BRIEF REPORT
Congenital Primary Cutaneous Anaplastic Large-Cell Lymphoma: A Case Report An Na Seo, MD, PhD,* Seok-Jong Lee, MD, PhD,† Yoon Hyuk Choi, MD,† Ho Yun Chung, MD,‡ Jooryung Huh, MD, PhD,§ and Ghil Suk Yoon, MD, PhD*
Abstract: Primary cutaneous anaplastic large-cell lymphoma (C-ALCL) is the second most common type of primary cutaneous T-cell lymphoma. The median age of onset of C-ALCL is 60 years. Presented here is a case of congenital CD30-positive (CD30+) primary C-ALCL in a 10-day-old neonate who presented with a large erythematous indurative plaque in the right postauricular area. A systemic workup of the patient excluded other potential causes. The neonate was treated with wide excision, but chemotherapy or radiation therapy was not administered, as the patient’s parents did not consent to such treatment. The patient has been monitored for 30 months after excision and there has been no disease recurrence. C-ALCL rarely occurs in children, and to the best of our knowledge, this is the first reported case of a neonate with congenital primary C-ALCL. Key Words: primary cutaneous anaplastic large-cell lymphoma, CD30, congenital onset (Am J Dermatopathol 2015;37:398–400)
INTRODUCTION Primary cutaneous anaplastic large-cell lymphoma (C-ALCL) is the second most common type of primary cutaneous T-cell lymphoma.1 C-ALCL typically occurs in elderly individuals but very rarely in children.1,2 To the best of our knowledge, cases of congenital primary C-ALCL have not been reported previously. This is a report of an unusual case of a 10-day-old neonate with an erythematous crusted plaque on the posterior aspect of the auricle present since birth. The patient was diagnosed with congenital primary C-ALCL with characteristic CD30 marker expression.
CASE REPORT A 10-day-old neonate with a congenital erythematous indurative plaque on the right posterior aspect of the auricle was referred to our From the Departments of *Pathology, †Dermatology, and ‡Plastic and Reconstructive Surgery, Kyungpook National University Hospital, Kyungpook National University School of Medicine, Daegu, Korea; and §Department of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea. The authors declare no conflicts of interest. A. N. Seo and S.-J. Lee have contributed equally. Reprints: Ghil Suk Yoon, MD, PhD, Department of Pathology, Kyungpook National University Hospital, Kyungpook National University School of Medicine, 680 Gukchaebosang-ro, Jung-gu, Daegu 700-842, Korea (e-mail: [email protected]). Copyright © 2014 Wolters Kluwer Health, Inc. All rights reserved.
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dermatology clinic (Fig. 1). The neonate appeared to be in good health and did not have B symptoms or high fever. Findings of antenatal care and screening, the labor and delivery process, and the family history of the patient were unremarkable. Neither the parents nor the neonate had any history of mycosis fungoides (MF) or human immunodeficiency virus infection. The firm-bounded reddish plaque was located at the posterior border of the right auricle, extending laterally to the occipital scalp; it was 3 · 2 cm in size with no ulceration. Microscopic examination of a skin biopsy specimen revealed diffuse proliferation or nodular infiltration with cohesive sheets of atypical cells extending through the dermis into the subcutis (Figs. 2A, B). Angiocentric distribution of tumor cells, but no angiodestruction, was observed in some areas. The sheet-like lesion consisted of atypical medium-to-large cells, with irregular nuclei and clear or eosinophilic cytoplasm. Mitosis, apoptosis, and atypia were frequently noted, but necrosis was not evident. Small clusters of mixed reactive inflammatory cells, including histiocytes, lymphocytes, and neutrophils, were found around the tumor. There were very few eosinophils and plasma cells. Most of the atypical large tumor cells were positive for CD30 (Fig. 2C), CD45, and vimentin expression, whereas some atypical tumor cells