Pediatric NonHodgkin Lymphomas
University of Utah
Salt Lake City, UT
Non-Hodgkin's lymphoma (NHL) makes up approximately 7% of all pediatric cancers diagnosed in the US
(750-800 cases diagnosed/year), comprising 3% of tumors in children younger than 5 and 8-9% of tumors in
children between 5-20 years of age. The numbers of NHL diagnosed in children under the age of 15 has
remained relatively constant over the past 20 years, but the rates in adolescents 15 and older has risen
steadily. Males are affected 2 to 3 times more frequently than females, and white children have
approximately twice the rate of lymphoma as do African Americans, with Hispanics having an intermediate
incidence of disease between whites and African Americans. There is also an increased incidence of NHL
in children with inherited or acquired autoimmune disorders, including HIV, Wiscott-Aldrich syndrome,
severe combined immune deficiency, ataxia-telangiectasia, common variable immunodeficiency or those on
immune suppression drugs following solid organ transplant.
NHL in the pediatric age group differs from adult lymphomas both in the distribution of subtypes of
lymphoma and clinical presentation as well as in response to therapy. Pediatric lymphomas are almost
exclusively clinically aggressive lymphomas with indolent tumors, such as follicular lymphomas being
distinctly unusual. Precursor (lymphoblastic) lymphomas are common in children, comprising almost 30% of
pediatric NHL, compared to <5% of adult NHL. Pediatric NHL also differs from adult disease in that
nearly half of the NHL are of T-cell phenotype (including both precursor and mature T-cell phenotypes),
unlike adults where T-cell phenotype is seen in <10% of cases. Extranodal disease is much more common
in children than in adults, and high stage (Stage III or IV) disease with involvement of bone marrow or
the CNS is also much more common.
There are four main subtypes of pediatric NHL that are recognized by the WHO Classification that make
up >95% of NHL in patients less than 20 years of age. These include precursor B and T-cell lymphomas
(lymphoblastic lymphoma), Burkitt and atypical Burkitt lymphoma, diffuse large B-cell lymphoma (DLBCL)
and CD30 positive anaplastic large cell lymphoma (ALCL). All are treated by systemic multi-agent
chemotherapy with choice of drugs and duration of treatment dictated by the histologic subtype. Current
therapies have cure rates of better than 85% for most patients with limited (Stage I or II) disease.
Radiotherapy has limited use, usually as treatment for acute respiratory distress, superior vena cava
syndrome or active CNS involvement. Because of the excellent response to therapy, surgery also has
limited use, and is mainly employed for diagnosis or relief from symptoms of rapidly growing tumors (i.e.
bowel obstruction or intussusceptions in Burkitt lymphoma). Because of the rapid growth of many of the
tumors, pediatric patients are susceptible to tumor lysis syndrome or acute obstructive symptoms.
Precursor T and B-cell lymphomas (lymphoblastic lymphomas) make up about 30% of pediatric NHL, and 90%
are of precursor T-cell origin. The precursor T-cell lymphomas will show variable expression of T-cell
surface antigens with frequent expression of CD1a and TdT as well as co-expression of CD4 and CD8. CD3
is often expressed in the cytoplasm rather than the cell surface. CD10 expression is seen in one third
to one half of cases, and aberrant expression of myeloid or B-cell antigens may be seen. Clonal T-cell
receptor (TCR) gene rearrangements may be seen in some, but not all cases. About one third of cases will
show cytogenetic abnormalities involving either the alpha or delta locus of the TCR and one quarter will
have abnormalities or deletions of the TAL-1 locus at (9q). The definition of lymphoblastic lymphoma is
somewhat arbitrary in the precursor cell lymphoproliferative processes, with a cut off of <25% bone
marrow lymphoblasts defining lymphoma and >25% blasts considered as acute lymphoblastic leukemia
(ALL). The most common clinical presentation of T-lymphoblastic lymphoma is a mediastinal or
supradiaphragmatic mass with or without pleural effusions and variable cervical lymphadenopathy. Other,
extranodal sites may also be involved. Respiratory compromise secondary to airway compression is a
common complication of the rapidly growing mediastinal mass. About 10% of lymphoblastic lymphomas are
precursor B-cell origin (expressing CD19, CD24, CD10, CD79a and TdT), and these are more likely to
present in skin, soft tissue, bone, tonsils or in peripheral lymph nodes (often solitary), and appear to
not progress to full-blown ALL in most cases. Treatment of lymphoblastic lymphoma is currently based on
leukemia-type regimes with long term (12-24 month) duration of therapy with up to ten different agents
including high dose methotrexate, vincristine, daunorubicin asparaginase and prophylactic cranial
radiation. This approach has lead to 85-90% EFS in high stage disease. Limited stage disease is also
treated with systemic leukemic type regimes with similar outcomes. Earlier approaches of treatment with
more conventional NHL therapies led to frequent relapses, often as ALL. CNS prophylaxis is needed, even
in limited stage disease, to achieve an EFS of 85%.
