Cell kinetics in Burkitt lymphoma

Iversen, Olav Hilmar; Iversen, Ulla; Ziegler, John L.; Bluming, Avrum Z.

doi:10.1016/0014-2964(74)90148-0

Cited by 103 publications

(28 citation statements)

References 12 publications

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“…There is evidence in the literathat stathmokinetic methods may be used favourably to study tumour kinetics over a 4-h period (Iversen, 1967;Refsum and Berdal, 1 967; Smith, Thomas and Riches, 1974). Anaphases and telophases were not seen in the sections from tumours exposed to Colcemid, and this leads us to believe that the block was complete, and supports previous observations in Burkitt's lymphoma (Iversen et al, 1974). The small Colcemid effect in one of the florid tumours was probably partly due to impaired vascular supply, areas of necrosis being seen in the histological sections.…”

Section: Cellular Kineticssupporting

confidence: 85%

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Growth kinetics of Kaposi's sarcoma

Taylor¹,

Iversen²,

Bjerknes³

1977

Br J Cancer

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Summary.-This is a study of The rate of cell production found in this tumour is lower than the values reported in the literature for other malignancies. The calculated mitotic duration is long, but similar to previously reported values. The cell loss factor is high: in the static tumour it is 1-0, and in the regressing tumours greater than 1.0. In regressing tumours, the rate of cell loss was 30% higher than the rate of cell production. These tumours did not differ histologically from nearly florid tumours which were increasing in size. It is postulated that regression is determined by local vascular or mechanical factors, supplemented possibly by delayed hypersensitivity responses in some patients.

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Section: Cellular Kineticssupporting

confidence: 85%

“…The growth rate of Kaposi's sarcoma is similar to that of Hodgkin's disease (Charbit, Malaise and Tubiana, 1971), but much slower than Burkitt's lymphoma, which has a doubling time of 3 days (Iversen et al, 1974).…”

Section: Cellular Kineticsmentioning

confidence: 87%

Growth kinetics of Kaposi's sarcoma

Taylor¹,

Iversen²,

Bjerknes³

1977

Br J Cancer

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“…Examination at this time revealed a firm, tender suprapubic mass measuring about hours. 9,20,21 Also, the fact that the patient presented with lower lip paraesthesia sharply contrasts with earlier reports [22][23][24][25][26] that this tumour does not usually produce sensory loss due to the non-involvement of the fifth or seventh nerves in their extracranial course.…”

Section: Discussioncontrasting

confidence: 50%

Burkitt's lymphoma presenting as lower lip paraesthesia in a 24 year old Nigerian. Case report

Ugboko

Ndukwe

Adelusola

et al. 1999

Australian Dental Journal

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An unusal case of stage D Burkitt's lymphoma in a 24 year old Nigerian female undergraduate is reported. There was a four month history of left lower lip paraesthesia followed three months later by a slowly progressive ‘pimple‐sized’ nodular mandibular swelling arising from the mental foramen region. A full‐blown, rapidly developing abdominal mass manifested only three weeks after a biopsy of the mandibular swelling. Aspiration of the latter and a histologic report of the mandibular mass confirmed Burkitt's lymphoma. The patient responded very well to appropriate chemotherapy. Clinicians should not overlook insidious jaw swellings in any adult residing in the endemic zone of Burkitt's lymphoma, in view of the fact that successful therapy is dependent on early diagnosis. Mental nerve paraesthesia is very rarely seen in Burkitt's lymphoma.

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“…6 BL has the highest proliferative index of any known human cancer; it progresses rapidly, with the tumors doubling in size every 24-26 hours. 7 eBL is hypothesized to be of a multifactorial etiology, encompassing environmental factors, infectious factors (i.e., EBV and malaria infection), immune system disturbances, and potentially, host genetic predisposition. 2,8,9 Although the precise pathogenic mechanisms for eBL have not been fully elucidated, genetic susceptibility has been found to play an important role in the development and progression of BL.…”

Section: Introductionmentioning

confidence: 99%

Interleukin-6 and Interleukin-10 Gene Promoter Polymorphisms and Risk of Endemic Burkitt Lymphoma

Oduor¹,

Chelimo²,

Ouma³

et al. 2014

The American Society of Tropical Medicine and Hygiene

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Abstract. Overexpression of interleukin-6 (IL-6) and IL-10 in endemic Burkitt lymphoma (eBL) may facilitate tumorigenesis by providing a permissive cytokine milieu. Promoter polymorphisms influence interindividual differences in cytokine production. We hypothesized that children genetically predisposed for elevated cytokine levels may be more susceptible to eBL. Using case-control samples from western Kenya consisting of 117 eBL cases and 88 ethnically matched healthy controls, we tested for the association between eBL risk and IL-10 (rs1800896, rs1800871, and rs1800872) and IL-6 (rs1800795) promoter single nucleotide polymorphisms (SNPs) as well as IL-10 promoter haplotypes. In addition, the association between these variants and Epstein Barr Virus (EBV) load was examined. Results showed that selected IL-10 and IL-6 promoter SNPs and IL-10 promoter haplotypes were not associated with risk eBL or EBV levels in EBV-seropositive children. Findings from this study reveal that common variants within the IL-10 and IL-6 promoters do not independently increase eBL risk in this vulnerable population.

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Cell kinetics in Burkitt lymphoma

Cited by 103 publications

References 12 publications

Growth kinetics of Kaposi's sarcoma

Growth kinetics of Kaposi's sarcoma

Burkitt's lymphoma presenting as lower lip paraesthesia in a 24 year old Nigerian. Case report

Interleukin-6 and Interleukin-10 Gene Promoter Polymorphisms and Risk of Endemic Burkitt Lymphoma

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