CD30-positive Anaplastic Large Cell Lymphoma Research Articles

SGN-35C: A Novel CD30-Directed Antibody-Drug Conjugate for the Treatment of Lymphomas

SGN-35C is an antibody drug conjugate composed of an anti-CD30 antibody conjugated to a camptothecin-derived topoisomerase 1 (TOP1) inhibitor payload. SGN-35C was designed to leverage the antibody backbone from brentuximab vedotin (BV) and the novel mechanism of action of camptothecin-derived ADCs. Here, we evaluated the mechanism of action, cytotoxicity, and safety in in vitro and in vivo models. To characterize the mechanism of action of SGN-35C in vitro and in vivo experiments were performed in CD30-positive anaplastic large cell lymphoma (ALCL), Hodgkin lymphoma (HL) cell lines, and versions of these cell lines that are resistant to BV. SGN-35C binding, internalization, induction of DNA damage, cell cycle analysis, and in vitro cytotoxicity were evaluated. To assess if payload released in CD30-positive cells could kill adjacent CD30-negative cells, an in vitro bystander assay of CD30-positive and CD30-negative co-cultures was developed. The in vivo antitumor activity of SGN-35C was evaluated in animals bearing subcutaneous lymphoma models. SGN-35C antitumor activity was evaluated in a xenograft model of heterogeneous CD30 expression consisting of a mixture of a BV-resistant Karpas-299 cell line mixed with parental Karpas-299 cells to assess bystander activity in vivo. The tolerability of SGN-35C was assessed in a non-human primate model. SGN-35C binding to CD30-positive cells was similar to the unconjugated anti-CD30 antibody and demonstrated internalization into CD30-expressing cells. Treatment of cells with SGN-35C for 24 hours led to an increase of the DNA damage marker phospho-γH2A.X, which induced an increase in the fraction of cells in S-phase, consistent with the mechanism of camptothecin-based TOP1 inhibitors. Cytotoxicity was observed in ALCL and HL cell lines treated with SGN-35C, including an ALCL cell line resistant to BV. In a mixture of CD30-positive and CD30-negative cells, SGN-35C treatment induced cytotoxicity of the CD30-negative cells, demonstrating that SGN-35C can elicit bystander activity. A single dose of SGN-35C led to significant tumor growth inhibition in animals bearing lymphoma xenografts, including a BV-resistant model and a model of heterogeneous CD30 expression, demonstrating that SGN-35C can elicit bystander activity in vivo. SGN-35C demonstrates a tolerability profile in non-human primates that is consistent with camptothecins. A Phase 1, first-in-human study is planned to evaluate the safety and anti-tumor activity of SGN-35C in lymphoid malignancies.

Dupilumab aggravates Sézary syndrome: The importance of accurate pathological diagnosis

