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Hindawi Publishing Corporation Case Reports in Oncological Medicine Volume 2013, Article ID 370179, 3 pages http://dx.doi.org/10.1155/2013/370179 Case Report Burkitt’s Lymphoma in a Pregnant Woman: Case Report and Review of the Literature 1 2 3 4 Carlos Zagalo, Francesca Pierdomenico, José Cabeçadas, and Pedro David Santos Egas Moniz, Health Sciences Institute, Quinta da Granja, Monte de Caparica, 2829-511 Caparica, Portugal Servi¸co de Hematologia, Instituto Portugues de Oncologia de Lisboa Francisco Gentil EPE, Rua Professor Lima Basto, 1099-023 Lisboa, Portugal Servi¸o c de Anatomia Patolog ´ ica, Instituto Portugues ˆ de Oncologia de Lisboa Francisco Gentil EPE, Rua Professor Lima Basto, 1099-023 Lisboa, Portugal Instituto Cien ˆ cias Biomed ´ icas Abel Salazar, Universidade do Porto, Rua de Jorge Viterbo Ferreira No. 228, 4050-313 Porto, Portugal Correspondence should be addressed to Pedro David Santos; email@example.com Received 30 March 2013; Accepted 20 April 2013 Academic Editors: L. Beex, J. M. Buchanich, D. V. Jones, C. V. Reyes, and K. Tanaka Copyright © 2013 Carlos Zagalo et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Burkitt’s lymphoma (BL) is an aggressive B-cell malignancy with very high proliferation rate, more common in males than females. Here, we describe a case of Burkitt’s lymphoma in a 24-week pregnant woman with cervical and abdominal involvement. The common genetic event of virtually all BL is a reciprocal chromosomal translocation involving the proto-oncogene MYC and one of the Ig gene heavy or light chain loci. Supportive treatment was administered until early delivery, aeft r which the patient was treated according to protocol LMB96. Pregnancy and tumorogenesis share some important events such as immunologic tolerance, angiogenesis, and editing the host immune response. Little is known about the relationship between these events in pregnancy and in tumorogenesis. 1. Introduction The sporadic form (5–15% associated with EBV) aeff cts mainly abdominal viscera, terminal ileum, caecum, mesen- Burkitt’s lymphoma was first described in 1957 by the Irish tery, and Waldeyer ring; the third variant is usually associated surgeon Dennis Parsons Burkitt, aeft r observation of a so- with HIV infection, and 45% of patients are coinfected with called “sarcoma of the jaws” in children in Uganda, Africa. EBV. Burkitt’s lymphoma is more common in males than Burkitt’s lymphoma (BL) is a highly aggressive non-Hodgkin females . lymphoma (NHL), with a very fast growth rate, oen ft aeff cting The common genetic event of virtually all BL is a recipro- extranodal sites or with leukemic presentation . Burkitt’s cal chromosomal translocation involving the proto-oncogene lymphoma is usually diagnosed in children and young adults MYC (on chromosome 8) and one of the Ig gene heavy or and, to a lesser extent, in middle-aged adults . Based on light chain loci (on chromosomes 2, 14, or 22) . The vast epidemiology, three different forms of Burkitt’s lymphoma majority of Burkitt’s lymphomas exhibit t(8; 14)(q24; q32). have been described until now, an endemic form, a sporadic As aresultofthe reciprocal chromosomaltranslocation,the form, and one related to HIV infection. eTh endemic form oncogene c-myc is overexpressed under the influence of Ig (verycommoninAfricaand PapuaNew Guinea)isstrongly enhancers regulatory regions. Constitutive expression of c- associated (95%) with Epstein-Barr virus (EBV) infection and myc oncogene promotes an increased B-cell proliferation, as malaria  and usually aeff cts children that present with facial bones involvement. well as a reduced capacity for induction of apoptosis . 