Burkitt lymphoma (BL) and atypical Burkitt lymphoma account for about 40% of pediatric NHL. Most of
the cases appear to be of the sporadic type and lack evidence of the EBV genome (<30% of cases).
These are mature B-cell neoplasms expressing CD19, CD20, CD22 and CD79a with cell surface IgM and light
chains and somatic mutation of the Ig genes. BL frequently presents as extranodal disease involving gut,
ovary and bones. Presentation of abdominal disease often presents with abdominal pain, nausea, vomiting
and other signs of acute bowel obstruction. BL has a high incidence of CNS and bone marrow involvement,
which may be seen in up to 20% of cases. CNS disease may present as cranial nerve palsies, seizures or
cord compression. Bone marrow involvement often presents as cytopenias and a leukemic form of Burkitt
lymphoma (previously designated as ALL L3) may be seen. Atypical Burkitt's lymphoma (also termed
Burkitt-like lymphoma or high grade B-cell lymphoma) is more likely to present as peripheral node
disease, and lacks morphologic features of classic BL such as a prominent starry sky pattern and
cytologic homogeneity. Pathologic identification of atypical Burkitt lymphoma remains problematic with
poor intra-observer agreement, as many of the features of increased cytologic pleomorphism may be
difficult to distinguish without optimal fixation and slide preparation. Burkitt lymphoma has a very
high mitotic rate (99-100% by MIB-1 or Ki-67 immunostaining), accounting for the typical acute clinical
presentations. It has been proposed that Burkitt and atypical Burkitt lymphoma be defined on the basis
of cytogenetic/molecular findings that include a c-myc translocation. Previous studies of Burkitt-like
lymphomas in adult populations have seen combinations of c-myc and bcl-2 translocations. Cytogenetics of
Burkitt-like cases in pediatric trials find a much higher number of c-myc translocations with bcl-2
translocations being very rare, suggesting that the disease is more closely related to BL in the
pediatric population. Additional cytogenetic abnormalities, including duplication of 1q21-32 and
deletion of 13q are also very common. Treatment of Burkitt and atypical Burkitt lymphomas is by a very
intense but short duration therapeutic approach. Most regimes currently used last for 4-6 months and
show 85-95% EFS even in high stage disease. Poorer outcome is seen with leukemic disease, but still is
near 75% (compared to 20% in 1977!). CNS disease, with current therapeutic regimes, does not impart
independent adverse prognosis.
DLBCL makes up approximately 20% of pediatric NHL and is more common in adolescents and older
children. In the pediatric group, DLBCL is more likely to present as higher stage disease, with up to
70% presenting with Stage III disease, often involving mediastinum or abdomen (although abdominal disease
is not as frequently seen as with the Burkitt lymphomas). Extranodal disease in tonsils, testes and
other organs is also common. Stage IV disease (involving CNS or marrow is rare (<5%). DLBCL will
have a mature B-cell phenotype with expression of CD20 and cell surface immunoglobulin (with exception of
some primary mediastinal large B-cell lymphomas). Other subtypes of DLBCL seen in adults, such as
T-cell rich large B-cell lymphoma or mediastinal large B-cell lymphoma, are also seen in children. DLBCL
is not associated with any specific cytogenetic abnormalities, although >80% will display cytogenetic
abnormalities, which are often complex. Detection of the t(14;18)(q32;q21) that characterizes many adult
DLBCL has not been described in pediatric DLBCL or pediatric follicular lymphomas, although the t(8;14)
seen in BL is well described in pediatric cases that have classic morphologic features of DLBCL.