We report a case of Sézary syndrome aggravated by dupilumab. Although a diagnosis of atopic dermatitis was made previously, our retrospective diagnosis was cutaneous T-cell lymphoma. A 72-year-old woman was referred for evaluation of erythema over her entire body. She had received a diagnosis of atopic dermatitis (AD) based on skin biopsy elsewhere 7 years earlier. Since her symptoms were resistant to topical corticosteroids and oral antihistamines, dupilumab was started. She noticed peripheral lymph node enlargement 11 months after the commencement of dupilumab. Physical examination revealed generalized erythroderma with desquamation (Figure 1A,B) and lymphadenopathy in the neck, axilla, and inguinal region. A biopsy from her abdomen showed dense infiltrations of atypical lymphoid cells in the upper dermis with epidermotropism (Figure 1C,D). Immunohistochemically, the infiltrating cells were positive for CD3 and CD4; CD8 was almost negative. There was a 50% deletion of CD7 (Figure 1E–H). Her peripheral blood (PB) white blood cell count was 7660/μL, with 35% abnormal lymphocytes (2681/μL). Although CD4+/CD26− or CD4+/CD7− cells were not assessed, CD4/CD8 ratio was 10.59.1, 2 Human T-lymphotropic virus-1 antibody was negative. Monoclonal gene rearrangement of T-cell receptor β-chain was identified in her PB by Southern blot analysis. Inguinal lymph node biopsy showed partial effacement by atypical lymphocytes. The diagnosis was Sézary syndrome (SS), stage IVA2 (T4N3MXB2). Taking into account the risk of tumor lysis syndrome due to high tumor burden, we selected conventional multiagent chemotherapy as an initial therapy before using a molecular-targeted drug. Dupilumab was discontinued; cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) were started. After two cycles of CHOP, biweekly intravenous mogamulizumab was introduced. Her skin lesions gradually improved. The PB abnormal lymphocyte count decreased. Her disease was well controlled with mogamulizumab for 17 months. We reviewed the previous biopsy specimen. Dense dermal infiltrates with atypical cells and epidermotropism were seen (Figure 1I,J). These infiltrates were positive for CD3 and CD4. CD8-positive cells were sparse. There was a 30% deletion of CD7 (Figure 1K–N). The atypical cells were CCR4+ and CD68−. Although a diagnosis of AD was made previously, our retrospective diagnosis was cutaneous T-cell lymphoma (CTCL). Dupilumab is a monoclonal antibody which inhibits both IL-4 and IL-13 signaling pathways by binding specifically to the α subunit of the IL-4 receptor. Several cases of CTCL that developed or worsened after dupilumab use have been reported. A proposed mechanism of CTCL due to dupilumab is the involvement of IL-13 receptor α2 (IL-13Rα2), which is expressed on CTCL cells and promotes tumor progression. When dupilumab blocks IL-4 and IL-13 receptors, serum IL-13 levels increase. Because dupilumab inhibits IL-13Rα1 but not IL-13Rα2 signaling, increased IL-13 levels due to dupilumab stimulate IL-13Rα2, leading to the activation and proliferation of lymphoma cells.3 To our knowledge, there are 36 cases3-19 of CTCL worsened by dupilumab based on the diagnosis of AD or eczema have been reported. Of these 36 patients, 18 underwent skin biopsy prior to dupilumab therapy; no evidence of CTCL was described in 16 patients.3-10 In one remaining patient, the authors re-evaluated the biopsy specimen taken before dupilumab treatment and revised the diagnosis to early CTCL-not otherwise specified.10 In another patient, the first skin biopsy taken before dupilumab was compatible with AD; however, the diagnosis of mycosis fungoides was made by the second biopsy taken on the first day of dupilumab treatment. After 6 months of dupilumab treatment, the third biopsy turned out CD30-positive anaplastic large-cell lymphoma.11 When using dupilumab for AD, clinicians should be alert to the development or worsening of CTCL. Skin biopsy with immunohistochemical examination is strongly recommended before dupilumab therapy, especially in patients with erythroderma and elderly patients. The authors declare no conflict of interest. Approval of the research protocol: N/A. Informed Consent: N/A. Registry and the Registration No.: N/A. Animal Studies: N/A.

249 Differences of spatially resolved transcriptome profile between mycosis fungoides with CD30-positive large cell transformation and primary cutaneous anaplastic large cell lymphoma

249 Differences of spatially resolved transcriptome profile between mycosis fungoides with CD30-positive large cell transformation and primary cutaneous anaplastic large cell lymphoma

CD30-positive anaplastic large-cell lymphoma associated with mycosis fungoides after treatment with dupilumab

CD30-positive anaplastic large-cell lymphoma associated with mycosis fungoides after treatment with dupilumab

The peripheral T-cell lymphoma: can we pivot from the chemotherapy-predicated paradigm?

Peripheral T-cell lymphomas (PTCL) are uncommon and aggressive diseases that are difficult to study. Combination chemotherapy such as cyclophosphamide, doxorubicin, vincristine, and prednisone has been the mainstay of treatment for almost 30 years, but outcomes remain poor. The development of new targeted therapies is changing the landscape of how we treat patients with these difficult diseases. For instance, the addition of brentuximab vedotin to combination chemotherapy enhanced the outcomes in patients with CD30-positive anaplastic large cell lymphomas, but there is still a need for better therapies in the other numerous subtypes. Here we discuss the data for the existing treatment paradigm of PTCL as well as the merits of shifting toward a chemotherapy-free approach.

Safety profile of brentuximab vedotin in Japanese patients with relapsed/refractory Hodgkin lymphoma or systemic anaplastic large cell lymphoma: a post-marketing surveillance study.

