The gross appearance of the capsules as well as the presence, extent and depth of tumor cells on the luminal side and number of sections involved by lymphoma were determined by review of routine stains and CD30 immunohistochemistry.
While our understanding of the biology of CD30 in lymphoma continues to evolve, our need to detect and measure its expression at the protein level remains critically important for diagnosis and patient care.
CD30 is promising target as it is universally expressed in virtually all classical Hodgkin lymphomas, anaplastic large cell lymphomas, and in a proportion of other lymphoma types, including cutaneous T cell lymphomas and diffuse large B cell lymphomas.
CD8<sup>+</sup> LyP with lack of expression of CD30 may have distinct histopathologic features that resemble mycosis fungoides and LyP type B. Clinically, they are indistinguishable from their CD30<sup>+</sup> counterparts, signifying the importance of clinical correlation to avoid the erroneous diagnosis of lymphoma.
Recently, the tumor necrosis factor receptor superfamily cluster of differentiation 30 (CD30) has been thought to be implicated in malignant cells in organs affected by Hodgikin lymphoma or in a prognostic marker of diffuse large B cell lymphoma.
Their specific features and relationship to CD30-expressing Hodgkin and Reed/Sternberg (HRS) cells of Hodgkin lymphoma are unclear but highly relevant, because numerous patients with lymphoma are currently treated with an anti-CD30 immunotoxin.
Areas covered: The following article examines the current and emerging monoclonal antibody-based therapies for CTCL, with a particular focus on mycosis fungoides, primary cutaneous anaplastic large cell CD30+ lymphoma and Sezary syndrome.
CD30 expression in extranodal natural killer/T-cell lymphoma, nasal type among 622 cases of mature T-cell and natural killer-cell lymphoma at a single institution in South China.
Once a diagnosis of lymphoma is established, it is important to exclude systemic anaplastic lymphoma kinase-negative ALCL involving the breast, primary cutaneous ALCL, and other CD30(+) lymphoproliferative disorders.
This review gives a critical overview about anti-CD30 therapies with unconjugated, engineered, and conjugated mAbs and the therapeutic challenges of treatment of CD30(+) lymphoma.
Some of the A20-mCD99L2- cells exhibited H/RS‑cell like morphology, a decreased proliferative ability, a prolonged G2 phase and increased CD30 and CD15 expression.
To mobilize both adoptive and innate immune cells for an anti-tumor attack we fused the pro-inflammatory cytokines IL2 and IL12 to an anti-CD30 scFv antibody in a dual cytokine fusion protein to accumulate both cytokines at the malignant CD30(+) Hodgkin/Reed-Sternberg cells in the lymphoma lesion.
In the context of the MD lymphoma microenvironment (and potentially in other CD30(hi) lymphomas as well), our results show that the neoplastic transformation is a continuum and the non-neoplastic cells are actually pre-neoplastic precursor cells and not merely immune bystanders.
A 47-year-old woman developed numerous violaceous nodules in the perineal and upper thigh area 3 years after multimodal treatment and complete remission of primary anaplastic large-cell CD30+ lymphoma.
A distinct pathologic entity characterized by expression of the anaplastic lymphoma kinase (ALK) protein (hence described as ALK lymphoma) has emerged within the heterogeneous group of CD30 anaplastic large-cell lymphomas.
The lymphoma was partially positive for CD30, diffusely positive for EBV by in situ hybridization, and clonal for T-cell receptor gene rearrangement and cytogenetic abnormalities.
Studies of LyP and cutaneous ALCL tissues and cell lines suggest a dual role for CD30/CD30 ligand interactions in regression of LyP and progression to lymphoma.
We discuss the diagnostic and clinical implications in the case of a 42-yr-old female with a peripheral CD30+ lymphoma that displayed both characteristic B- and T-cell surface antigens and clonal rearrangement of B- and T-cell antigen receptor gene loci.