with expression of CD8 were infrequently seen within tumor burden. However, there was no immunoreactivity with antibodies against CD3, CD4, CD20, CD79a, CD15, terminal deoxynucleotidyl transferase, granzyme B, CD56, CD34, epithelial membrane antigen (EMA), and anaplastic lymphoma kinase (ALK) (Fig. 2D). Epstein–Barr virus–encoded RNA, analyzed by in situ hybridization of paraffin-embedded skin tissue, was not detected within the atypical large-cell infiltrate (Fig. 3A). Rearrangements of the T-cell receptor gamma-chain locus, analyzed by GeneScan (Applied Biosystems), were shown monoclonality. Finally, fluorescence in situ hybridization of the ALK gene using the Vysis LSI ALK dual-color break-apart probe (Abbott Laboratories, Abbott Park, IL) was performed on paraffin-embedded biopsy tissue (Samsung Medical Center, Seoul, Korea). Analysis of 50 nonoverlapping nuclei revealed no chromosomal translocation, t(2;5)(p23;q35), between the ALK gene on chromosome 2 and the nucleophosmin (NPM) gene on chromosome 5 (Fig. 3B). Therefore, the histopathology, immunohistochemistry, and molecular pathology of the tumor were consistent with congenital primary C-ALCL. Positron emission tomography–computed tomography, used for systemic examination of the patient, revealed a limited local right postauricular aspect with intense fludeoxyglucose uptake (maximum standardized uptake value, 1.7). Brain magnetic resonance imaging, spinal magnetic resonance imaging, abdominal computed tomography, and ultrasound imaging revealed no abnormality. A bone marrow aspirate biopsy showed no evidence of bone marrow involvement, and cerebrospinal fluid was normal. The hematological laboratory data were also unremarkable. Therefore, the disease was considered to be localized to the skin, without systemic involvement. After 25 days, the patient underwent surgery. A wide excision was made, and a palpable postauricular lymph node biopsy was performed. The lymph node also contained tumor cells, but the patient did not receive chemotherapy or radiation therapy owing to the lack of parental consent. The patient has been monitored for Am J Dermatopathol Volume 37, Number 5, May 2015
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Am J Dermatopathol Volume 37, Number 5, May 2015
Primary Cutaneous Anaplastic Large-Cell Lymphoma
FIGURE 1. A and B, Erythematous indurative plaque on the posterior aspect of the right auricle before excision. 30 months after surgery and there has been no disease recurrence or palpable lymphadenopathy.
DISCUSSION Cutaneous CD30+ T-cell lymphoproliferative disorders are a specific subtype of cutaneous T-cell lymphoma,1,3,4 comprising lymphomatoid papulosis (LyP), primary C-ALCL, and borderline lesions,1,4 identified by their clinical presentation, longitudinal observation, and histology.1,3,4 Primary C-ALCL is the second most common type of cutaneous T-cell lymphoma, accounting for approximately
10%–20% of cutaneous T-cell lymphoma cases.5 Diagnosis of primary C-ALCL is based on the following criteria: (1) immunophenotypic expression of the CD30 antigen (on .75% of the tumor cells), (2) no clinical evidence of Lyp, (3) no history of or concurrent Lyp, MF, or other cutaneous lymphoma, and (4) no extracutaneous manifestations.3 A few cases of primary C-ALCL have been described in children,2,6,7 but to the best of our knowledge, the identification of primary C-ALCL in a 10-day-old neonate is the first reported case of congenital C-ALCL. To differentially diagnose primary C-ALCL, several diseases were considered and subsequently ruled out. Specifically, unlike Hodgkin lymphoma or diffuse large B-cell
FIGURE 2. Histopathology and immunohistochemical stains of the tumor. A, Extensive infiltration of the atypical mononuclear cell is present in the dermis. B, Sheet-like appearance of atypical medium-to-large cells and mitosis were observed. C, The tumor cells were CD30 expression. D, ALK no expression. Copyright 2014 Wolters Kluwer Health, Inc. All rights reserved.
