This report suggests that if there are suspicious intraoperative manifestations, carrying out a biopsy simultaneously, using Hematoxylin and eosin (HE) staining, and a comprehensive Immunohistochemistry (IHC) panel are essential to diagnosing PC-ALCL to prevent misdiagnosis.
CD39 was overexpressed by peripheral blood T-cells in Sezary syndrome and mycosis fungoides, and in skin-infiltrating lymphocytes of Sezary syndrome, mycosis fungoides, subcutaneous panniculitis-like T-cell lymphoma and primary cutaneous CD30-positive lymphoproliferation. Our study emphasizes the interest in using CD39/CD73/adenosine pathway blocking agents for cutaneous T cell lymphomas treatment.
P2, N=11, Recruiting, Lawson Health Research Institute | Not yet recruiting --> Recruiting | Trial completion date: Mar 2026 --> Jul 2026 | Trial primary completion date: Nov 2025 --> Feb 2026
3 months ago
Enrollment open • Trial completion date • Trial primary completion date
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TNFRSF8 (TNF Receptor Superfamily Member 8) • IL2 (Interleukin 2)
Positive CD30 expression was a favorable prognostic factor for ENKTL, and CD30 expression could restratify the survival of patients in clinical subgroups.
Since ALCL may have a variable expression of T-cell antigens, the diagnosis may easily be missed when CD45 and/or CD3 is negative, and screening epithelial stains for carcinoma (e.g., p63 and EMA) are positive. CD30 must be performed to raise the consideration of ALCL when reniform nuclei are observed.
3 months ago
Journal
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ALK (Anaplastic lymphoma kinase) • TNFRSF8 (TNF Receptor Superfamily Member 8) • PTPRC (Protein Tyrosine Phosphatase Receptor Type C) • TP63 (Tumor protein 63)
Flow cytometric immunophenotyping is a quick, sensitive, high-yield tool for evaluating the immunophenotype of mast cells. An abnormal FCI finding should prompt careful histologic evaluation and sensitive KIT D816V mutation testing to address the possibility of SM. CD2, CD25, and CD30 are important markers for the detection of immunophenotypic aberrancy of mast cells, and their frequencies of aberrancy differ across SM subtypes.
In conclusion, 44% of ALCL patients, regardless of histological subtypes, showed a loss of/decrease in CD30 expression after receiving BV-containing therapy, but this phenomenon was not observed in CHL patients. A higher cumulative dose of BV and a lower amount of CD30 antigen in tumor cells in the initial biopsy materials might be predictors of a loss of/decrease in CD30 expression in ALCL patients.
Recent years have seen the introduction of novel agents into clinical practice; most of these target CD30, such as anti-CD30 monoclonal antibodies and conjugated antibodies (brentuximab vedotin), bispecific antibodies and cellular therapies, particularly anti-CD30 CAR-T cells. This paper briefly reviews the biology of CD30 that makes it a good therapeutic target and describes the anti-CD30 therapies that have emerged to date.
These entities are currently treated similarly with CHOP or CHOEP for CD30-negative diseases or brentuximab vedotin plus CHP for CD30-positive diseases, followed by consolidation with autologous stem cell transplant in first remission...Although current treatment strategies lump most disease entities together, future treatment will include distinct strategies for each disease subtype that optimizes therapy for individuals. This movement towards individualized therapy will ultimately lead to dramatic improvements in prognosis for patients with PTCL.
3 months ago
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • TNFRSF8 (TNF Receptor Superfamily Member 8)
Distinguishing between EBV+ nodal T-cell and NK-cell lymphoma from ALCL is important because treatment strategy and prognosis differ. CD30 expression offers a potential therapeutic target for patients with this aggressive disease.
PLMLs usually present in the elderly with a short duration of illness. Herein, we describe a case of CD30 positive diffuse large B-cell PLML in a young 21-years-old male with review of literature.
Additionally, CRISPR BNIP3 knockout caused proliferation defects and increased sensitivity to apoptosis. All the findings reveal a strong relationship between mitophagy and adverse prognosis of EBV DLBCL and discover a new regulatory mechanism of BNIP3-mediated mitophagy, which may help develop effective treatment regimens with anti-CD30 antibody brentuximab vedotin to improve the prognosis of CD30 EBV DLBCL patients.
4 months ago
Journal • IO biomarker
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BCL2 (B-cell CLL/lymphoma 2) • TNFRSF8 (TNF Receptor Superfamily Member 8) • BNIP3 (BCL2 Interacting Protein 3)
While the LMP2A-expressing MHV-68 behaved similarly to wildtype MHV-68, virally induced constitutively active CD30-signaling in GC B cells led to the expansion of a pre-plasmablastic population. The findings underscore the potential of our novel tools to address crucial questions about the interaction between herpesviral infections and deregulated cellular gene-expression in future studies.
