Diffuse large B-cell lymphoma represents approximately 30%–40% of all diagnoses of non-Hodgkin’s Lymphoma and may represent up to 80% of all lymphomas that arise in the palatine tonsils. Several studies have attempted to correlate clinical, laboratorial, and tissue factors with the prognosis of the lymphomas, such as the International Prognostic Index, the tissue expression of some proteins, and the lymphocyte count at the time of diagnosis, as well as to correlate Epstein-Barr virus (EBV) infection with worse prognoses. Patients with palatine tonsil DLBCL, from Salvador, Bahia, Brazil, were studied in order to identify prognostic factors. Twenty-four patients with DLBCL were studied. The factors that negatively influenced the patients’ survival rates were the lymphocyte count at the time of diagnosis <1.000/mm3 and the Bcl-2 protein expression. There was no CD5 expression in these lymphomas, and neither was there an association with EBV infection. 1. Introduction The palatine tonsils, along with the nasopharyngeal lymphoid tissue, the base of the tongue, and the oropharyngeal wall make up Waldeyer’s ring. This ring is located at the entrance of the respiratory and digestive tract, being the second most common site of extranodal lymphomas, after the gastrointestinal tract [1, 2]. These tumors represent 15 to 20% of all lymphomas and half of the head and neck lymphomas. Approximately 50% of Waldeyer’s ring lymphomas arise in the palatine tonsils in presentation, and in approximately 20% of the cases they are bilateral [3]. Most lymphomas found in the palatine tonsils are the B-cell type, and, of these, diffuse large B-cell lymphoma (DLBCL) represents most of the cases, reaching as much as 80% in some of the groups studied [3, 4]. Although morphologically indistinct, some molecular studies support the hypothesis that DLBCL makes up a heterogeneous group of lymphomas that has different prognostic implications [5]. Classically, the International Prognostic Index (IPI) has been used to predict the survival of patients with DLBCL [6]; however, it is not useful in all cases. Studies using DNA microarray analysis show that the DLBCL gene expression profile similar to B cells germinal center would have a better clinical prognosis than the profile similar to activated B cells [5, 7]. Transposing this gene profile to a protein expression, Hans et al. [8] proposed an algorithm to classify DLBCL patients, using three immunohistochemical markers (CD10, Bcl-6, and MUM1). The profile that was similar to the germinal center (GC) presented a better survival rate than the
References
[1]
A. Yuen and C. Jacobs, “Lymphomas of the head and neck,” Seminars in Oncology, vol. 26, no. 3, pp. 338–345, 1999.
[2]
R. M. Nathu, N. P. Mendenhall, N. M. Almasri, and J. W. Lynch, “Non-Hodgkin's lymphoma of the head and neck: a 30-year experience at the University of Florida,” Head and Neck, vol. 21, no. 3, pp. 247–254, 1999.
[3]
E. Zucca, E. Roggero, F. Bertoni, A. Conconi, and F. Cavalli, “Primary extranodal non-Hodgkin's lymphomas. Part 2: head and neck, central nervous system and other less common sites,” Annals of Oncology, vol. 10, no. 9, pp. 1023–1033, 1999.
[4]
M. M. S. Neto, E. M. Jalil, and I. Araújo, “Linfomas n？o-Hodgkin extranodais em Salvador-Bahia: aspectos clínicos e classifica？？o histopatológica segundo a OMS-2001,” Revista Brasileira de Hematologia e Hemoterapia, vol. 30, pp. 36–40, 2008, http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1516-84842008000100010.
[5]
A. A. Alizadeh, M. B. Eisen, R. E. Davis et al., “Distinct types of diffuse large B-cell lymphoma identified by gene expression profiling,” Nature, vol. 403, no. 6769, pp. 503–511, 2000.
[6]
M. Shipp, D. Harrington, and J. Anderson, “The international non-Hodgkin’s lymphoma prognostic factors project. A predictive model for aggressive non-Hodgkin’s lymphoma,” The New England Journal of Medicine, vol. 329, pp. 987–994, 1993.
[7]
A. Rosenwald, G. Wright, W. C. Chan et al., “The use of molecular profiling to predict survival after chemotherapy for diffuse large-B-cell lymphoma,” New England Journal of Medicine, vol. 346, no. 25, pp. 1937–1947, 2002.
[8]
C. P. Hans, D. D. Weisenburger, T. C. Greiner et al., “Confirmation of the molecular classification of diffuse large B-cell lymphoma by immunohistochemistry using a tissue microarray,” Blood, vol. 103, no. 1, pp. 275–282, 2004.
[9]
J. Muris, C. Meijer, W. Vos et al., “Immunohistochemical profiling based on Bcl-2, CD10 and MUMI expression improves risk stratification in patients with primary nodal diffuse large B cell lymphoma,” Journal of Pathology, vol. 208, no. 5, pp. 714–723, 2006.
[10]
M. Yamaguchi, M. Seto, M. Okamoto et al., “De novo CD5+ diffuse large B-cell lymphoma: a clinicopathologic study of 109 patients,” Blood, vol. 99, no. 3, pp. 815–821, 2002.