www.amjdermatopathology.com |
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Seo et al
Am J Dermatopathol Volume 37, Number 5, May 2015
FIGURE 3. A, Photomicrograph of Epstein–Barr virus in situ hybridization study, positive blue cells were not observed in atypical large mononuclear cells. B, Photomicrograph of ALK fluorescence in situ hybridization analysis, translocation was not detected.
lymphoma, the large tumor cells did not express CD15 and CD20, respectively,8 and in contrast to Lyp, most of the large tumor cells (.95%) expressed CD30. The mixed inflammatory cell infiltrate was commonly found at the periphery of the lesion rather than within the tumor.9 In addition, unlike tumor-stage MF with large cell transformation, the tumor was a sporadic congenital lesion without history of MF and not progressive.10 As the lesion was localized, C-ALCL was the most likely diagnosis. Peripheral T-cell lymphoma, not otherwise specified, was not considered. Primary C-ALCL manifests as a solitary, asymptomatic, and clustered nodule or plaque, with or without ulceration.11 The lesion may be a rapidly progressive mass,3,7 and multifocal and multicentric lesions are occasionally observed.11 Nodal and extranodal site involvement is more common in children and adolescents with primary ALK-positive systemic ALCL (S-ALCL) than that in C-ALCL patients.2 However, extracutaneous dissemination (such as in the regional lymph node) occurs in approximately 10% of C-ALCL patients.11 This case showed regional lymph node involvement in the adjacent auricle. It is important to distinguish C-ALCL from S-ALCL with cutaneous involvement because the treatment and prognosis of patients with C-ALCL and S-ALCL differ significantly. Misdiagnosis of C-ALCL may lead to unnecessary aggressive treatment.4 ALK-positive S-ALCLs typically express EMA and carry a t(2;5)/NPM-ALK translocation.1,2,4,12 In contrast, primary C-ALCL usually lacks both ALK activity and EMA expression.4,5 In this case, immunohistochemical staining demonstrated that the tumor was CD30+, ALK and EMA negative, and lacked the t(2;5)/NPM-ALK chromosomal translocation. S-ALCL has a worse prognosis than C-ALCL and requires systemic agent chemotherapy.1 In adult C-ALCL patients, the currently accepted treatment modality for localized lesions is simple surgical excision or local radiation, which are both sufficient.5,11 However, in advanced rapidly progressing cases or in those with extracutaneous involvement, multiagent chemotherapy and lowdose methotrexate or doxorubicin are administered.5,11 In contrast to adult C-ALCL, there are no well-established treatment guidelines for pediatric C-ALCL because of its rarity.2 In summary, a precise diagnosis of C-ALCL is important because of significant differences in prognosis and treatment regimens. Systemic workup and flow cytometric analysis of cell surface markers may help to prevent misdiagnosis and overtreatment in patients with cutaneous involvement.
1. Vaid R, Cohen B. Primary cutaneous CD30 positive anaplastic large cell lymphoma in an adolescent. Pediatr Dermatol. 2009;26:721–724. 2. Santiago-et-Sanchez-Mateos D, Hernandez-Martin A, Colmenero I, et al. Primary cutaneous anaplastic large cell lymphoma of the nasal tip in a child. Pediatr Dermatol. 2011;28:570–575. 3. Modi S, Yang DJ, Sule N, et al. Primary cutaneous CD30+ large-cell lymphoma presenting as a scrotal plaque. Dermatol Online J. 2009;15:9. 4. Bekkenk MW, Geelen FA, van Voorst Vader PC, et al. Primary and secondary cutaneous CD30(+) lymphoproliferative disorders: a report from the Dutch Cutaneous Lymphoma Group on the long-term followup data of 219 patients and guidelines for diagnosis and treatment. Blood. 2000;95:3653–3661. 