eMedicine Specialties > Dermatology > Lymphoma and Related Processes

Cutaneous CD30+ (Ki-1) Anaplastic Large-Cell Lymphoma

Author: Cary Chisholm, MD, Resident Physician, Department of Pathology, Texas A&M Health Science Center College of Medicine
Coauthor(s): Daniel D Bennett, MD, Assistant Professor, Department of Internal Medicine, Texas A&M Health Science Center College of Medicine; Senior Staff, Department of Dermatology, Scott and White Memorial Hospital
Contributor Information and Disclosures

Updated: Feb 26, 2010

Introduction

Background

CD30+ lymphoproliferative disorders include a wide spectrum of disease with lymphomatoid papulosis at the benign end of the spectrum and cutaneous CD30+ anaplastic large-cell lymphomas (ALCLs) at the malignant end. Borderline lesions lie somewhere in between.1,2 Cutaneous CD30+ (Ki-1) ALCL is clinically and pathologically heterogeneous, leading to some difficulty in its diagnosis and classification. Expression of CD30 (an activation marker for B or T cells) in more than 75% of neoplastic cells characterizes this group of lymphoproliferative disorders.3

Based on clinical manifestations, cutaneous CD30+ ALCL can be subdivided mainly into a primary cutaneous form without extracutaneous involvement at presentation or a systemic form with secondary skin involvement at presentation. The primary cutaneous form (see History) generally has a better prognosis than the systemic form with secondary skin involvement. Sometimes (in up to 25% of cases), spontaneous regression of the primary cutaneous form occurs despite high-grade anaplastic cytology of neoplastic lymphocytes.

Cutaneous CD30+ ALCL can be further classified into different groups according to histologic features (eg, pleomorphic, immunoblastic, monomorphic, small-cell predominant, Hodgkin disease–related, and other uncommon variants); immunophenotype (eg, T, null, B, rarely B and T); and other clinical features, such as ALCL arising in patients who are HIV positive and ALCL occurring after another lymphoproliferative process (eg, lymphomatoid papulosis (LyP), mycosis fungoides, Hodgkin disease).

Multiple patterns of cutaneous CD30+ ALCL are recognized. Three are recognized by the World Health Organization (common, lymphohistiocytic, and small cell); however, several others have been described in the literature, for example, neutrophil rich, subcutaneous, and inflammatory.4,5

Pathophysiology

Cytogenetic studies and subsequent cloning of the translocation t(2;5) have shown a high degree of association with systemic forms of cutaneous CD30+ (Ki-1) anaplastic large cell lymphoma (ALCL). This genetic abnormality is not specific for anaplastic morphologic features and is more common in the monomorphic and small-cell variants. This translocation creates a novel fusion protein, nucleophosmin-anaplastic lymphoma kinase (NPM-ALK), which has transforming properties in vitro and can cause large-cell lymphoma in vivo when transfected into murine bone marrow.

NPM-ALK expression is most often seen in young patients with the monomorphic or small-cell variant of ALCL who present with advanced-stage disease and have tumors with a CD30+, T- or null-cell phenotype. NPM-ALK expression is less frequently detected in older patients and in ALCL of pleomorphic histology.6 The t(2;5) is rare in the primary cutaneous form of ALCL. This points to a molecular etiology of primary cutaneous CD30+ ALCL distinct from that of extracutaneous (systemic form) CD30+ lymphoproliferative disease.

Several other mutations have been reported. Recurrent copy number alterations have been reported by several authors, and these include gains of chromosomes 6p, 7q, and 19 and losses of 6q, 9, and 18.7,8 Van Kester et al report that gains of the 7q region, which harbors the MET oncogene, were found in 45% of cases. Additionally, alterations in the FOXO1A and BRCA2 regions of 13q, the PRDM16/MEL1 region of 1p, and the TP53 region of 17p have been described. Each of these genes has been associated in cancer pathogenesis.9 Translocations involving the interferon regulatory factor-4 (IRF4) have also been identified in cutaneous ALCL. IRF4 is joined with the multiple myeloma oncogene-1 (MUM1), creating a fusion protein, MUM1/IRF4. The significance of MUM1/IRF4 expression is unclear, and further study is needed on its oncogenic potential and prevalence in systemic ALCL and LyP.10

The neoplastic cells are CD30+ positive and typically have a T-helper phenotype (ie, CD3+, CD4+, CD8-). Pan–T-cell antigens (CD2, CD3, CD5, CD7) may be partially lost. Monoclonal rearrangement of the T-cell receptor (TCR) gene is observed in most cases. However, Bonzheim et al reported that only 2 (4%) of 47 ALCLs expressed TCR-beta protein.11 Moreover, both TCR-beta+ ALCLs lacked CD3 and ZAP-70 (ie, molecules indispensable for the transduction of cognate TCR signals). Thus, defective expression of TCRs is a common characteristic of all types of ALCL, which may contribute to the dysregulation of intracellular signaling pathways controlling T-cell activation and survival.

