Because of the effect of time on allele burden in PV, we restricted clinical correlations to patients in whom JAK2V617F allele burden was performed within 5 years of diagnosis (n ¼ 77, median age at diagnosis 66 years, 43% women). Blood counts at presentation in these 77 patients included medians of 18.6 g/dl for hemoglobin, 439  10 9 /l for platelet count and 11.8  10 9 /l for leukocyte count. At a median follow-up of 38 months, eight deaths, one leukemic transformation and two post-PV myelo- fibrosis were documented. Arterial and venous thrombosis occurred in 10 (13%) and four (5%) patients at diagnosis and in 15 (19.5%) and four (5%) patients during follow-up, respectively. Linear regression analysis for continuous variables revealed that JAK2V617F allele burden correlated directly with leukocyte count (Po0.0001) but not with hemoglobin level (P ¼ 0.39), platelet count (P ¼ 0.85), or age (P ¼ 0.85). Similarly, allele burden was not affected by gender (P ¼ 0.9). Allele burden (considered as a continuous variable) was significantly higher in the presence of pruritus (P ¼ 0.003) or microvascular symptoms (P ¼ 0.03) but not palpable splenomegaly (P ¼ 0.89) or cytotoxic therapy during follow-up (n ¼ 57 versus 20 patients not receiving such therapy; P ¼ 0.3). Mutant allele burden was similar between the 14 patients who presented with major thrombosis (both arterial and venous) and the 63 patients who did not (P ¼ 0.32); similarly, allele burden was not significantly different in those patients who developed major thrombosis during follow-up (n ¼ 19) compared to those who did not (n ¼ 58; P ¼ 0.95). The results did not change when arterial thrombosis (P ¼ 0.38 at diagnosis and 0.75 during follow-up) was analyzed separately from venous thrombosis (P ¼ 0.51 at diagnosis and 0.49 during follow-up). The above-mentioned results regarding clinical correlations of bone marrow JAK2V617F allele burden remained the same, for the most part, when allele burden was treated as a categorical variable with either two groups above and below the median value or three groups with allele burdens upto 25% (n ¼ 55), between 25 and 50% (n ¼ 10) and above 50% (n ¼ 12), respectively. The only different outcome was the loss of significant correlation involving microvascular symptoms and pruritus when allele burden was categorized into three groups. Finally, the number of events in terms of death, leukemic transformation, or development of post-PV myelofibrosis was too small to allow valid statistical comparisons of survival or disease transformation. Taken together, the findings from the current study are underwhelming in terms of clinical relevance of bone marrow JAK2V617F allele burden in PV. The strongest and most consistent correlation was leukocytosis, an observation that warrants the inclusion of leukocyte count as a covariate in any statistical analysis of prognostic relevance that includes JAK2V617F allele burden. This result is pertinent to the recent emphasis on the prognostic relevance of leukocytosis in both PV and ET. 7 Our findings also underline the potential confounding effect of sample accrual time on result interpretation. Finally, we underscore the fact that the current study utilized DNA from archived bone marrow and should not be compared with other studies that have used either DNA 2 or mRNA (Vannucchi AM et al. Blood 2006; 108: Abstract no. 5) from purified granulocytes. A Tefferi 1 , JJ Strand 1 , TL Lasho 1 , RA Knudson 2 , CM Finke 1 , N Gangat 1 , A Pardanani 1 , CA Hanson 3 and RP Ketterling 2 1 Division of Hematology, Mayo Clinic, Rochester, MN, USA; 2 Laboratorie of Cytogenetics, Mayo Clinic, Rochester, MN, USA and 3 Laboratorie of Hematopathology, Mayo Clinic, Rochester, MN, USA E-mail: tefferi.ayalew@mayo.edu References 1 Scott LM, Tong W, Levine RL, Scott MA, Beer PA, Stratton MR et al. JAK2 exon 12 mutations in polycythemia vera and idiopathic erythrocytosis. N Engl J Med 2007; 356: 459–468. 2 Tefferi A, Lasho TL, Schwager SM, Strand JS, Elliott M, Mesa R et al. The clinical phenotype of wild-type, heterozygous, and homozygous JAK2V617F in polycythemia vera. Cancer 2006; 106: 631–635. 3 Vannucchi AM, Pancrazzi A, Bogani C, Antonioli E, Guglielmelli P. A quantitative assay for JAK2(V617F) mutation in myeloproliferative disorders by ARMS-PCR and capillary electrophoresis. Leukemia 2006; 20: 1055–1060. 4 Levine RL, Belisle C, Wadleigh M, Zahrieh D, Lee S, Chagnon P et al. X-inactivation-based clonality analysis and quantitative JAK2V617F assessment reveal a strong association between clonality and JAK2V617F in PV but not ET/MMM, and identifies a subset of JAK2V617F-negative ET and MMM patients with clonal hematopoiesis. Blood 2006; 107: 4139–4141. 5 Gale RE, Allen AJ, Nash MJ, Linch DC. Long-term serial analysis of X-chromosome inactivation patterns and JAK2 V617F mutant levels in patients with essential thrombocythemia show that minor mutant- positive clones can remain stable for many years. Blood 2007; 109: 1241–1243. 6 Kittur J, Knudson RA, Lasho TL, Finke CM, Gangat N, Wolanskyj AP et al. Clinical Correlates of JAK2V617F Allele Burden in Essential Thrombocythemia. Cancer 2007; in press. 7 Gangat N, Wolanskyj AP, McClure RF, Li CY, Schwager S, Wu W et al. Risk stratification for survival and leukemic transformation in essential thrombocythemia: a single institutional study of 605 patients. Leukemia 2007; 21: 270–276. History of infections and vaccinations and risk of lymphoid neoplasms: does influenza immunization reduce the risk? Leukemia (2007) 21, 2075–2079; doi:10.1038/sj.leu.2404738; published online 17 May 2007 Lymphoid neoplasms (LN) are malignancies of lymphocytes, the primary effectors of the immune system. LN are a heterogeneous group including non-Hodgkin’s lymphoma (NHL), Hodgkin’s lymphoma (HL), multiple myeloma (MM) and chronic lympho- cytic leukaemia (CLL) and comprises numerous histological subtypes integrated in the third edition of the WHO Interna- tional Classification in Oncology since 2001. Altogether, for the year 2000, the annual number of incident cases of LN in France was estimated to be over 17 000 and the number of deaths to almost 9000. The incidence of NHL increased more than 3% Letters to the Editor 2075 Leukemia