5. Koh LP, Wong LC, Ng SB, et al. Primary cutaneous anaplastic large cell lymphoma of the vulva: a typical cutaneous lesion with an ‘atypical’ presenting site. Int J Hematol. 2009;90:388–391. 6. Rubie H, Gladieff L, Robert A, et al. Childhood anaplastic large cell lymphoma Ki-1/CD30: clinicopathologic features of 19 cases. Med Pediatr Oncol. 1994;22:155–161. 7. Tomaszewski MM, Moad JC, Lupton GP. Primary cutaneous Ki-1 (CD30) positive anaplastic large cell lymphoma in childhood. J Am Acad Dermatol. 1999;40:857–861. 8. Menon MP, Pittaluga S, Jaffe ES. The histological and biological spectrum of diffuse large B-cell lymphoma in the World Health Organization classification. Cancer J. 2012;18:411–420. 9. Stein H, Foss HD, Durkop H, et al. CD30(+) anaplastic large cell lymphoma: a review of its histopathologic, genetic, and clinical features. Blood. 2000;96:3681–3695. 10. Kadin ME, Hughey LC, Wood GS. Large-cell transformation of mycosis fungoides-differential diagnosis with implications for clinical management: a consensus statement of the US Cutaneous Lymphoma Consortium. J Am Acad Dermatol. 2014;70:374–376. 11. Newlove T, Loyd A, Patel R, et al. Primary cutaneous anaplastic largecell lymphoma. Dermatol Online J. 2010;16:2. 12. Hosoi M, Ichikawa M, Imai Y, et al. A case of anaplastic large cell lymphoma, ALK positive, primary presented in the skin and relapsed with systemic involvement and leukocytosis after years of follow-up period. Int J Hematol. 2010;92:667–668.
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However, standardized treatment guidelines for pediatric C-ALCL have not yet been established. Therefore, centralized and collaborative long-term follow-up studies of pediatric C-ALCL patients are necessary to determine optimal treatment regimens, the risk of relapse, and patient prognosis. ACKNOWLEDGMENTS We are indebted to Seungeun Lee, MD and Yoon-La Choi, MD, PhD in Samsung Medical Center (Seoul, Korea) for generous help in the ALK FISH study. REFERENCES
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Congenital Primary Cutaneous Anaplastic Large-Cell Lymphoma: A Case Report An Na Seo, MD, PhD,* Seok-Jong Lee, MD, PhD,† Yoon Hyuk Choi, MD,† Ho Yun Chung, MD,‡ Jooryung Huh, MD, PhD,§ and Ghil Suk Yoon, MD, PhD*
Abstract: Primary cutaneous anaplastic large-cell lymphoma (C-ALCL) is the second most common type of primary cutaneous T-cell lymphoma. The median age of onset of C-ALCL is 60 years. Presented here is a case of congenital CD30-positive (CD30+) primary C-ALCL in a 10-day-old neonate who presented with a large erythematous indurative plaque in the right postauricular area. A systemic workup of the patient excluded other potential causes. The neonate was treated with wide excision, but chemotherapy or radiation therapy was not administered, as the patient’s parents did not consent to such treatment. The patient has been monitored for 30 months after excision and there has been no disease recurrence. C-ALCL rarely occurs in children, and to the best of our knowledge, this is the first reported case of a neonate with congenital primary C-ALCL. Key Words: primary cutaneous anaplastic large-cell lymphoma, CD30, congenital onset (Am J Dermatopathol 2015;37:398–400)
INTRODUCTION Primary cutaneous anaplastic large-cell lymphoma (C-ALCL) is the second most common type of primary cutaneous T-cell lymphoma.1 C-ALCL typically occurs in elderly individuals but very rarely in children.1,2 To the best of our knowledge, cases of congenital primary C-ALCL have not been reported previously. This is a report of an unusual case of a 10-day-old neonate with an erythematous crusted plaque on the posterior aspect of the auricle present since birth. The patient was diagnosed with congenital primary C-ALCL with characteristic CD30 marker expression.