Brentuximab vedotin (BV) was initially approved in Japan for the treatment of relapsed/refractory (R/R) CD30-positive Hodgkin lymphoma (HL) and systemic anaplastic large cell lymphoma (sALCL). As requested by the Japanese Ministry of Health, Labour and Welfare, we conducted a post-marketing surveillance (PMS) study to assess the safety of BV in Japanese patients with R/R HL or sALCL. PMS forms were collected from 284 patients (182 with HL, 101 with sALCL and one with another lymphoma) treated between April and September 2014. The median age was 62 (range 14–93) years and the median number of treatment cycles was 5.5 for HL and 4 for sALCL. Adverse drug reactions (ADRs) were reported in 74.3% of patients. The most commonly observed ADRs included peripheral sensory neuropathy (39.1%; grade ≥ 3, 6.3%), neutropenia (34.5%; grade ≥ 3, 22.2%) and lymphopenia (7.0%; grade ≥ 3, 5.3%). Ten patients had fatal ADRs including interstitial lung disease (n = 3). This study showed that BV has an acceptable safety profile in Japanese patients with R/R HL and R/R sALCL in the clinical practice setting. However, close monitoring rare, but potentially fatal, ADRs such as pulmonary toxicity may be warranted, especially in patients with prior or ongoing pulmonary disorders. Electronic supplementary materialThe online version of this article (10.1007/s12185-020-03039-w) contains supplementary material, which is available to authorized users.

Incidence of Anaplastic Large Cell Lymphoma and Breast-Implant-Associated Lymphoma-An Analysis of a Certified Tumor Registry over 17 Years.

Background: Breast-implant-associated anaplastic large cell lymphoma (BI-ALCL) and primary breast ALCL are rare extranodal manifestations of non-Hodgkin lymphoma. The rarity of both diseases, along with unreleased sales data on breast implants and constant updates of classification systems impede the calculation of an exact incidence. Methods: The database of the Tumor Center Regensburg in Bavaria was searched for patients with CD30-positive and ALK-negative anaplastic large cell lymphoma between 2002 and 2018. These lymphomas were identified by the ICD-O-3 morphology code “97023” and were cross-checked by searching the diagnosis by name the and ICD-10 code C84.7. Furthermore, we tried to calculate the incidence rates and corresponding 95% confidence intervals, standardized to 1,000,000 implant years of breast-implant-associated anaplastic large cell lymphoma and primary breast anaplastic large cell lymphoma. Results: Twelve ALK-negative and CD30-positive anaplastic large cell lymphomas were identified out of 170,405 malignancies. No case was found within the breast tissue and none of the patients had a previous history of breast implant placement. In five cases, lymph node involvement in close proximity to the breast was observed. Conclusion: We found a low incidence of anaplastic large cell lymphoma and no association to breast implants in these patients. A review of the current literature revealed inconsistent use of classification systems for anaplastic large cell lymphomas and potential overestimation of cases.

Impressive response of CD30‐negative, treatment‐refractory mycosis fungoides to brentuximab vedotin

Brentuximab vedotin is a CD30-antibody/drug conjugate which has demonstrated excellent response in treating CD30-positive mycosis fungoides (MF) and anaplastic large cell lymphoma (ALCL). In this report, we present a patient with CD30-negative MF refractory to multiple other lines of therapy who demonstrated a dramatic response to brentuximab. This paradoxical response may be due to inadequate detection of CD30 expression by immunohistochemical techniques. From this case we see that even in the setting of apparent CD30 negativity, brentuximab may be a viable treatment option for patients who require bridging to stem cell transplant or seek successful palliation. This case highlights the point that rigid inclusion criteria for MF trials without use of more sensitive techniques to confirm lack of CD30 expression may inappropriate.

Anaplastic Large Cell Lymphoma Associated with Double-Lumen Breast Implants: A Case Report and Review of the Literature

Background: Breast implant-associated anaplastic large cell lymphoma (ALCL) is commonly associated with diagnostic delay due to the insidious nature of presentation with late periprosthetic fluid collection, mass or locoregional adenopathy. Case Presentation: A 75-year-old woman with a remote history of right breast cancer treated with modified radical mastectomy and immediate reconstruction with a double-lumen silicone implant presented 13 years later with volume asymmetry. The implant was removed and a saline implant was placed. Five years later, she presented with acute onset of right breast enlargement and pain. Ultrasound revealed an associated periprosthetic fluid accumulation. Cytology showed anaplastic lymphoma kinasenegative, CD30-positive ALCL without associated systemic disease. The patient was treated with implant removal and total capsulectomy. Conclusion: Due to the insidious presentation of ALCL, a high index of clinical suspicion must be maintained when evaluating patients for delayed presentation of volumetric discrepancy. Treatment typically entails implant removal. Indications for additional systemic treatment include extracapsular spread of ALCL or presence of a periprosthetic tumour.