Although the extensive molecular analysis that has been done on adult DLBCL has not been carried out on
pediatric cases, extensive immunophenotypic analysis has suggested that nearly all of the pediatric cases
display a germinal center phenotype (positive for bcl-2, bcl-6 and/or CD-10, and lacking expression of
MUM-1 and/or CD138). Treatment of pediatric DLBCL with intense, short multiagent chemotherapy lasting
between 6 weeks to 6 months with 90-100% 5 year EFS in limited (Stage I-II) and 80-95% 3year EFS in
advanced stage disease. Therapeutic approaches include therapy that is directed towards mature B-cell
disease (both DLBCL and Burkitt lymphoma) or therapy designed specifically for large cell disease (both B
and T-cell phenotypes) has been used.
Anaplastic large cell lymphoma (ALCL) comprises approximately 10% of pediatric NHL in the US, but
appears to have a higher incidence in some European cohorts. ALCL in the pediatric population is most
often high stage (III or IV) systemic disease, with 40-60% of children having involvement of extranodal
sites such as bone, soft tissue and skin as well as nodal disease. All morphologic subtypes, including
the common type and lymphohistiocytic, and small cell variants are seen. ALCL is typically mature T-cell
disease by immunophenotyic analysis or demonstration of clonal TCR gene rearrangements. All will express
CD30, and in contrast to adults where ALK overexpression may be seen in 50-60% of cases, >95% of
pediatric cases will demonstrate evidence of ALK over-expression by immunohistochemistry or FISH
analysis. As with adults, a wide variety of translocation partners involving the ALK locus are seen in
the pediatric age group and, to date, there has been no association with response or therapeutic
outcome. ALCL varies from many of the other types of pediatric NHL in that patients are susceptible to
late relapses, often occurring 4-8 years after initial diagnosis. Treatment approaches have varied from
NHL based CHOP type regimes to regimes directed more specifically at T-cell disease using doxorubicin,
prednisone and vincristine (APO) over a 5-36 month period. Both approaches give short-term response
rates of 75%. However EFS at 5 years falls to 50-60% in many studies, due to late relapses. Poor
prognostic factors include extensive organ or skin involvement and B-symptoms. Relapses may be
aggressive (waxing and waning disease) or rapidly aggressive disease. Salvage therapy includes bone
marrow transplantation or second line NHL therapies with 40-50% 3-year survivals.
Although lymphoblastic lymphoma, Burkitt and atypical Burkitt lymphoma, DLBCL and ALCL make up >90%
of pediatric tumors, a small number of other lymphomas have been seen in children. These include
low-grade tumors such as follicular lymphomas and marginal zone lymphomas as well as rare aggressive
peripheral T-cell lymphomas (exclusive of ALCL), gamma delta hepatosplenic lymphoma, mycosis fungoides
and NK cell neoplasms. Follicular lymphoma is probably the most commonly seen of these rare NHLs, and
appears to be distinctly different from adult follicular center cell lymphomas in that it is commonly low
stage (often Stage I) or extranodal (testes) disease and are often predominantly large cell processes.
These tumors may also have different pathogenetic mechanisms, as many do not over-express bcl-2 by
immunohistochemistry and lack the characteristic t(14;18) seen in adult follicular center cell tumors.
Many of the marginal zone type lymphomas in the pediatric population occur in immunosuppressed patients.