In recent years, targeted therapies such as ALK inhibitors and brentuximab vedotin (BV) have been developed. Weekly vinblastine treatment and hematopoietic stem cell transplantation have also been reported to be effective therapies. This article reviews pediatric ALK-positive ALCL, focusing on risk factors and treatment strategies for pediatric patients with relapsed or refractory ALK-positive ALCL.
High-throughput RNA sequencing analysis revealed that CD30 deficiency led to a decrease of FOXO-autophagy axis in T cells upon TCR stimulation. Thus, CD30 positively regulates T-cell-dependent immune response and T cell proliferation.
After treatment with rituximab combined with chemotherapy, the EBV+DLBCL patients had a complete response rate and a overall response rate of 55... The majority of EBV+DLBCL patients were non-GCB. β2-Microglobulin level and bone marrow invasion were independent risk factors for PFS in patients with EBV+DLBCL, while β2-Microglobulin and HB were independent risk factors for OS in patients with EBV+DLBCL. The therapeutical potentials of targeted medicines, such as CD30 inhibitors and PD-1 inhibitors, deserve to be explored in the future.
MethodsA diverse panel of EBV+ T/NK lymphoma cell lines including SNK1, MECO4, SNK6, SNT8, SNK10, SNT15 and SNT16 were evaluated for sensitivity to MMAE alone and with specific BH3 family inhibitors including A1331852, inhibiting BCL-XL, venetoclax inhibiting and BCL-2 and the MCL-1 inhibitor S63845 (Generon). These data show the potential of BV with BCL-XL inhibition to be an effective and tolerable treatment for ENKTL. We are now planning a detailed preclinical study to better understand the efficacy and safety of this combination in vivo and progress towards a future clinical trial.
Moreover, endogenous extracellular CD30, such as sCD30 shed by ADAM10/17, and CD30-positive EVs may be responsible for the BV-induced cell death. Correctively, extracellular CD30 concentrations, including EV, may be useful as biomarkers for BV therapy in ATL.
The most common side effect of BV was peripheral neuropathy; 22 patients (25.9%, 22/85) experienced peripheral neuropathy (all grades). s : The treatment outcomes of patients with relapsed or refractory CD30-positive lymphoma improved with BV treatment, and the safety profile was manageable.
In cutaneous biopsies, both primary cutaneous DUSP22-translocated ALCL and LyP with DUSP22 rearrangements are characterized by a biphasic pattern with significant small cell epidermotropism. A distinct protein expression profile with preserved T Cell Receptor (TCR) expression, positivity for CD30, LEF1, HLA, and CD58, and negativity for cytotoxic marker expression as well as phospho-STAT3 protein is consistently found in these cases.
6 months ago
Review • Journal • IO biomarker
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TNFRSF8 (TNF Receptor Superfamily Member 8) • STAT3 (Signal Transducer And Activator Of Transcription 3) • CD58 (CD58 Molecule) • DUSP22 (Dual Specificity Phosphatase 22) • USP22 (Ubiquitin Specific Peptidase 22)
These results indicate that BCL11b may be involved in CD30 differentiation and PTCL prognosis. The detection and targeting of BCL11b and CD30 may provide new strategies for the treatment and classification of PTCL.
We hereby present an extraordinary case of CD30+PCLPD with DUSP22-IRF4 rearrangement and novel expression of gamma/delta T-cell immunophenotype in a young patient. Although the gamma/delta T-cell immunophenotype has been described in many other T-cell lymphomas, this is the first reported association with CD30+PCLPD with DUSP22-IRF4 rearrangement.
Various treatment strategies were used, including observation (n = 3), discontinuation/reduction of immunosuppression (n = 3), rituximab (n = 4), and steroids (n = 4)...These cases suggest clinicopathologic presentations resembling lymphomatoid papulosis with atypical, large CD30-positive, EBV-positive cells could comprise first sign of potentially serious immunodeficiency and should prompt evaluation for EBV viremia. These cases also broaden the current picture of immunodeficiency-associated lymphoproliferative disorders to include lymphomatoid papulosis-like clinical presentations.
This rare variant of ENKTL, characterized by the predominance of anaplastic cells and diffuse CD30 expression, exhibits high aggressiveness and should be differentiated from ALK-negative ALCL. Awareness of this uncommon variant is crucial in preventing misdiagnosis and ensuring the timely initiation of therapy.