CASE REPORT A 10-day-old neonate with a congenital erythematous indurative plaque on the right posterior aspect of the auricle was referred to our From the Departments of *Pathology, †Dermatology, and ‡Plastic and Reconstructive Surgery, Kyungpook National University Hospital, Kyungpook National University School of Medicine, Daegu, Korea; and §Department of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea. The authors declare no conflicts of interest. A. N. Seo and S.-J. Lee have contributed equally. Reprints: Ghil Suk Yoon, MD, PhD, Department of Pathology, Kyungpook National University Hospital, Kyungpook National University School of Medicine, 680 Gukchaebosang-ro, Jung-gu, Daegu 700-842, Korea (e-mail: [email protected]). Copyright © 2014 Wolters Kluwer Health, Inc. All rights reserved.
398
| www.amjdermatopathology.com
dermatology clinic (Fig. 1). The neonate appeared to be in good health and did not have B symptoms or high fever. Findings of antenatal care and screening, the labor and delivery process, and the family history of the patient were unremarkable. Neither the parents nor the neonate had any history of mycosis fungoides (MF) or human immunodeficiency virus infection. The firm-bounded reddish plaque was located at the posterior border of the right auricle, extending laterally to the occipital scalp; it was 3 · 2 cm in size with no ulceration. Microscopic examination of a skin biopsy specimen revealed diffuse proliferation or nodular infiltration with cohesive sheets of atypical cells extending through the dermis into the subcutis (Figs. 2A, B). Angiocentric distribution of tumor cells, but no angiodestruction, was observed in some areas. The sheet-like lesion consisted of atypical medium-to-large cells, with irregular nuclei and clear or eosinophilic cytoplasm. Mitosis, apoptosis, and atypia were frequently noted, but necrosis was not evident. Small clusters of mixed reactive inflammatory cells, including histiocytes, lymphocytes, and neutrophils, were found around the tumor. There were very few eosinophils and plasma cells. Most of the atypical large tumor cells were positive for CD30 (Fig. 2C), CD45, and vimentin expression, whereas some atypical tumor cells with expression of CD8 were infrequently seen within tumor burden. However, there was no immunoreactivity with antibodies against CD3, CD4, CD20, CD79a, CD15, terminal deoxynucleotidyl transferase, granzyme B, CD56, CD34, epithelial membrane antigen (EMA), and anaplastic lymphoma kinase (ALK) (Fig. 2D). Epstein–Barr virus–encoded RNA, analyzed by in situ hybridization of paraffin-embedded skin tissue, was not detected within the atypical large-cell infiltrate (Fig. 3A). Rearrangements of the T-cell receptor gamma-chain locus, analyzed by GeneScan (Applied Biosystems), were shown monoclonality. Finally, fluorescence in situ hybridization of the ALK gene using the Vysis LSI ALK dual-color break-apart probe (Abbott Laboratories, Abbott Park, IL) was performed on paraffin-embedded biopsy tissue (Samsung Medical Center, Seoul, Korea). Analysis of 50 nonoverlapping nuclei revealed no chromosomal translocation, t(2;5)(p23;q35), between the ALK gene on chromosome 2 and the nucleophosmin (NPM) gene on chromosome 5 (Fig. 3B). Therefore, the histopathology, immunohistochemistry, and molecular pathology of the tumor were consistent with congenital primary C-ALCL. Positron emission tomography–computed tomography, used for systemic examination of the patient, revealed a limited local right postauricular aspect with intense fludeoxyglucose uptake (maximum standardized uptake value, 1.7). Brain magnetic resonance imaging, spinal magnetic resonance imaging, abdominal computed tomography, and ultrasound imaging revealed no abnormality. A bone marrow aspirate biopsy showed no evidence of bone marrow involvement, and cerebrospinal fluid was normal. The hematological laboratory data were also unremarkable. Therefore, the disease was considered to be localized to the skin, without systemic involvement. After 25 days, the patient underwent surgery. A wide excision was made, and a palpable postauricular lymph node biopsy was performed. The lymph node also contained tumor cells, but the patient did not receive chemotherapy or radiation therapy owing to the lack of parental consent. The patient has been monitored for Am J Dermatopathol Volume 37, Number 5, May 2015
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Am J Dermatopathol Volume 37, Number 5, May 2015
Primary Cutaneous Anaplastic Large-Cell Lymphoma
FIGURE 1. A and B, Erythematous indurative plaque on the posterior aspect of the right auricle before excision. 30 months after surgery and there has been no disease recurrence or palpable lymphadenopathy.
