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. 2009 Jul 6;206(7):1473–1483. doi: 10.1084/jem.20082842

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© 2009 Agopian et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 1. — Agricultural exposure drives a dramatic increase of t(14;18)⁺ clones in blood. (A) Evolution of t(14;18) frequency in PBMCs from control and exposed populations over time. The mean age at enrollment was 40 yr (±9 yr) for the controls and 43 yr (±9 yr) for the exposed individuals, with an average follow-up time of 7 and 9 yr, respectively. t(14;18) frequency was assessed at each time point by fluctuation SR-PCR. Horizontal lines indicate mean frequencies. p-values were calculated using the Mann-Whitney test. (B) Clonality analysis. Exposed (n = 26/51, 51%) and control (n = 6/46, 13%) samples with a high t(14;18) frequency (>10⁻⁵) in the last sampling period are shown and ordered according to increasing t(14;18) frequencies (the total number of clones in each individual for which more than one positive amplicon was found is summarized in Table S1). BCL2/J_H breakpoints (Table I and unpublished data) were identified by the cloning/sequencing of SR-PCR products (n ≈ 1,000) amplified from PBMCs, and were used to monitor the extent of polyclonality within t(14;18)⁺ cells in each individual. For each individual, independent BCL2/J_H clones are pictured in distinct shades and are represented from bottom to top according to increasing frequency.