PubMed · 16783785
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P Guilpain, R Delarue, M Matignon, L H Noël, B Knebelmann, F Fakhouri. 2006. Primary bilateral diffuse renal lymphoma.. https://doi.org/10.1002/ajh.20624
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A 57-year-old female with a history of diffuse large B-cell lymphoma (DLBCL) presented with a renal mass. Microscopic analysis of the nephrectomy specimen revealed DLBCL, confirmed by immunohistochemical analysis (CD45, CD20, CD3, pan-keratin) and polymerase chain reaction (PCR). Multiple spicules of metaplastic bone were identified within the tumor mass, but not within the uninvolved kidney parenchyma. No evidence of bone or dystrophic calcification was detected on the pre-nephrectomy computerized tomography (CT) scan. To our knowledge, this is the first incidence of osseous metaplasia occurring within DLBCL. The pathogenesis of osseous metaplasia is briefly discussed.
OBJECTIVE: A dietary compound curcumin hardwires to multiple cellular processes, with suppression of cell proliferation, induction of apoptosis, and inhibition of metastasis considered as the major mechanisms underlying its anticancer properties. Based on our recent evidence that curcumin triggers cell demise in follicular lymphoma (FL) cells, we aimed to identify curcumin-regulated genes of utmost importance for the treatment of follicular lymphoma. MATERIALS AND METHODS: Large-scale gene-expression profiling was performed during curcumin-triggered apoptosis (8-36 hours) in follicular lymphoma HF4.9 cells using Sentrix Human WG-6 BeadChips. Expression levels of selected differentially expressed genes were verified by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and immunoblotting. Chemical inhibitor studies (cyclosporin A and AMD3100) were performed to provide further insights into the functional significance of selected genes. RESULTS: Comprehensive transcriptional response is associated with curcumin treatment in HF4.9 cells, including differential expression of genes encoding apoptotic signaling proteins, tumor and metastasis suppressors, transcription and splicing factors, proteins involved in regulation of cell adhesion, migration (e.g., CXCR4), lymphoid development, or B-cell activation (e.g. CD20), and others. CXCR4 downregulation was confirmed by both qRT-PCR and immunoblotting. Importantly, curcumin induced downregulation of CXCR4 protein also in other FL cell lines, and similar effect was observed upon prolonged incubation with low concentration of curcumin. AMD3100 (a selective CXCR4 antagonist) alone enhanced neither spontaneous nor serum-starvation-induced death at 24 hours of treatment, but impaired long-term cell growth in a cell line-dependent fashion. CONCLUSIONS: To our knowledge this is the first study showing curcumin-induced downregulation of CXCR4, and at attainable in vivo concentration of the polyphenol. Other curcumin-regulated genes identified herein, e.g., CD20, are also seemingly pertinent to the pathophysiology of follicular lymphoma.
BACKGROUND: Numerous methods for quantitative fluorescence calibration (QFC) have been developed to quantify receptor expression on lymphocytes as potential disease biomarkers. CD20 expression in B-cell chronic lymphocytic leukemia (B-CLL) is one of the best examples of such a biomarker, but results from the use of different QFC methods vary considerably. METHODS: We measured CD20 expression on normal and B-CLL B-cells, using FITC and PE conjugates from the same monoclonal antibody (Mab). As a biological control and calibrator, we also measured CD4 expression on T-cells with FITC and PE Mab. Calibration curves were constructed using the CLSI (formerly NCCLS) consensus guidelines for QFC. Calibration with QuantiBRITE PE-labeled microspheres and the use of unimolar PE conjugates provided direct measurement of antibody bound per cell (ABC) for CD4 and CD20. Calibration for FITC conjugates was based on molecules of equivalent soluble fluorochrome (MESF), as determined by NIST RM 8640 microsphere standards. These MESF values were then converted to ABC, using the CD4 T-cell as a biologic calibrator, to normalize FITC and PE results for CD20 expression. RESULTS: On normal B cells, the mean ABC value for unimolar CD20-PE conjugate was 143,500 (CV +/- 19.1%). The mean ABC value for B-CLL B-cells stained with the same conjugate was 21,700 (CV +/- 42.0%). Using the CD4 T-cell as a biologic calibrator for FITC conjugate, the mean ABC value for CD20-FITC on normal B-cells was 199,300. CD20-FITC staining on B-CLL cells was generally too weak for accurate quantification. On normal T-cells, the mean ABC value for CD4 unimolar PE conjugate was (36,800 +/- 10.4)%, and it did not differ significantly in CLL samples. CONCLUSION: The expression of CD20 on normal and B-CLL lymphocytes can be quantified in ABC units using unimolar CD20-PE conjugates. In addition, CD4 expression on T-cells can be used as a biological calibrator to quantify CD20-FITC ABC, with reasonable agreement between the two conjugates with different fluorochromes. Issues regarding the accuracy of MESF microsphere calibrators and effective F/P ratios for FITC conjugates will require additional laboratory studies.