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The cause of death was due to HL in 9 patients; pulmonary embolism, pneumonia, and aortic stenosis accounted for the other deaths. FLC elevation was significantly associated with age >45, advanced stage, poor ECOG PS, albumin 15,000), B symptoms, elevated sedimentation rate, and unfavorable IPS. There was no association of FLC elevation with lymphopenia (WBC http://www.selleckchem.com/products/birinapant-tl32711.html to build a multivariable model for OS. After adjusting for GFR, elevated FLC remained associated with EFS: HR = 4.20, (95% CI: 1.57�C11.23), P = 0.004. Elevated FLC were associated with poor EFS in both early (HR = 6.94, 1.32�C36.4, P = 0.02) and advanced stage patients (HR = 3.07, 0.92�C10.27, P = 0.07); FLC hazard ratio estimates were also similar across GHSG categories (data not shown). An abnormal FLC ratio without elevated FLC was not associated with outcome (data not shown). Classical HL is a unique tumor in that the majority of cells in the microenvironment are nonmalignant, consisting of reactive T- and B-cells, eosinophils, neutrophils, macrophages, http://www.selleckchem.com/products/Gemcitabine-Hydrochloride(Gemzar).html and plasma cells [14]. The malignant cells��the Reed-Sternberg cells��have been demonstrated to be incapable of secreting functional Ig molecules and therefore would not be expected to produce FLC [15, 16]. In our study, the FLC elevation is polyclonal in nature (elevated kappa and lambda light chains with a normal ratio) which supports the hypothesis http://www.selleck.cn/products/azd9291.html that the FLC is being secreted by polyclonal B-cells, presumably in the HL microenvironment, although this needs to be established. It is known that polyclonal increase in FLC can be due to a number of host factors, such as increased age, impaired renal function, and general inflammation or immune stimulation [17]. In our study, we observed an association of polyclonal elevated FLC with more general host attributes (older age, B symptoms, and poor PS) and with sedimentation rate, an inflammatory marker. It is hypothesized that patients with elevated FLC will have elevations in inflammatory cytokines and chemokines. This should be evaluated in future studies to better understand the pathogenesis. Serum FLC has the potential to be a useful clinical tool in the care of patients with HL. FLC quantitative analysis could be incorporated into a prognostic index used at diagnosis, which may be useful in predicting those patients who would benefit from a more aggressive first line of treatment.