Due to the small numbers of pediatric patients, a clear treatment approach for these diseases has not
been established, and many are treated with adult based therapies or with immune based therapies (such as
use of Rituximab for less aggressive B-cell disease). The prognosis in these young patients remains
The prognosis for children with NHL has improved markedly in the past 20 years and most patients have
excellent outcomes with short-intensive therapies with mature B-cell neoplasms and long-term therapy with
precursor lesions. Challenges in improving outcome with treatment of ALCL, finding effective salvage
therapies for the small numbers of patients that fail therapy in other entities and in minimizing toxic
side effects due to the intensive treatment regimes remain. Late effects, such as sterility,
cardiomyopathy and secondary tumors are still seen in some patients and because of the predicted long
life spans of many of the patients remain problematic. Use of less toxic or alternative therapies, such
as immune-based therapies (very rarely used in children in contrast to adults) or better prognostic risk
identification to allow minimization of therapy for some patients are challenges remaining in therapy of
- Agnarsson BA, Kadin ME. Peripheral T-cell lymphomas in children. Semin Diagn Pathol 12:314-324, 1995.
- Alessandri AJ, Pritchard SL, et al. A population based study of pediatric anaplastic large cell lymphoma. Cancer 94:1830-1835, 20002.
- Attarbaschi A, Mann G, et al. The role of surgery in the treatment of pediatric B-cell non-Hodgkin's lymphoma. J Pediatr Surg 37:1470-1475, 2002.
- Brugieres L, LeDelay H, et al. CD30+ anaplastic large cell lymphoma in children: analysis of 82 patients enrolled in two consecutive studies of the French Society of Pediatric Oncolocy. Blood 92:3591-3598, 1998.
- Brunning RD, Borowitz M, et al. Precursor B lymphoblastic leukaemia/lymphoma. . In Jaffe ES, Harris NL, Stein H, Vardiman JW (eds) Pathology and Genetics of Tumours of Haematopoietic and Lymphoid Tissues. IARC Press, Lyon. p 111-114, 2001.
- Brunning RD, Borowitz M, et al. Precursor T lymphoblastic leukaemia/lymphoma. . In Jaffe ES, Harris NL, Stein H, Vardiman JW (eds) Pathology and Genetics of Tumours of Haematopoietic and Lymphoid Tissues. IARC Press, Lyon. p 115-117, 2001.
- Cairo MS. Current advances and future strategies in B large cell lymphoma in children and adolescents. Proc Am Soc Oncol 21:512-519, 2002.
- Cairo MS, Raetz E, et al. Non-Hodgkin lymphoma in children. In Kufe D, Pollack RE, Weishelbaum RR, Bast RC, Gansler TS, Holland JF, Frei E (eds) Cancer Medicine, 6th ed. BC Decker Inc., London, p 2337-2348, 2003.
- Chu PG, Chang KL, et al. Practical applications of immunohistochemistry in hematolymphoid neoplasms. Ann Diagnost Pathol 3:104-133, 1999.
- Corr P, Vaithilingum M, et al. Parotid MALT lymphoma in HIV infected children. J Ultrasound Med 16:615-617, 1997.
- Delsol G, Ralfiaer E, et al. Anaplastic large cell lymphoma. . In Jaffe ES, Harris NL, Stein H, Vardiman JW (eds) Pathology and Genetics of Tumours of Haematopoietic and Lymphoid Tissues. IARC Press, Lyon. p 230-235, 2001.
- Diebold J, Jaffe ES, et al. Burkitt lymphoma. In Jaffe ES, Harris NL, Stein H, Vardiman JW (eds) Pathology and Genetics of Tumours of Haematopoietic and Lymphoid Tissues. IARC Press, Lyon. p 181-184, 2001.
- Drexler HG, Gignac SM, et al. Pathobiology of the NPM-ALK and variant fusion genes in anaplastic large cell lymphoma and other lymphomas. Leukemia 14:1533-1559, 2000.
- Duyster J, Bai RY, et al. Translocations involving anaplastic lymphoma kinase (ALK). Oncogene 20:5623-5637, 2001.
- Elenitoba-Johnson KSJ, Kumar S, et al. Marginal zone B-cell lymphoma in pediatric patients without immunodeficiency: a report of two cases. Am J Clin Pathol 107:92-98, 1997.