Biopsy diagnosis of CD30-positive anaplastic large T-cell lymphoma of ileum in necrotic biopsies

CD30 (Ki-1)-positive anaplastic large cell lymphoma (ALCL) has been reported only once in ileum. A 72-year-old presented with melena for 3 weeks duration. Endoscopy identified a large ulcerated tumor (3 cm × 4 cm × 4 cm) in ileum proximal to Bauhin’s valve. Punch biopsies showed broad coagulative necrosis without apparently viable cells, but cell contours were recognizable. Diagnosis was impossible on HE-section, but it suggested malignancy. Since the patient denied second endoscopy, the author managed to make the diagnosis of necrotic punches. Immunohistocheimcally, the coagulative necrosis cells were positive for vimentin, CD45, CD3, CD4, CD5, CD10, CD15, CD30, CD43, CD45RO, p53, and Ki-67 (labeling = 78%). They were negative for cytokeratin (CK) AE 1/3, CK CAM5.2, CK5, CK6, CK7, CK8, CK18, CK19, CK20, EMA, p63, CD8, CD20, CD38, CD138, CD23, CD79α, κ-chain, λ-chain, bcl-2, bcl-6, cyclinD1, CD56, CD57, TdT, chromogranin, synaptophysin, NSE, S100 protein, smooth muscle actin, MUC1, MUC2, MUC5AC, MUC6, KIT and PDGFRA. Since CD30 and CD15 were strongly positive, Hodgkin’s disease and ALCL were considered. However, Hodgkin’s disease was unlikely because no apparent Hodgkin’s or Reed-Sternberg cells were seen. Therefore, CD30-positive ALCL was diagnosed. In addition, because the tumor cells expressed only T-cell markers, the diagnosis of CD30-positive T-cell ALCL was confirmed. The present study could not detect ALK, ALK/NPN, ALK-1, p80, and tissue destructive molecules such as perforins, TIA-1, and granzyme B because tumor cells were totally necrotic. Chromosomal translocation of t (2; 5) and TCR rearrangement could not be performed due to no viable cells. Post-diagnosis whole body examinations using CT, MRI, and PET showed bladder metastasis and multiple lymph node swellings in the para-aortic areas (Ann Arber Stage 4). The patient is now treated by chemotherapy and radiation for 5 months. The present study showed a very rare case of ileal CD30-positive T-cell ALCL and indicated that lymphoma diagnosis is possible even in coagulatively necrotic tissues.

New Therapies in T-cell Lymphoma

T-cell lymphomas represent 10–12% of all patients with non-Hodgkin lymphoma (NHL) in the Western world. When cutaneous T-cell lymphoma (CTCL) is excluded, peripheral T-cell lymphoma—not otherwise specified (PTCL-NOS), anaplastic large-cell lymphoma (ALCL), and angioimmunoblastic T-cell lymphoma (AITL) represent the overwhelming majority of patients in this population. These diseases remain a great challenge to treat. They are characterized by an aggressive presentation, extranodal disease, paraneoplastic phenomena, and resistance to standard chemotherapeutics. With the rapid development of new molecular gene profiling techniques, it is highly likely that these diseases will be subclassified by molecular abnormalities in the future. An evolving understanding of the tumor molecular pathogenesis will undoubtedly lead to further novel targeted therapies. Immunoconjugates, such as brentuximab vedotin (BV), have provided outstanding responses in relapsed, refractory CD30-positive ALCL. Histone deacetylase (HDAC) inhibitors have shown activity in PTCL and are potentially synergistic with proteasome inhibitors. Denileukin diftitox is an interesting recombinant DNA fusion protein linking fragments of the diphtheria toxin to interleukin-2 (IL-2) that is tested in clinical trials. Crizotinib, a highly specific anaplastic lymphoma kinase (ALK) inhibitor, has shown great promise in small number of patients with ALK-positive ALCL; the future of patients with this disorder looks very promising. Biomarker-driven chemotherapeutics is becoming a critical part of the state-of-the-art treatment in early- and late-phase clinical trials. It is crucial that future trials include sensible biomarker-based designs when future treatments are used in these challenging disorders.