2 Case Reports in Oncological Medicine Burkitt’s lymphoma/leukemia was one of the rfi st malig- nancies shown to be curable with intensive chemotherapy, and the majority of children and young adult patients are curable today with aggressive combination chemotherapy regimens . 2. Case Presentation A twenty-five years old woman, in the 24th week of gestation, presentedwithavoluminous cervical mass locatedonthe left front neck. She had first noticed an enlargement of her neck 3 months earlier, and, apart from tiredness, she was completely asymptomatic. On observation, she had an isolated cervical mass of Figure 1: Ki67 almost 100%. about 5× 10cm long,hardonpalpation,not mobile. Fine needle aspiration showed a high grade B-cell lym- phoma, CD10+ (flow cytometry), and the biopsy to the cer- vical lesion confirmed the diagnosis of Burkitt’s lymphoma with gene break point on MYC (8q24) determined by FISH (fluorescent in situ hybridization). The tumour was CD20 (+), CD10 (+), Ki67 (+) (>90% of cells) (Figure 1), CD3 (−), BCL2 (−), and TdT (−). The patient is HIV-1 negative, HIV-2 negative,EBV Ig Gpositive, andEBV Ig Mnegative. As shewas pregnant at thetimeofdiagnosis,atotalbody MRI (magnetic resonance imaging) was used for staging instead of conventional CT scan. MRI revealed a cervical mass of 104× 63× 75 mm deviating the trachea and oesopha- gus leftwards and in the infra diaphragmatic compartment, amassmeasuring 135 × 116 × 94 mm in the right flank Figure 2: MR coronal cut revealing a fetus and the abdominal tum- and a fetus of approximately 25 weeks (Figure 2). There our mass. were no bone marrow infiltration and no central nervous system (CNS) infiltration, and the LDH level was elevated (1376𝜇 L/L). According to the Murphy/St. Jude staging classi- when immunotherapeutic approach is used . Rituximab is fication for Burkitt’s lymphoma, the patient was in stage III. In a monoclonal antibody specific to CD20 that induces death an intention to safely carry on the pregnancy until week 28 of on B cells by antibody-dependent cell-mediated cytotoxicity gestation, under monitoring by an obstetrician, chemother- . Early diagnosis and intense and short treatment regimens apy with agents potentially less harmful for the baby arewaysofincreasingcurerates . was proposed. Cyclophosphamide, doxorubicin, vincristine, Thisisaninteresting case notonlybecause it wasnot prednisone, plus rituximab (R-CHOP) was performed with possible to determine if it is purely extranodal BL (most reduction of the cervical mass; however, in two weeks’ time, common), butalsobecause thepatient waspregnant. the mass started growing again and LDH increased. Delivery A diagnosis of Burkitt’s lymphoma during pregnancy was performed at 28th week of gestation +5, and a healthy implies difficulties both in staging procedures and in treat- baby was born by caesarean section. After delivery, the patient ment decision. Conventional staging methods as CT and PET proceeded with conventional treatment for BL according to scan should not be performed, and BL treatment protocol LMB-96 protocol, group B , without major complications. such as LMB-96 includes high-dose methotrexate and cytara- Assessment of treatment response aeft r R-CYM (cytara- bine which are contraindicated during pregnancy. Using bine, methotrexate, and rituximab) by CT and PET scan alternative diagnostic means, chemotherapy regimens with showed complete remission, and the patient completed drugs potentially less harmful for the baby and a close follow- chemotherapy according to LMB96 group B protocol in up together with obstetric consult are crucial. August 2012, with persisting complete remission. Immunologic tolerance, establishment of a nutrient sup- ply system (angiogenesis), and evasion or editing the host 3. Discussion immune response are essential steps for