DISCUSSION Cutaneous CD30+ T-cell lymphoproliferative disorders are a specific subtype of cutaneous T-cell lymphoma,1,3,4 comprising lymphomatoid papulosis (LyP), primary C-ALCL, and borderline lesions,1,4 identified by their clinical presentation, longitudinal observation, and histology.1,3,4 Primary C-ALCL is the second most common type of cutaneous T-cell lymphoma, accounting for approximately
10%–20% of cutaneous T-cell lymphoma cases.5 Diagnosis of primary C-ALCL is based on the following criteria: (1) immunophenotypic expression of the CD30 antigen (on .75% of the tumor cells), (2) no clinical evidence of Lyp, (3) no history of or concurrent Lyp, MF, or other cutaneous lymphoma, and (4) no extracutaneous manifestations.3 A few cases of primary C-ALCL have been described in children,2,6,7 but to the best of our knowledge, the identification of primary C-ALCL in a 10-day-old neonate is the first reported case of congenital C-ALCL. To differentially diagnose primary C-ALCL, several diseases were considered and subsequently ruled out. Specifically, unlike Hodgkin lymphoma or diffuse large B-cell
FIGURE 2. Histopathology and immunohistochemical stains of the tumor. A, Extensive infiltration of the atypical mononuclear cell is present in the dermis. B, Sheet-like appearance of atypical medium-to-large cells and mitosis were observed. C, The tumor cells were CD30 expression. D, ALK no expression. Copyright 2014 Wolters Kluwer Health, Inc. All rights reserved.
www.amjdermatopathology.com |
399
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Seo et al
Am J Dermatopathol Volume 37, Number 5, May 2015
FIGURE 3. A, Photomicrograph of Epstein–Barr virus in situ hybridization study, positive blue cells were not observed in atypical large mononuclear cells. B, Photomicrograph of ALK fluorescence in situ hybridization analysis, translocation was not detected.
lymphoma, the large tumor cells did not express CD15 and CD20, respectively,8 and in contrast to Lyp, most of the large tumor cells (.95%) expressed CD30. The mixed inflammatory cell infiltrate was commonly found at the periphery of the lesion rather than within the tumor.9 In addition, unlike tumor-stage MF with large cell transformation, the tumor was a sporadic congenital lesion without history of MF and not progressive.10 As the lesion was localized, C-ALCL was the most likely diagnosis. Peripheral T-cell lymphoma, not otherwise specified, was not considered. Primary C-ALCL manifests as a solitary, asymptomatic, and clustered nodule or plaque, with or without ulceration.11 The lesion may be a rapidly progressive mass,3,7 and multifocal and multicentric lesions are occasionally observed.11 Nodal and extranodal site involvement is more common in children and adolescents with primary ALK-positive systemic ALCL (S-ALCL) than that in C-ALCL patients.2 However, extracutaneous dissemination (such as in the regional lymph node) occurs in approximately 10% of C-ALCL patients.11 This case showed regional lymph node involvement in the adjacent auricle. It is important to distinguish C-ALCL from S-ALCL with cutaneous involvement because the treatment and prognosis of patients with C-ALCL and S-ALCL differ significantly. Misdiagnosis of C-ALCL may lead to unnecessary aggressive treatment.4 ALK-positive S-ALCLs typically express EMA and carry a t(2;5)/NPM-ALK translocation.1,2,4,12 In contrast, primary C-ALCL usually lacks both ALK activity and EMA expression.4,5 In this case, immunohistochemical staining demonstrated that the tumor was CD30+, ALK and EMA negative, and lacked the t(2;5)/NPM-ALK chromosomal translocation. S-ALCL has a worse prognosis than C-ALCL and requires systemic agent chemotherapy.1 In adult C-ALCL patients, the currently accepted treatment modality for localized lesions is simple surgical excision or local radiation, which are both sufficient.5,11 However, in advanced rapidly progressing cases or in those with extracutaneous involvement, multiagent chemotherapy and lowdose methotrexate or doxorubicin are administered.5,11 In contrast to adult C-ALCL, there are no well-established treatment guidelines for pediatric C-ALCL because of its rarity.2 In summary, a precise diagnosis of C-ALCL is important because of significant differences in prognosis and treatment regimens. Systemic workup and flow cytometric analysis of cell surface markers may help to prevent misdiagnosis and overtreatment in patients with cutaneous involvement.