Atopic dermatitis with CD30-positive anaplastic large cell lymphoma

The association between long-term severe atopic dermatitis (AD) and lymphoma is a matter of debate. However, a substantial number of cases of severe AD with CD30+ anaplastic large cell lymphoma (ALCL) have been reported.We present the case of a 39-year-old female patient with long-term AD whose ALCL became systemic and nearly took a fatal course. She had been diagnosed with AD in early childhood and had been suffering from it ever since. Her disease severity had been mild and she was treated with [...]

Primary Cutaneous CD30-Positive Anaplastic Large-Cell lymphoma of the External Auditory Canal

Primary cutaneous T-cell lymphoma is rare. Cutaneous lymphoma is defined as primary when there is an absence of nodal or systemic disease during the first 6 months following diagnosis. We report what we believe to be the first documented case of a primary cutaneous CD30-positive anaplastic large-cell lymphoma of the external auditory canal. The patient was an elderly woman who presented with progressively worsening right otalgia and hypoacusis. Otoscopy revealed an erythematic, ulcerative, nonbleeding, localized lesion in the anterosuperior area of the external auditory canal. The patient underwent an excisional biopsy, and after the diagnosis was established, she underwent 22 sessions of radiotherapy. During follow-up, she exhibited no evidence of recurrence.

An Unusual Cause of Epigastric Pain

Question: A 64-year-old woman was hospitalized because of epigastric pain, back soreness, and poor appetite for 3 months. Her past and family histories were unremarkable. Physical examination showed epigastric tenderness without rebound pain and right axillary lymph node enlargement. Initial laboratory examination showed abnormalities as follows: Leukocyte count, 3.75 × 103/μL; hemoglobin level, 9.2 g/dL; platelet count, 148 × 103/μL; and aspartate aminotransferase, 92 U/L. Abdominal computed tomography demonstrated no significant changes. Upper gastrointestinal endoscopy identified elevated lesions with central ulcer on the greater curvature of stomach (Figure A) and in the duodenal bulb (Figure B). Magnified endoscopic observation with narrow band imaging was performed for the gastric lesion and revealed that it was surrounded by an elevation of gastric mucosa with normal gastric pits, indicating a submucosal tumor (Figure C). What is the most likely diagnosis? See the Gastroenterology web site (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and Images in GI. Excisional biopsies taken from gastric and duodenal lesions showed anaplastic large cell lymphoma (ALCL) characterized by the presence of large, anaplastic lymphoma cells around blood vessels (Figure D). Immunohistochemically, the tumor cells were positive for CD30 (Figure E) and Ki-67, but negative for ALK (anaplastic lymphoma kinase; Figure F), CD20, CD79a, and epithelial membrane antigen. The whole-body dual-modality 18F-fluorodeoxyglucose (FDG) positron emission tomography/computed tomography images showed multiple increase of FDG uptake around the pons, cerebellum, C-, T-, L-spines, pelvic bones, humeral and femoral bones, mandibular bones, mediastinum, left supraclavicle, axillary, and gastrointestinal and abdominal lymph nodes (Figure G). CD30-positive ALCL is a distinctive malignant large-cell lymphoma of T-cell lineage, often presenting in lymph node or extranodal sites, such as the skin (the most common site), bone, lung, spleen, and gastrointestinal tract.1Lu Y. Zhao X. Wang E. et al.ALK-negative anaplastic large cell lymphoma with extensive peripheral blood and bone marrow involvements manifested as “leukemic phase”.Leuk Res. 2010; 34: 475-482Crossref PubMed Scopus (19) Google Scholar, 2Ross C.W. Hanson C.A. Schnitzer B. CD30 (Ki-1)-positive, anaplastic large cell lymphoma mimicking gastrointestinal carcinoma.Cancer. 1992; 70: 2517-2523Crossref PubMed Scopus (30) Google Scholar Our patient showed an extremely rare manifestation of ALK-negative ALCL with extensive involvement of multiple organs. The treatment regimens for primary systemic ALCL are the same as those used for diffuse large B-cell lymphoma.3Armitage J.O. Mauch P.M. Harris N.L. et al.DeVita Jr, V.T. Hellman S. Rosenberg S.A. Cancer: principles and practice of oncology. 6th ed. Lippincott, Philadelphia2001: 2297-2298Google Scholar Without receiving chemotherapy, our patient died of respiratory failure 1 month later.