Malignant T cells are also able to evade apoptosis. Tumor necrosis factor-alpha (TNF-alpha) is one of the molecules that helps prevent cells from escaping cellular senescence. The TNF-alpha receptor is lost in certain strains of cutaneous ALCL, contributing to its tumorlike growth. TRAIL is another molecule that protects cells from malignant behavior. Cutaneous ALCL cells overexpress the cellular FLICE inhibitory protein (c-FLIP) and lose the Bcl-2 protein Bid, which suppress the TRAIL protective mechanism. Activation of CD30 leads to c-FLIP up-regulation. Thus, CD30 suppresses apoptosis.12

Primary cutaneous ALCL also shows higher expression of CCR10 and CCR8, which are chemokines that direct cells to the skin. This may explain why primary cutaneous ALCL has such a low rate of extracutaneous dissemination.9 CD95 (FAS protein that induces apoptosis) expression is preferentially expressed at high levels in all primary cutaneous forms of CD30+ lymphomas and suggests that CD95 may play a role in the regression of CD30+ skin lesions.

In situ hybridization has shown that systemic CD30+ ALCL is associated with the Epstein-Barr virus (EBV). In contrast, primary cutaneous CD30+ ALCL and LyP have not been linked with EBV using this method.13

Frequency

United States

The frequency of CD30+ anaplastic large cell lymphoma (ALCL) in the United States is not known.

International

Cutaneous CD30+ (Ki-1) anaplastic large-cell lymphomas (cutaneous CD30+ ALCL) comprise approximately 5% of all non-Hodgkin lymphomas (NHL). The primary cutaneous form of CD30+ ALCL makes up approximately 10% of the total primary cutaneous lymphoproliferative disorders and is the second most common primary cutaneous lymphoproliferative disorder after mycosis fungoides.

Mortality/Morbidity

The 5-year survival rate is typically around 90% for the primary cutaneous form of CD30+ anaplastic large cell lymphoma (ALCL).14 In fact, cases of primary cutaneous CD30+ ALCL may regress without therapeutic intervention.15 New data suggest that the 5-year overall survival and disease-specific survival in primary cutaneous CD30+ ALCL are affected by the extent of limb involvement. For patients without extensive limb disease, the 5-year survival remains around 90%. However, with extensive limb involvement by this disease, 5-year survival is around 50%. Those patients with extensive limb involvement have also been proven to have more rapid disease progression and decreased response to treatment.14

The prognosis of the systemic form with secondary cutaneous involvement depends on the expression of the ALK protein. Patients with expression of ALK have a 5-year survival rate ranging from 70-80%. The 5-year survival rate in patients without ALK expression ranges from 15-30%.

Survival in children with systemic ALCL also depends on what sites are involved. Mediastinal involvement, visceral involvement, and cutaneous involvement portend a worse prognosis. The presence of one of these factors decreases the 5-year survival rate from 89% to 61%.16 The Children's Cancer Group Study 5941 reported that only bone marrow involvement significantly changed the 5-year survival rate.17

Sex

The male-to-female ratio for CD30+ anaplastic large cell lymphoma (ALCL) is 3:2.

Age

Patients with primary cutaneous forms of anaplastic large cell lymphoma (ALCL) are generally older (median age, 61 y) than patients with the systemic form of ALCL (median age, 24 y) and, in contrast to the latter group, do not show a bimodal age distribution.

When separated by extent of limb involvement, patients with extensive limb involvement had a significantly higher age at presentation (median age, 73 y) compared with those without such limb involvement (median age, 48 y).14 In primary cutaneous disease, involvement of the lower extremity may be associated with a worse prognosis.

Clinical

History

  • The primary cutaneous form of cutaneous CD30+ (Ki-1) anaplastic large cell lymphoma (cutaneous CD30+ ALCL) is defined by skin-only involvement without systemic dissemination at presentation. Draining regional lymph node involvement occurs in approximately 25% of patients with only skin lesions. Whether the patients only showing draining regional lymph node involvement should be considered to have a primary cutaneous form remains controversial.
  • Patients with widespread systemic and cutaneous disease at first presentation should be considered to have the systemic form with skin involvement.
  • Rarely, one may elicit a history of insect bite immediately preceding the appearance of the lesion.18
  • Some medications have also been associated with the onset of cutaneous CD30+ ALCL, including glatiramer acetate.19

Physical

  • Patients with cutaneous CD30+ (Ki-1) anaplastic large-cell lymphoma (cutaneous CD30+ ALCL) usually present with solitary or ulcerating nodules or tumors, as shown in the image below.

  • This ulcerated nodule of localized primary cutane...

    This ulcerated nodule of localized primary cutaneous CD30+ anaplastic large cell lymphoma is relatively nonspecific in appearance. Courtesy of Dr. Ronald Grimwood.