[11]
M. A. Piris, F. Pezella, J. C. Martinez-Montero et al., “p53 and bcl-2 expression in high-grade B-cell lymphomas: correlation with survival time,” British Journal of Cancer, vol. 69, no. 2, pp. 337–341, 1994.
[12]
D. H. Kim, J. H. Baek, Y. S. Chae et al., “Absolute lymphocyte counts predicts response to chemotherapy and survival in diffuse large B-cell lymphoma,” Leukemia, vol. 21, no. 10, pp. 2227–2230, 2007.
[13]
L. F. Porrata, K. Ristow, T. M. Habermann, T. E. Witzig, D. J. Inwards, and S. N. Markovic, “Absolute lymphocyte count at the time of first relapse predicts survival in patients with diffuse large B-cell lymphoma,” American Journal of Hematology, vol. 84, no. 2, pp. 93–97, 2009.
[14]
M. Engel, M. F. Essop, P. Close, P. Hartley, G. Pallesen, and C. Sinclair-Smith, “Improved prognosis of Epstein-Barr virus associated childhood Hodgkin's lymphoma: study of 47 South African cases,” Journal of Clinical Pathology, vol. 53, no. 3, pp. 182–186, 2000.
[15]
S. Park, J. Lee, Y. Ko et al., “The impact of Epstein-Barr virus status on clinical outcome in diffuse large B-cell lymphoma,” Blood, vol. 110, no. 3, pp. 972–978, 2007.
[16]
J. M. Middeldorp, A. Brink, A. van den Brule, and C. Meijer, “Pathogenic roles for Epstein-Barr virus (EBV) gene products in EBV-associated proliferative disorders,” Critical Reviews in Oncology/Hematology, vol. 45, no. 1, pp. 1–36, 2003.
[17]
A. A. Bahnassy, A.-R. N. Zekri, N. Asaad et al., “Epstein-Barr viral infection in extranodal lymphoma of the head and neckcorrelation with prognosis and response to treatment,” Histopathology, vol. 48, no. 5, pp. 516–528, 2006.
[18]
I. Araújo, H. D. Foss, M. Hummel et al., “Frequent expansion of Epstein-Barr virus (EBV) infected cells in germinal centres of tonsils from an area with a high incidence of EBV- associated lymphoma,” Journal of Pathology, vol. 187, no. 3, pp. 326–330, 1999.
[19]
S. H. Swerdlow, E. Campo, N. L. Harris, et al., Eds., WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues, IARC, Lyon, France, 2008.
[20]
S. A. Rosenberg, “Validity of the Ann Arbor staging classification for the non-Hodgkin's lymphomas,” Cancer Treatment Reports, vol. 61, no. 6, pp. 1023–1048, 1977.
[21]
P. Sannino and S. Shousha, “Demonstration of oestrogen receptors in paraffin wax sections of breast carcinoma using the monoclonal antibody 1D5 and microwave oven processing,” Journal of Clinical Pathology, vol. 47, no. 1, pp. 90–92, 1994.
[22]
A. Krol, S. Le Cessie, S. Snijder, J. C. Kluin-Nelemans, P. M. Kluin, and E. M. Noordijk, “Waldeyer's ring lymphomas: a clinical study from the comprehensive cancer center west population based NHL registry,” Leukemia and Lymphoma, vol. 42, no. 5, pp. 1005–1013, 2001.
[23]
D. Hasenclever and V. Diehl, “A prognostic score for advanced Hodgkin's disease,” New England Journal of Medicine, vol. 339, no. 21, pp. 1506–1514, 1998.
[24]
M. Siddiqui, K. Ristow, S. N. Markovic et al., “Absolute lymphocyte count predicts overall survival in follicular lymphomas,” British Journal of Haematology, vol. 134, no. 6, pp. 596–601, 2006.
[25]
D. Behl, L. F. Porrata, S. N. Markovic et al., “Absolute lymphocyte count recovery after induction chemotherapy predicts superior survival in acute myelogenous leukemia,” Leukemia, vol. 20, no. 1, pp. 29–34, 2006.
[26]
K. B. B. Pagnano, J. Vassallo, I. Lorand-Metze, F. F. Costa, and S. T. O. Saad, “p53, Mdm2, and c-Myc overexpression is associated with a poor prognosis in aggressive non-Hodgkin’s lymphomas,” American Journal of Hematology, vol. 67, no. 4, pp. 84–92, 2001.
[27]
F. R. Kerbauy, G. Colleoni, S. Saad et al., “Detection and possible prognostic relevance of p53 gene mutations in diffuse large B-cell lymphoma. An analysis of 51 cases and review of the literature,” Leukemia and Lymphoma, vol. 45, no. 10, pp. 2071–2078, 2004.
[28]
K. K. Wong, N. Prepageran, and S. C. Peh, “Prognostic subgroup distribution in diffuse large B-cell lymphoma of the upper aerodigestive tract,” Pathology, vol. 41, no. 2, pp. 133–139, 2009.