1. Vaid R, Cohen B. Primary cutaneous CD30 positive anaplastic large cell lymphoma in an adolescent. Pediatr Dermatol. 2009;26:721–724. 2. Santiago-et-Sanchez-Mateos D, Hernandez-Martin A, Colmenero I, et al. Primary cutaneous anaplastic large cell lymphoma of the nasal tip in a child. Pediatr Dermatol. 2011;28:570–575. 3. Modi S, Yang DJ, Sule N, et al. Primary cutaneous CD30+ large-cell lymphoma presenting as a scrotal plaque. Dermatol Online J. 2009;15:9. 4. Bekkenk MW, Geelen FA, van Voorst Vader PC, et al. Primary and secondary cutaneous CD30(+) lymphoproliferative disorders: a report from the Dutch Cutaneous Lymphoma Group on the long-term followup data of 219 patients and guidelines for diagnosis and treatment. Blood. 2000;95:3653–3661. 5. Koh LP, Wong LC, Ng SB, et al. Primary cutaneous anaplastic large cell lymphoma of the vulva: a typical cutaneous lesion with an ‘atypical’ presenting site. Int J Hematol. 2009;90:388–391. 6. Rubie H, Gladieff L, Robert A, et al. Childhood anaplastic large cell lymphoma Ki-1/CD30: clinicopathologic features of 19 cases. Med Pediatr Oncol. 1994;22:155–161. 7. Tomaszewski MM, Moad JC, Lupton GP. Primary cutaneous Ki-1 (CD30) positive anaplastic large cell lymphoma in childhood. J Am Acad Dermatol. 1999;40:857–861. 8. Menon MP, Pittaluga S, Jaffe ES. The histological and biological spectrum of diffuse large B-cell lymphoma in the World Health Organization classification. Cancer J. 2012;18:411–420. 9. Stein H, Foss HD, Durkop H, et al. CD30(+) anaplastic large cell lymphoma: a review of its histopathologic, genetic, and clinical features. Blood. 2000;96:3681–3695. 10. Kadin ME, Hughey LC, Wood GS. Large-cell transformation of mycosis fungoides-differential diagnosis with implications for clinical management: a consensus statement of the US Cutaneous Lymphoma Consortium. J Am Acad Dermatol. 2014;70:374–376. 11. Newlove T, Loyd A, Patel R, et al. Primary cutaneous anaplastic largecell lymphoma. Dermatol Online J. 2010;16:2. 12. Hosoi M, Ichikawa M, Imai Y, et al. A case of anaplastic large cell lymphoma, ALK positive, primary presented in the skin and relapsed with systemic involvement and leukocytosis after years of follow-up period. Int J Hematol. 2010;92:667–668.
400
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| www.amjdermatopathology.com
However, standardized treatment guidelines for pediatric C-ALCL have not yet been established. Therefore, centralized and collaborative long-term follow-up studies of pediatric C-ALCL patients are necessary to determine optimal treatment regimens, the risk of relapse, and patient prognosis. ACKNOWLEDGMENTS We are indebted to Seungeun Lee, MD and Yoon-La Choi, MD, PhD in Samsung Medical Center (Seoul, Korea) for generous help in the ALK FISH study. REFERENCES
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