- Finn LS, Viswanatha DS, et al. Primary follicular lymphoma of the testes in childhood. Cancer 85:1626-1635, 1999.
- Frizzera G, Murphy SB, et al. Follicular (nodular) lymphoma in childhood: a rare clinicopathological entity, a report of eight cases from four cancer centers. Cancer 44:2218-2235, 1979.
- Garcia-Sanchez F, Menaguez J, et al. Hepatosplenic gamma-delta T-cell malignant lymphoma: report of the first case in childhood including molecular minimal disease follow-up. Br J Haematol 90:943-946, 1995.
- Goldsby RE, Carroll WL. The molecular biology of pediatric lymphomas. J Pediatr Hematol/Oncol 20:283-296, 1998.
- Golub TR. Genomic approaches to the pathogenesis of hematologic malignancy. Curr Opin Hematol 8:252-261, 2001.
- Gordon BG, Weisenberger DD, et al. Peripheral T-cell lymphoma in childhood and adolescence: a clinicopathologic study of 22 patients. Cancer 71:257-263, 1993.
- Harris NL, Jaffe ES, et al. A revised European-American classification of lymphoid neoplasms: a proposal from the International Lymphoma Study Group. Blood 84:1361-1392, 1994.
- Head DR, Behm FG. Acute lymphoblastic leukemia and the lymphoblastic lymphomas of childhood. Semin Diagn Pathol 12:325-334, 1995.
- Hutchinson RE, Bernard CW, et al. B-cell lineage confers a favorable outcome among children and adolescents with large-cell lymphoma: a Pediatric Oncology Group study. J Clin Oncol 13:2023-2032, 1995.
- Hutchinson RE, Finch C, et al. Burkitt lymphoma is immunophenotypically different from Burkitt-like lymphoma in young persons. Ann Oncol 11:35-38, 2000.
- Irivani S, Singleton TP, et al. Precursor B lymphoblastic lymphoma presenting as lytic bone lesions. Am J Clin Pathol 112:836-843, 1999.
- Joshi VV, Gagnon GA, et al. The spectrum of mucosa-associated lymphoid tissue lesions in pediatric patients infected with HIV: a clinicopathologic study of six cases. Am J Clin Pathol 107:592-600, 1997.
- Kadin ME, Morris S. The t(2;5) in human lymphomas. Leuk Lymphoma 29:249-256. 1998.
- Kinney MC, Kadin ME. The pathologic and clinical spectrum of anaplastic large cell lymphoma and correlation with ALK gene dysregulation. Am J Clin Pathol 111:S56-S67, 1999.
- Koch SE, Zackheim HS, et al. Mycosis fungoides beginning in childhood and adolescence. J Am Acad Dermatol 17:563-570, 1987.
- Laver JH, Mahmoud H, et al. Results of a randomized phase III trial in children and adolescents with advanced stage diffuse large cell non-Hodgkin's lymphoma: a Pediatric Oncology Group study. Leuk Lymphoma 43:105-109, 2002.
- Lin P, Jones D, et al. Precursor B-cell lymphoblastic lymphoma: a predominantly extranodal tumor with low propensity for leukemic involvement. Am J Surg Pathol 24:1480-1490, 2000.
- Lin K-H, Su I-J, et al. Peripheral T-cell lymphoma in childhood: a report of five cases in Taiwan. Med Pediatr Oncol 23:26-35, 1994.
- Link MP, Roper M, et al. Cutaneous lymphoblastic lymphoma with pre-B markers. Blood 61:838-841, 1983.
- Link M, Shuster JJ, et al. Treatment of children and young adults with early-stage non-Hodgkin's lymphoma. N Engl J Med 337:1259-1266, 1997.
- Lones M, Auperin A, et al. Mature B-cell lymphoma/leukemia in children and adolescents: intergroup pathologist consensus with the Revised European-American Lymphoma classification. Ann Oncol 11:47-51, 2000.
