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P lasma E pstein‐ B arr virus DNA for pediatric B urkitt lymphoma diagnosis, prognosis and response assessment in M alawi
Author(s) -
Westmoreland Katherine D.,
Montgomery Nathan D.,
Stanley Christopher C.,
ElMallawany Nader Kim,
Wasswa Peter,
van der Gronde Toon,
Mtete Idah,
Butia Mercy,
Itimu Salama,
Chasela Mary,
Mtunda Mary,
Kampani Coxcilly,
Liomba N. George,
Tomoka Tamiwe,
Dhungel Bal M.,
Sanders Marcia K.,
Krysiak Robert,
Kazembe Peter,
Dittmer Dirk P.,
Fedoriw Yuri,
Gopal Satish
Publication year - 2017
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.30682
Subject(s) - medicine , hazard ratio , cohort , prospective cohort study , lymphoma , surgery , chemotherapy , confidence interval
Point‐of‐care tools are needed in sub‐Saharan Africa (SSA) to improve pediatric Burkitt lymphoma (BL) diagnosis and treatment. We evaluated plasma Epstein–Barr virus (pEBV) DNA as a pediatric BL biomarker in Malawi. Prospectively enrolled children with BL were compared to classical Hodgkin lymphoma (cHL) and nonlymphoma diagnoses. Pediatric BL patients received standardized chemotherapy and supportive care. pEBV DNA was measured at baseline, mid‐treatment, and treatment completion. Of 121 assessed children, pEBV DNA was detected in 76/88 (86%) with BL, 16/17 (94%) with cHL, and 2/16 (12%) with nonlymphoma, with proportions higher in BL versus nonlymphoma ( p < 0.001) and similar in BL versus cHL ( p = 0.69). If detected, median pEBV DNA was 6.1 log 10 copies/mL for BL, 4.8 log 10 copies/mL for cHL, and 3.4 log 10 copies/mL for nonlymphoma, with higher levels in BL versus cHL ( p = 0.029), and a trend toward higher levels in BL versus nonlymphoma ( p = 0.062). pEBV DNA declined during treatment in the cohort overall and increased in several children before clinical relapse. Twelve‐month overall survival was 40% in the cohort overall, and for children with baseline pEBV detected, survival was worse if baseline pEBV DNA was ≥6 log 10 copies/mL versus <6 log 10 copies/mL ( p = 0.0002), and also if pEBV DNA was persistently detectable at mid‐treatment versus undetectable ( p = 0.041). Among children with baseline pEBV DNA detected, viremia was the only significant risk factor for death by 12 months in multivariate analyses (adjusted hazard ratio 1.35 per log 10 copies/mL, 95% CI 1.04–1.75, p = 0.023). Quantitative pEBV DNA has potential utility for diagnosis, prognosis, and response assessment for pediatric BL in SSA.