a normal pregnancy Whereas MYC translocation is found in almost all BL, it may and also for tumorogenesis. Epithelial-mesenchymal transi- be seen as well in some cases of diffuse large B-cell lymphoma tion, loss of integrin, and E-cadherin expression are essential (DLBCL) which is much more common, and may have a for the invasion processes in pregnancy and tumor growth. dieff rent treatment approach [ 7]. Vasculogenic mimicry (nonendothelial cell assumes form Burkitt’s lymphoma’s brief and intense treatment regi- and function of a vascular structure) is a process observed mens have led to high cure rates even in adults, especially in extra villous trophoblast (EVT) cells (invasion of spiral Case Reports in Oncological Medicine 3 arteries of maternal decidua, early in placental development)  S. G. Holtan, D. J. Creedon, P. Haluska, and S. N. Markovic, “Cancer and pregnancy: parallels in growth, invasion, and and in some aggressive melanoma cells, sharing the same immune modulation and implications for cancer therapeutic event—expression of galectin 3 . Immunologic modula- agents,” Mayo Clinic Proceedings,vol.84, no.11, pp.985–1000, tion is also a phenomenon encountered both in pregnancy, and in tumor proliferation which allows the presence, growth, and development of semiallogeneic cells (fetus and tumour). 40%ofcells of thedecidua,inapregnant uterus,are immune cells (NK, macrophages and dendrocytes). Uterus NK (70% of uterus immune cells) are CD16 (−)which meansthat they lack cytotoxic capacity. They also secrete galectin-1, responsible for induction of a tolerant behaviour in dendritic cells (DC). CD16 (−)NKcellsinfiltratedintumours,likerenal cell carcinoma, have been taken as responsible for reducing cytotoxic activity and modulating DC immune activity on these tumours . Regulatory T cells (present both in nor- mal pregnancy and cancer) have an important role in increas- ing tumor blood vessel density and in impaired antitumor immunity . Still very little is known about the relationship between these events in pregnancy and in tumorogenesis. Conflict of Interests The authors declare no conflict of interests. References  K. Booth, D. P. Burkitt, D. J. Bassett, R. A. Cooke, and J. Bid- dulph, “Burkitt lymphoma in Papua, New Guinea,” British Jour- nal of Cancer,vol.21, no.4,pp. 657–664, 1967.  V.T.DeVitaJr.,S.Hellman,andS.A.Rosenberg,“Non-Hodgkin lymphoma,” in Cancer: Principles and Practice of Oncology,vol. 2, pp. 2099–2139, Lippincott Williams & Wilkins, Philadelphia, Pa, USA, 8th edition, 2008.  C. Bellan, L. Stefano, D. F. Giulia, E. A. Rogena, and L. Lorenzo, “Burkitt lymphoma versus diffuse large B-cell lymphoma: a practical approach,” Hematological Oncology,vol.27, no.4,pp. 182–185, 2009.  G.Brady,G.J.MacArthur, andP.J.Farrell,“Epstein-Barr virus and Burkitt lymphoma,” Postgraduate Medical Journal,vol.84, no.993,pp. 372–377, 2008.  M. J. Allday, “How does Epstein-Barr virus (EBV) complement the activation of Myc in the pathogenesis of Burkitt’s lympho- ma?” Seminars in Cancer Biology,vol.19, no.6,pp. 366–376,  C.Patte,A.Auperin, M. Gerrardetal.,“Resultsofthe random- ized international FAB/LMB96 trial for intermediate risk B- cell non-Hodgkin lymphoma in children and adolescents: it is possible to reduce treatment for the early responding patients,” Blood,vol.109,no. 7, pp.2773–2780,2007.  C. Mosse and K. Weck, Molecular Pathology of Hematolymphoid Diseases, Springer Science+Business Media, Dordrecht, The Netherlands, 2010.  I.T.Aldoss, D. D. Weisenburger,K.Fuetal.,“AdultBurkitt lym- phoma: advances in diagnosis and treatment,” Oncology,vol.22, no.13, pp.1508–1517,2008.  M. Jason and H. 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Published: May 12, 2013
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