Primary esophageal CD30-positive ALK-positive anaplastic large cell lymphoma with MUM1 expression

We report a case of primary esophageal CD30+/ALK+/MUM1+ anaplastic large cell lymphoma (ALCL) and discuss its diagnosis and treatment, specifically in regard to the unusual expression of the B cell marker, MUM1. A 29-year-old Mexican male presented with an esophageal mass with stenosis and dysphagia. Endoscopic samples were sent for hematoxylin–eosin staining and immunohistochemical analysis. Pathologic and immunohistochemical examination resulted in a diagnosis of primary ALCL of the esophagus with CD30+/ALK+/MUM1+ phenotype. This diagnosis was confirmed by molecular analysis [fluorescence in situ hybridization (FISH)]. Initially, two cycles of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy were given, but the patient exhibited progressive disease. Subsequent treatment consisted of four cycles of ifosfamide, carboplatin, and etoposide (ICE). As of the 12-month follow-up examination, the patient is in complete remission. This case suggests that ALCL of the esophagus should be considered in the differential diagnosis of esophageal neoplasms. Biopsy through esophagoscopy or surgical exploration is recommended, and treatment with chemotherapy or radiotherapy can achieve long-term survival.

CD30-Positive Anaplastic Large Cell Lymphoma の1例

CD30-Positive Anaplastic Large Cell Lymphoma の1例

Childhood primary cutaneous CD30-positive anaplastic large cell lymphoma: A child case with spontaneous regression.

Childhood primary cutaneous CD30-positive anaplastic large cell lymphoma: A child case with spontaneous regression.

Primary Esophageal CD30-Positive ALK-Positive Anaplastic Large Cell Lymphoma: A Case Report and Literature Review

To introduce a case of primary esophageal CD30-positive ALK-positive anaplastic large cell lymphoma (ALCL) and discuss its diagnosis and treatment. Esophagectomy was done for a 37-year-old male with a submucosal lesion after a frozen section failed to give a definite diagnosis. Samples were sent for hematoxylin-eosin staining and immunohistochemical analysis. Six cycles of CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) chemotherapy were given and the patient was followed up. The operation was uneventful. Postoperative pathologic and immunohistochemical examination yielded a diagnosis of primary CD30-positive and ALK-positive ALCL of the esophagus. The patient was in complete remission at the 14-month follow-up. ALCL of the esophagus should be considered in the differential diagnosis of esophageal submucosal lesions. Biopsy through either esophagoscopy or surgical exploration, chemotherapy, and radiotherapy can be chosen for long-term survival.

CD30 positive anaplastic large‐cell lymphoma mimicking Langerhans cell histiocytosis

The presence of CD 1a+ dendritic cells (DC) has been well described in T-cell lymphoproliferative disorders, and the presence of large numbers of DCs has rarely been reported as a mimicker of Langerhans cell histiocytsis (LCH). We present the case of a 56-year-old female with a solitary nodule on the chin whose case was referred to our institution for confirmation of the diagnosis of LCH. Skin biopsy showed an ulcerated nodule containing a wedge-shaped infiltrate comprised of large atypical cells and cells with prominent grooved nuclei. The constellation of histologic and immunologic features favored a CD30 lymphoproliferative disorder of T-cell lineage even though there were accompanying numerous dendritic histiocytes and CD1a positive Langerhans cells. The sheets of CD30 positive atypical lymphoid cells which express T-cell markers were consistent with CD30 positive lymphoproliferative disease and favor CD30 positive anaplastic large-cell lymphoma (ALCL) over Langerhans histiocytosis. The absence of Anaplastic Lymphoma Kinase (ALK) staining favored a primary cutaneous origin. This case signifies a CD 30+ ALCL of the skin which histopathologically mimics a LCH. Ezra N, Van Dyke GS, Binder SW. CD30 positive anaplastic large-cell lymphoma (ALCL) mimicking Langerhans cell histiocytosis (LCH).

Primary cutaneous lymphomas: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up

Primary cutaneous lymphomas: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up