Received March 7, 2006; accepted for publication March 7, 2006.

　　Lymphoma biology is a rapidly moving field. Until the most recent decade, large-cell lymphoma was considered a single entity and classified as such in earlier lymphoma pathologic classification schema. The differentiation was almost exclusively based on classic histology. Advances in immunoperoxidase technology and molecular biology have opened the biologic door to a better understanding of subtypes that have their clinical and molecular characteristics.

　　The purpose of this series is to update interested clinicians on new terminology and unique biologic features that contribute to the now widely used World Health Organization designations for these entities. The initial series will include disorders known as primary mediastinal, anaplastic large-cell, post-transplant lymphoproliferative disease, Burkitt’s, intravascular, and T-cell–rich B-cell lymphoma. Others could be added, but these represent some of the more frequently encountered of the subtypes.

　　There is, of course, a great deal more to be learned about large-cell lymphoma. Clinical differences exist in the natural history of some of the extranodal large-cell lymphomas, such as a primary testicular B-cell large-cell lymphoma compared to nodal B-cell large-cell lymphoma. The various entities of T-cell large-cell lymphoma have been generally characterized as resistant to conventional chemotherapy with the exception of anaplastic T-cell large-cell lymphoma, which is described in this series.

　　It is becoming apparent that nodal B-cell large-cell lymphoma is a heterogeneous disease. The technique of gene micro-array has defined genetic signatures that can be correlated with therapeutic outcome [1–4]. This technology has the potential to define unique and vital changes in genes that may play a vital role in the behavior of the disease. Defining these abnormalities is likely to lead to the development of specific agents that target the gene and its product. These techniques have also defined molecular genetic relationships between mediastinal B-cell lymphoma and Hodgkin’s lymphoma [5].

　　In this initial series, all authors chosen are young academics who are or have been active in the lymphoma programs associated with Dana-Farber/Partners CancerCare, an entity which encompasses the Harvard Medical School–affiliated institutions Dana-Farber Cancer Institute, Massachusetts General Hospital, and the Brigham and Women’s Hospital.

　　References
 
Monti S, Savage KJ, Kutok JL et al. Molecular profiling of diffuse large B-cell lymphoma identifies robust subtypes including one characterized by host inflammatory response. Blood 2005;105:1851–1861.
Rosenwald A, Wright G, Chan WC et al. The use of molecular profiling to predict survival after chemotherapy for diffuse large-B-cell lymphoma. N Engl J Med 2002;346:1937–1947.
Shipp MA, Ross KN, Tamayo P et al. Diffuse large B-cell lymphoma outcome prediction by gene-expression profiling and supervised machine learning. Nat Med 2002;8:68–74.
Lossos IS, Czerwinski DK, Alizadeh AA et al. Prediction of survival in diffuse large- B-cell lymphoma based on the expression of six genes. N Engl J Med 2004;350:1828–1837.
Savage KJ, Monti S, Kutok JL et al. The molecular signature of mediastinal large B-cell lymphoma differs from that of other diffuse large B-cell lymphomas and shares features with classical Hodgkin lymphoma. Blood 2003;102:3871–3879.

查询更多Special相关信息在本站>>

《肿瘤学家医学期刊》2006年4月第11卷第4期