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    This ulcerated nodule of localized primary cutane...

    This ulcerated nodule of localized primary cutaneous CD30+ anaplastic large cell lymphoma is relatively nonspecific in appearance. Courtesy of Dr. Ronald Grimwood.

  • Lesions are typically reddish brown and indurated.
  • Lymphadenopathy may be present because involvement of the draining regional lymph nodes occurs in approximately 25% of patients. (This does not appear to be associated with a worse prognosis.)
  • In one study, 30% of patients with cutaneous ALCL lesions had ichthyosiform eruptions, all of which were consistent with acquired ichthyosis. Fourteen percent of patients with mycosis fungoides also had some form of ichthyosis. No patients with cutaneous B-cell lymphoma had ichthyosiform eruptions.20

Causes

  • In the systemic form of cutaneous CD30+ anaplastic large-cell lymphoma (ALCL), the translocation t(2;5) results in a novel fusion protein (NPM-ALK) and may play an important role for the development of disease. The primary cutaneous form, however, does not commonly show this translocation, and the etiology remains unknown.
  • A relationship with insect bites has been proposed. A 2009 study by Lamant et al studied 5 such cases. The initial diagnosis of these lesions was consistent with nonmalignant inflammatory disease. One patient even had involvement of one draining lymph node, which was initially diagnosed as lymphadenitis rich in macrophages. Application of the ALK immunostain to biopsy sample from all 5 cases showed positive cells that were also CD30 and epithelial membrane antigen (EMA) positive, including in the lymph node. One of the 5 patients subsequently developed disseminated disease with pulmonary involvement and later died. It is proposed that the insect bite–associated antigens and inflammatory cytokines select for and encourage proliferation of T cells bearing the t(2;5) translocation.18

More on Cutaneous CD30+ (Ki-1) Anaplastic Large-Cell Lymphoma

Overview: Cutaneous CD30+ (Ki-1) Anaplastic Large-Cell Lymphoma
Differential Diagnoses & Workup: Cutaneous CD30+ (Ki-1) Anaplastic Large-Cell Lymphoma
Treatment & Medication: Cutaneous CD30+ (Ki-1) Anaplastic Large-Cell Lymphoma
Follow-up: Cutaneous CD30+ (Ki-1) Anaplastic Large-Cell Lymphoma
Multimedia: Cutaneous CD30+ (Ki-1) Anaplastic Large-Cell Lymphoma
References
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Further Reading

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Keywords

cutaneous CD30+ (Ki-1) anaplastic large-cell lymphoma, anaplastic large-cell lymphoma, ALCL, cutaneous anaplastic large-cell lymphoma, cutaneous CD30+ ALCL, cutaneous ALCL, CD30+ ALCL, regressing atypical histiocytosis, RAH, CD30+ cutaneous large T-cell lymphoma, pseudo-Hodgkin disease, pseudo-Hodgkin's disease, non-Hodgkin lymphoma, NHL, pseudo-Hodgkin lymphoma

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Contributor Information and Disclosures

Author

Cary Chisholm, MD, Resident Physician, Department of Pathology, Texas A&M Health Science Center College of Medicine
Cary Chisholm, MD is a member of the following medical societies: College of American Pathologists, Texas Medical Association, and United States and Canadian Academy of Pathology
Disclosure: Nothing to disclose.

Coauthor(s)

Daniel D Bennett, MD, Assistant Professor, Department of Internal Medicine, Texas A&M Health Science Center College of Medicine; Senior Staff, Department of Dermatology, Scott and White Memorial Hospital
Daniel D Bennett, MD is a member of the following medical societies: American Academy of Dermatology, American Contact Dermatitis Society, American Medical Association, Dermatology Foundation, National Psoriasis Foundation, Society for Investigative Dermatology, and Texas Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Günter Burg, MD, Professor and Chairman Emeritus, Department of Dermatology, University of Zürich School of Medicine; Delegate of The Foundation for Modern Teaching and Learning in Medicine Faculty of Medicine, University of Zürich, Switzerland
Günter Burg, MD is a member of the following medical societies: American Academy of Dermatology, American Dermatological Association, International Society for Dermatologic Surgery, North American Clinical Dermatologic Society, and Pacific Dermatologic Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Daniel S Loo, MD, Associate Professor of Dermatology, Residency Program Director, Department of Dermatology, Tufts Medical Center
Daniel S Loo, MD is a member of the following medical societies: American Academy of Dermatology and Association of Professors of Dermatology
Disclosure: Nothing to disclose.

CME Editor

Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania
Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology
Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds Investigator; Genentech Grant/research funds investigator; Centocor Consulting fee Consulting; Abbott Grant/research funds investigator; Abbott Consulting fee Consulting; Novartis  investigator; Pfizer Grant/research funds investigator; Celgene Consulting fee DMC Chair; NIAMS and NHLBI Grant/research funds investigator

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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