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AIDS-Related Malignancy
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2020
Mark Bower, Elena Gervasi, Alessia Dalla Pria
Burkitt lymphoma is a highly curable malignancy in the general population using intensive chemotherapy regimens of short duration combined with central nervous system penetrating therapy. These regimens have been adopted in the management of HIV-BL and small studies have demonstrated the feasibility of administering more intensive chemotherapy regimens, such as rituximab-cyclophosphamide, vincristine, doxorubicin, methotrexate/ifosfamide, etoposide, cytarabine ([R]-CODOX-M/IVAC) and cyclophosphamide, vincristine, doxorubicin, dexamethasone, methotrexate, cytarabine (hyperCVAD). Studies report response rates and 2-year event-free survivals similar to those observed in HIV-negative patients treated with the same regimen, with no increase in toxicity, suggesting that a uniform approach to treatment of BL should be used, regardless of HIV status.
The Non-Hodgkin’s Lymphomas and Plasma Cell Dyscrasias
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
Lynne V. Abruzzo, L. Jeffrey Medeiros
The histologic features of Burkitt-like lymphoma resemble Burkitt’s lymphoma. The cytologic features of the neoplastic cells are intermediate between Burkitt’s lymphoma and diffuse large B-cell lymphoma. Like Burkitt’s lymphoma, the nuclei of the malignant cells are the same size or smaller than benign macrophages. However, like diffuse large B-cell lymphoma, there is greater nuclear pleomorphism, and the nuclear chromatin is more vesicular with more prominent nucleoli (Fig. 12). In some cases it may not be possible to distinguish between Burkitt-like and diffuse large B-cell lymphoma.
Indeterministic Causality
Published in Donald Gillies, Causality, Probability, and Medicine, 2019
The first step consisted in epidemiological investigations of cervical cancer which took place in the late 1950s and early 1960s. These showed that cervical cancer (Vonka and Hamš iková , 2007, p. 132) “had the character of an infectious disease and that the causative agent was transmitted by sexual intercourse.” In the second half of the 1960s, the first case of a human cancer caused by a virus was proposed and came to be increasingly accepted by the medical community. This was the causation of Burkitt’s lymphoma by the Epstein-Barr virus (see Clarke, 2011, pp. 25–52, and 2012, pp. 181–184 for details).
CAR-NK cells: a promising cellular immunotherapy in lymphoma
Published in Expert Opinion on Biological Therapy, 2023
Shaghayegh Khanmohammadi, Nima Rezaei
Monoclonal antibodies against CD20 (rituximab) are commonly used in patients with NHL, which is usually effective; however, drug resistance may affect its efficacy. To examine the effect of CD20-specific NK cells on NHL, Müller et al. generated CAR-NK cells with CD20-specific scFv antibody fragment and CD3ζ chain as the signaling domain from the NK-92 cell line (with retroviral vector). Their result showed that CD20-specific CAR-NK cells enhanced cytotoxicity towards NK-sensitive CD20-expressing cells. Additionally, the CAR-NK cells overcame the resistant lymphoma cells [77]. Chu et al. tested the efficacy of anti-CD20 CAR-NK cells in treating aggressive B-cell NHL from NSG mice in vitro and in vivo. Peripheral blood NK cells were engineered by mRNA nucleofection to target CD20+ B-NHL. Engineered CAR-NK cells had enhanced in vitro cytotoxicity towards both rituximab-resistant and rituximab-sensitive lymphoma cells. CAR-NK-treated NSG mice had prolonged survival and reduced tumor size in comparison with the control group [78]. In another study on Burkitt lymphoma by Chu et al., romidepsin (a histone deacetylase inhibitor) and CAR-NK cells showed synergic cytotoxic activities in vivo and in vitro. Romidepsin can increase the cytotoxicity of anti-CD20 CAR-modified expanded peripheral blood NK cells via NKG2D by inducing the expression of NKG2D ligands MICA/B in rituximab-sensitive and rituximab-resistant Burkitt lymphoma cells [9].
Adult Burkitt lymphoma- an Island between lymphomas and leukemias
Published in Journal of Community Hospital Internal Medicine Perspectives, 2019
James Turro, Pratiksha Singh, Manbeer Singh Sarao, Satish Tadepalli, Pramil Cheriyath
Burkitt lymphoma is a rare, aggressive and rapidly fatal, B-cell Non-Hodgkin’s lymphoma (NHL). The World Health Organization (WHO) defines it as a highly aggressive but curable lymphoma that often presents in extra-nodal sites or as acute leukemia” [1]. It was first described in 1958 by Dr. Dennis Parsons Burkitt in a 5-year old boy from Uganda who presented with swelling of both jaws. The symmetrical nature and progression of these swellings to other parts of the body piqued Dr. Burkitt’s curiosity. He described the disease as a tumor of lymphatic origin, which now bears his eponym. Currently, the disease is known to have an incidence of 0.4/100,000 age-adjusted to the USA standard population [2]. It has trimodal age-specific incidence peaks in males at ages 10, 40 and 75 years, and bimodal pediatric and geriatric peaks in females [3]. The cure rate decreases significantly with age, dramatically in patients > 60 years of age.
Low expression of Mda-7/IL-24 and high expression of C-myb in tumour tissues are predictors of poor prognosis for Burkitt lymphoma patients
Published in Hematology, 2018
Ming Ma, Riyang Zhao, Xingxiao Yang, Lianmei Zhao, Lihua Liu, Cong Zhang, Xuexiao Wang, Baoen Shan
Burkitt lymphoma is one of the most common subtypes of paediatric haematopoietic malignancy and accounts for approximately 40% of newly diagnosed non-Hodgkin’s lymphoma in children and adolescents [1]. Although high-dose combination chemotherapy is an effective strategy for the treatment of Burkitt lymphoma, a poor prognosis is inevitable for the patients due to recurrence, invasion of bone marrow tissue and development of chemotherapy resistance [2,3]. However, the exact mechanisms involved in occurrence and progression of Burkitt lymphoma remain unclear. Haemopoietic tumours, including Burkitt lymphoma, are characterized by a block in terminal differentiation. Therefore, acquiring more knowledge of the key molecules involved in affecting cell differentiation may provide new therapeutic targets for treatment of Burkitt lymphoma and further improve the survival rates of patients.