Burkitt Lymphoma: beyond discoveries

Mbulaiteye, Sam M.

doi:10.1186/1750-9378-8-35

Cited by 17 publications

(21 citation statements)

References 33 publications

(38 reference statements)

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“…Assuming our results are not due to chance, IL-6 could contribute to lymphomagenesis by thwarting the apoptosis feedback loops in B cells that are triggered in B cells that have developed c-MYC chromosomal translocations to prevent the propagation of cells with chromosomal instability [11]. IL-6 is a pleiotropic cytokine that may exert local effects via the fixed IL-6 receptor (IL-6Rα) on initiated B cells (classical signaling pathway) or systemic effects by engaging its soluble receptor (sIL-6Rα) on activated B cells (trans-signaling pathway) [12].…”

mentioning

confidence: 99%

“…IL-6 is a pleiotropic cytokine that may exert local effects via the fixed IL-6 receptor (IL-6Rα) on initiated B cells (classical signaling pathway) or systemic effects by engaging its soluble receptor (sIL-6Rα) on activated B cells (trans-signaling pathway) [12]. Our results also could be due to secretion of IL-6 by eBL tumor cells [11]. If so, then levels of IL-6 might be correlated with disease burden.…”

mentioning

confidence: 99%

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Elevated serum levels of interleukin‐6 in endemic Burkitt lymphoma in Ghana

Aka¹,

Emmanuel²,

Vila

et al. 2014

Hematological Oncology

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mentioning

confidence: 99%

mentioning

confidence: 99%

Elevated serum levels of interleukin‐6 in endemic Burkitt lymphoma in Ghana

Aka¹,

Emmanuel²,

Vila

et al. 2014

Hematological Oncology

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“…As noted, chromosomal translocations involving cellular myc are a hallmark of BL and central to the genetic basis of cancer. 53 This translocation may be mediated by deregulated expression of AID, which is highly expressed in GC B cells. The most common variant of c-myc, accounting for about 85% of cases, is t(8;14)(q24;q32).…”

Section: Retinoic Acid and C-mycmentioning

confidence: 99%

Malaria, Epstein–Barr virus infection and the pathogenesis of Burkitt's lymphoma

Mawson

Majumdar

2017

Intl Journal of Cancer

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A geographical and causal connection has long been recognized between malaria, Epstein-Barr virus (EBV) infection and Burkitt's lymphoma (BL), but the underlying mechanisms remain obscure. Potential clues are that the malaria parasite Plasmodium falciparum selectively absorbs vitamin A from the host and depends on it for its biological activities; secondly, alterations in vitamin A (retinoid) metabolism have been implicated in many forms of cancer, including BL. The first author has proposed that the merozoite-stage malaria parasite, emerging from the liver, uses its absorbed vitamin A as a cell membrane destabilizer to invade the red blood cells, causing anemia and other signs and symptoms of the disease as manifestations of an endogenous form of hypervitaminosis A (Mawson AR, Path Global Health 2013;107(3):122-9). Repeated episodes of malaria would therefore be expected to expose the tissues of affected individuals to potentially toxic doses of vitamin A. It is proposed that such episodes activate latent EBV infection, which in turn activates retinoid-responsive genes. Expression of these genes enhances viral replication and induces germinal center (GC) B cell expansion, activation-induced cytidine deaminase (AID) expression, and c-myc translocation, which in turn predisposes to BL. Thus, an endogenous form of retinoid toxicity related to malaria infection may be the common factor linking frequent malaria, EBV infection and BL, whereby prolonged exposure of lymphatic tissues to high concentrations of retinoids may combine to induce B-cell translocation and increase the risk of Burkitt's lymphoma.

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“…The endemic BL in Africa was first described in Ugandan children by Dr. Denis Burkitts in 1958 at Mulago Hospital [3]. The tumor is the most common childhood malignancy in Africa [3,4].…”

Section: Introductionmentioning

confidence: 99%

“…The endemic BL in Africa was first described in Ugandan children by Dr. Denis Burkitts in 1958 at Mulago Hospital [3]. The tumor is the most common childhood malignancy in Africa [3,4]. The commonest sites of tumor growth are the face (jaw tumors), abdomen or both and the third most frequent site is the central nervous system [5,6].…”

Section: Introductionmentioning

confidence: 99%

Survival Factors of Burkitts Lymphoma Patients at Discharge: The Case of St. Mary’s Hospital Lacor in Northern Uganda

Mike¹

2014

AJHR

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Abstract:The purpose was to explore the contribution of the presenting demographic, clinical and laboratory characteristics to the survival status at discharge and duration of admission. The study used secondary data of the Burkitts Lymphoma (BL) patients who were admitted at St. Mary's Hospital Lacor between the period 2003 and 2009. Regressive methods were developed to establish the factors explaining the dependent variables. Whereas majority of the admissions were males (60%), the proportion of females diagnosed with the cancer progressively increased more than that of males over years. Regardless of any other anatomic site involved; 74 percent of the patients had abdominal tumors, 49 percent had tumors in the face and 23 percent had tumors in the CNS. Females were more likely to have abdominal tumor involvement than males. On the other hand, males were twice more likely to have facial or CNS tumor involvement than the females. Over 80 percent of the patients were staged C or D suggesting delays in seeking for treatment. Patients with adnominal or CNS tumor involvement were more likely to be staged C or D. Seven percent died within the average admission period of 96 days. All deaths were observed among stages C and D patients. The duration of admission between the discharged dead and alive was significantly different. Stage C and D patients tended to have longer duration of admission. Further, older patients tended to have a longer duration of admission than the younger ones. Other variables such as sex, and site tumor involvement did not have a significant effect on the duration of admission. The duration of admission and survival status tended to influence each other. Though marginal, age at admission had a significant role to play in explaining the length of admission. The deaths before admission were observed among stage C and D patients, of which over 80% of the patients were staged. This calls in a community-level follow-up study to assess their survival. The above findings suggest an accelerated risk to death among the discharged stage C and D patients.

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Burkitt Lymphoma: beyond discoveries

Cited by 17 publications

References 33 publications

Elevated serum levels of interleukin‐6 in endemic Burkitt lymphoma in Ghana

Elevated serum levels of interleukin‐6 in endemic Burkitt lymphoma in Ghana

Malaria, Epstein–Barr virus infection and the pathogenesis of Burkitt's lymphoma

Survival Factors of Burkitts Lymphoma Patients at Discharge: The Case of St. Mary’s Hospital Lacor in Northern Uganda

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