoma: https://doi.org/10.1056/NEJMoa0905680
- Young and Rickinson, Nat Rev Cancer 2004: Epstein-Barr virus, 40 years on: https://doi.org/10.1038/nrc1452

## Connected records

- biomarkers: [CD30 expression (CD30-positive)](https://onco.cc/biomarkers/cd30-expression/)
- cancers: [Advanced-stage classical Hodgkin lymphoma (stage III to IV)](https://onco.cc/cancers/advanced-stage-classical-hodgkin-lymphoma/), [ALK-negative anaplastic large cell lymphoma](https://onco.cc/cancers/alk-negative-anaplastic-large-cell-lymphoma/), [ALK-positive anaplastic large cell lymphoma](https://onco.cc/cancers/alk-positive-anaplastic-large-cell-lymphoma/), [Breast implant-associated anaplastic large cell lymphoma](https://onco.cc/cancers/breast-implant-associated-alcl/), [Cutaneous T-cell lymphoma (mycosis fungoides and Sezary syndrome)](https://onco.cc/cancers/cutaneous-t-cell-lymphoma/), [Diffuse large B-cell lymphoma](https://onco.cc/cancers/dlbcl/), [Early-stage classical Hodgkin lymphoma (stage I to II)](https://onco.cc/cancers/early-stage-classical-hodgkin-lymphoma/), [EBV-positive diffuse large B-cell lymphoma](https://onco.cc/cancers/ebv-positive-dlbcl/), [HIV-associated (AIDS-related) lymphomas](https://onco.cc/cancers/hiv-associated-lymphoma/), [Hodgkin lymphoma](https://onco.cc/cancers/hodgkin-lymphoma/), [Lymphomatoid papulosis](https://onco.cc/cancers/lymphomatoid-papulosis/), [Mediastinal grey zone lymphoma](https://onco.cc/cancers/mediastinal-grey-zone-lymphoma/), [Mycosis fungoides](https://onco.cc/cancers/mycosis-fungoides/), [Nodal T-follicular helper cell lymphoma, angioimmunoblastic type (angioimmunoblastic T-cell lymphoma)](https://onco.cc/cancers/angioimmunoblastic-t-cell-lymphoma/), [Non-Hodgkin lymphoma (all types)](https://onco.cc/cancers/non-hodgkin-lymphoma/), [Peripheral T-cell lymphomas (including cutaneous T-cell lymphoma)](https://onco.cc/cancers/peripheral-t-cell-lymphoma/), [Primary cutaneous anaplastic large cell lymphoma](https://onco.cc/cancers/primary-cutaneous-anaplastic-large-cell-lymphoma/), [Primary mediastinal (thymic) large B-cell lymphoma](https://onco.cc/cancers/primary-mediastinal-b-cell-lymphoma/), [Relapsed and refractory classical Hodgkin lymphoma](https://onco.cc/cancers/relapsed-refractory-hodgkin-lymphoma/)
- drugs: [Brentuximab vedotin](https://onco.cc/drugs/brentuximab-vedotin/), [EB-CAR30-NK](https://onco.cc/drugs/eb-car30-nk/)
- pathways: [Antigen presentation & immune editing](https://onco.cc/pathways/antigen-presentation-immunoediting/), [Inflammation & NF-κB](https://onco.cc/pathways/inflammation-nfkb/), [Mitosis & the spindle assembly checkpoint](https://onco.cc/pathways/mitotic-spindle-checkpoint/), [Myeloid suppression: TAMs, MDSCs & don't-eat-me signals](https://onco.cc/pathways/myeloid-suppression-axis/), [Oncogenic viruses](https://onco.cc/pathways/oncogenic-viruses/), [Tumour microenvironment (TME)](https://onco.cc/pathways/tumor-microenvironment/)
- terms: [Antigen escape: how a lymphoma loses the thing the drug was aimed at](https://onco.cc/terms/lymphoma-bio-antigen-escape/), [Epstein-Barr virus latency programmes, and why they decide which lymphoma](https://onco.cc/terms/lymphoma-bio-ebv-latency/), [Reed-Sternberg cell](https://onco.cc/terms/reed-sternberg-cell/), [The Hodgkin microenvironment: when the cancer cell is the minority](https://onco.cc/terms/lymphoma-bio-hodgkin-microenvironment/)
- trials: [Brentuximab Vedotin Plus Lenalidomide and Rituximab for the Treatment of Relapsed/Refractory DLBCL](https://onco.cc/trials/nct04404283/), [ECHELON-1](https://onco.cc/trials/echelon-1/), [RADAR](https://onco.cc/trials/radar-hodgkin/)
- ideas: [A radiotherapy-free cure for early Hodgkin lymphoma that actually holds](https://onco.cc/ideas/lymphoma-ev-radiotherapy-free-early-hodgkin/), [CD30 CAR-T for multiply relapsed Hodgkin lymphoma](https://onco.cc/ideas/idea-cd30-car-t-hodgkin/), [Randomised evidence for the T-cell lymphomas, including the ones that are not in Europe or North America](https://onco.cc/ideas/lymphoma-ev-randomised-evidence-for-the-t-cell-lymphomas/)
- key papers: [Brentuximab vedotin combination for relapsed diffuse large B-cell lymphoma](https://onco.cc/key-papers/paper-echelon-3-brentuximab-lenalidomide-rituximab-dlbcl-jco-2025/), [ECHELON-1: brentuximab vedotin replacing bleomycin in first-line chemotherapy for advanced Hodgkin lymphoma](https://onco.cc/key-papers/paper-echelon-1-brentuximab-avd-nejm-2018/), [SWOG S1826: nivolumab plus AVD chemotherapy versus brentuximab-AVD for advanced Hodgkin lymphoma in adolescents and adults](https://onco.cc/key-papers/paper-swog-s1826-nivolumab-avd-nejm-2024/)
- roadmaps: [Lymphoma roadmap: from a jaw tumour in Uganda and the first human cancer virus to gene-expression subtypes, PET-adapted chemotherapy, CAR-T cells, bispecific antibodies and the genetics-directed trials now recruiting](https://onco.cc/roadmaps/lymphoma-roadmap/)
- technologies: [Antibody-drug conjugate (ADC)](https://onco.cc/technologies/adc/)

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