- Lones MA, Perkins SL, et al. Large-cell lymphoma arising in the mediastinum of children and adolescents is associated with excellent outcome: a Children's Oncolocgy Group report. J Clin Oncol 18:3845-3853, 2000.
- Lorsbach RB, Shay-Seymore D, et al. Clinicopathologic analysis of follicular lymphoma occurring in children. Blood 99:1959-1964, 2002.
- Macpherson N, Lesack D, et al. Small noncleaved, non-Burkitt (Burkitt-like) lymphoma: cytogenetics predict outcome and reflect clinical presentation. J Clin Oncol 17:1558-1567, 1999.
- Magrath IT. Small noncleaved cell lymphomas (Burkitt and Burkitt-like lymphomas). In Magrath IT (ed) The Non-Hodgkin's Lymphomas, 2nd ed. Arnold, New York, p 781-811, 1997.
- Massimo M, Gasparini M, et al. Ki-1 (CD30) anaplastic large cell lymphoma in children. Ann Oncol 6:915-920, 1995.
- Murphy SB. Classification, staging and end results of treatment of childhood non-Hodgkin's lymphomas: dissimilarities from lymphomas in adults. Semin Oncol 7:332-339, 1980.
- Murphy SB. Pediatric lymphomas: recent advances and commentary on Ki-1-positive anaplastic large cell lymphomas of childhood. Ann Oncol 5:S31-S33, 1994.
- Nakawaga A, Nakmura S, et al. CD30-positive anaplastic large cell lymphoma in childhood: expression of the p80 npm/alk and absence of Epstein-Barr virus, Mod Pathol 10:210-215, 1997.
- Neth O, Seideann K, et al. Precursor B-cell lymphoblastic lymphoma in childhood and adolescence: clinical features, treatment and results in trials BFM86 and 90. Med Pediatr Oncol 35:20-27, 2000.
- Patte C, Auperin A, et al. The Societe Francaise d'Oncologie Pediatrique LMB89 protocol: highly effective multiagent chemotherapy tailored to the tumor burden and initial response in 561 unselected children with B-cell lymphomas and L3 leukemia. Blood 97:3370-3379, 2001.
- Patte C, Philip T, et al. High survival rate in advanced B-cell lymphomas and leukemias without CNS involvement with a short intensive polychemotherapay: results from the French Pediatric Oncology Society of a randomized trial of 216 children. J Clin Oncol 9:123-132, 1991.
- Perkins SL. Work-up and diagnosis of pediatric non-Hodgkin's lymphomas. Pediatr Develop Pathol 3:374-390, 2000.
- Perkins SL, Segal GH, et al. Classification of non-Hodgkin's lymphomas in children. Semin Diagn Pathol 12:303-313, 1995.
- Piccozzi V, Coleman C. Lymphoblastic lymphoma. Semin Oncol 17:96-103, 1990.
- Pilozzi E, Muller0Hermelink H, et al. Gene rearrangements in T-cell lymphoblastic lymphoma. J Pathol 188:267-270, 1999.
- Pinto A, Hutchinson R, et al. Follicular lymphomas in pediatric patients. Mod Pathol 3:308-313, 1990.
- Pollak BH, Jenson HB, et al. Risk factors for pediatric human immunodeficiency virus-related malignancy. JAMA 18:2393-2399, 2003.
- Pulford K, Lamant L, et al. Detection of anaplastic lymphoma kinase (ALK) and nucleolar protein nucleophosmin (NPM)-ALK proteins in normal and neoplastic cells with the monoclonal protein ALK1. Blood 89:1394-1404, 1997.
- Reiter A, Riehm H. Large cell lymphomas in children. In Magrath IT (ed) The Non-Hodgkin's Lymphomas, 2nd ed. Arnold, New York, p 829-851, 1997.
- Reiter A, Schrappe M, et al. Non-Hodgkin's lymphomas of childhood and adolescence: results of treatment stratified for biologic subtype and stage-a report of the Berlin-Frankfort-Munster group. J Clin Oncol 13:359-372, 1995.
- Reiter A, Schrappe M, et al. Intensive ALL-type therapy without localized radiotherapy provides a 90% event-free survival for children with T-cell lymphoblastic lymphoma: a BFM group report. Blood 95:416-421, 2000.
- Rossbach HC, Chamizo W, et al. Hepatosplenic gamma/delta T-cell lymphoma with isochromosome 7q, translocation t(7;21) and tetrasomy 8 in a nine-year-old girl. J Pediatr Hematol Oncol 24:154-157, 2002.
- Rubie H, Glafieff L, et al. Childhood anaplastic large cell lymphoma Ki-1/CD30: clinicopathologic features of 19 cases. Med Pedaitr Oncol 22:155-161, 1994.
- Sandlund JT, Downing JR, et al. Non-Hodgkin's lymphoma in childhood. N Engl J Med 334:1238-1248, 1998.
- Sandlund JT, Mcgrath IT: Lymphoblastic lymphoma. In Magrath IT (ed) The Non-Hodgkin's Lymphomas, 2nd ed. Arnold, New York, p813-828, 1997.
- Sandlund JT, Murphy SB, et al. CNS involvement in children with newly diagnosed non-Hodgkin's lymphoma. J Clin Oncol 18:30183024, 2000.
- Seidemann K, Tiemann M, et al. Primary mediastinal large B-cell lymphoma with sclerosis in pediatric and adolescent patients: treatment and results from three therapeutic studies of the Berlin-Frankfurt-Munster Group. J Clin Oncol 21:1782-189, 2003.
- Shad A, Mcgrath I. Malignant non-Hodgkin's lymphoma in childhood. In Pizzo PA, Poplack DG (eds): Principles and Practice of Pediatric Oncology, 3rd ed. Lippincott-Raven, Philadelphia, p545-547, 1997.
- Sherman CG, Zielenska M, et al. Morphological and phenotypic features in pediatric large cell lymphoma and their correlation with ALK expression and the t(2;5)(p23;q35) translocation. Pediatr Dev Pathol 4:129-137, 2001.
- Soslow R, Baergen R, et al. B-lineage lymphoblastic lymphoma is a clinicopathologic entity distinct from other histologically aggressive lymphomas with blastic morphology.. Cancer 85:2648-2654, 1999.
- Spina D, Leocini L, et al. Cellular kinetic and phenotypic heterogeneity in and among Burkitt and Burkitt-like lymphomas. J Pathol 182:145-150, 1997.
- Spreafico F, Massimino M, et al. Intensive, very short-term chemithrapy for advanced Burkitt's lymphoma in children. J Clin Oncol 20:2783-2788, 2002.
- Taddesse-Heath L, Pittaluga S, et al. Marginal zone B-cell lymphoma in children and young adults. Am J Surg Pathol 27:522-531, 2003.
- Taniguchi S, Horio T, et al. Mycosis fungoides in the tumor stage treated by PUVA: a successful trial in a 12 year old girl. Dermatologica 160:409-413, 1980.
- Thomas DA, Kantarjian HM. Lymphoblastic lymphoma. Hematol Oncol Clin North Am 15:51-95, 2001.
- Uckun FM, Sensel MG, et al. Biology and treatment of childhood T-lineage acute lymphoblastic leukemia. Blood:735-746, 1998.
- Weiss RL, Lazarus KH, et al. Natural killer-like T-cell lymphoma in the small intestine of a child without evidence of enteropathy. Am J Surg Pathol 21:964-969, 1997.
- Weitzman S, Suryanarayan K, et al. Pediatric non-Hodgkin's lymphoma: clinical and biological prognostic factors and risk allocation. Curr Oncol Rep 4:107-113, 2002.
- Winberg C, Nathwani, B, et al. Follicular (nodular) lymphoma during the first two decades of life: a clinicopathologic study of 12 patients. Cancer 48:2223-2235, 1981.
- Wright D, McKeever P, et al. Childhood non-Hodgkin's lymphomas in the United Kingdom: findings from the UK Children's Cancer Study Group. J Clin Pathol 50:128-134, 1997.