Closed-Loop Recycling of Copper from Waste Printed Circuit Boards Using Bioleaching and Electrowinning Processes

International audienceIn the present study, a model of closed-loop recycling of copper from PCBs is demonstrated, which involves the sequential application of bioleaching and electrowinning to selectively extract copper. This approach is proposed as part of the solution to resolve the challenging ever-increasing accumulation of electronic waste, e-waste, in the environment. This work is targeting copper, the most abundant metal in e-waste that represents up to 20% by weight of printed circuit boards (PCBs). In the first stage, bioleaching was tested for different pulp densities (0.25–1.00% w/v) and successfully used to extract multiple metals from PCBs using the acidophilic bacterium, Acidithiobacillus ferrooxidans. In the second stage, the method focused on the recovery of copper from the bioleachate by electrowinning. Metallic copper foils were formed, and the results demonstrated that 75.8% of copper available in PCBs had been recovered as a high quality copper foil, with 99 + % purity, as determined by energy dispersive X-ray analysis and Inductively-Coupled Plasma Optical Emission Spectrometry. This model of copper extraction, combining bioleaching and electrowinning, demonstrates a closed-loop method of recycling that illustrates the application of bioleaching in the circular economy. The copper foils have the potential to be reused, to form new, high value copper clad laminate for the production of complex printed circuit boards for the electronics manufacturing industry. Graphic Abstract: [Figure not available: see fulltext.] © 2020, The Author(s)

Breast tumors from CHEK2 1100delC-mutation carriers: genomic landscape and clinical implications

Introduction: Checkpoint kinase 2 (CHEK2) is a moderate penetrance breast cancer risk gene, whose truncating mutation 1100delC increases the risk about twofold. We investigated gene copy-number aberrations and gene-expression profiles that are typical for breast tumors of CHEK2 1100delC-mutation carriers. Methods: In total, 126 breast tumor tissue specimens including 32 samples from patients carrying CHEK2 1100delC were studied in array-comparative genomic hybridization (aCGH) and gene-expression (GEX) experiments. After dimensionality reduction with CGHregions R package, CHEK2 1100delC-associated regions in the aCGH data were detected by the Wilcoxon rank-sum test. The linear model was fitted to GEX data with R package limma. Genes whose expression levels were associated with CHEK2 1100delC mutation were detected by the bayesian method. Results: We discovered four lost and three gained CHEK2 1100delC-related loci. These include losses of 1p13.3-31.3, 8p21.1-2, 8p23.1-2, and 17p12-13.1 as well as gains of 12q13.11-3, 16p13.3, and 19p13.3. Twenty-eight genes located on these regions showed differential expression between CHEK2 1100delC and other tumors, nominating them as candidates for CHEK2 1100delC-associated tumor-progression drivers. These included CLCA1 on 1p22 as well as CALCOCO1, SBEM, and LRP1 on 12q13. Altogether, 188 genes were differentially expressed between CHEK2 1100delC and other tumors. Of these, 144 had elevated and 44, reduced expression levels. Our results suggest the WNT pathway as a driver of tumorigenesis in breast tumors of CHEK2 1100delC-mutation carriers and a role for the olfactory receptor protein family in cancer progression. Differences in the expression of the 188 CHEK2 1100delC-associated genes divided breast tumor samples from three independent datasets into two groups that differed in their relapse-free survival time. Conclusions: We have shown that copy-number aberrations of certain genomic regions are associated with CHEK2 mutation 1100delC. On these regions, we identified potential drivers of CHEK2 1100delC-associated tumorigenesis, whose role in cancer progression is worth investigating. Furthermore, poorer survival related to the CHEK2 1100delC gene-expression signature highlights pathways that are likely to have a role in the development of metastatic disease in carriers of the CHEK2 1100delC mutation

CHEK2*1100delC and susceptibility to breast cancer:A collaborative analysis involving 10,860 breast cancer cases and 9,065 controls from 10 studies

Previous studies of families with multiple cases of breast cancer have indicated that a frameshift alteration in the CHEK2 gene, 1100delC, is associated with an elevated frequency of breast cancer in such families, but the risk associated with the variant in other situations is uncertain. To evaluate the breast cancer risk associated with this variant, 10,860 breast cancer cases and 9,065 controls from 10 case-control studies in five countries were genotyped. CHEK2*1100delC was found in 201 cases (1.9%) and 64 controls (0.7%) (estimated odds ratio 2.34; 95% CI 1.72-3.20; P=.0000001). There was some evidence of a higher prevalence of CHEK2*1100delC among cases with a first-degree relative affected with breast cancer (odds ratio 1.44; 95% CI 0.93-2.23; P=.10) and of a trend for a higher breast cancer odds ratio at younger ages at diagnosis (P=.002). These results confirm that CHEK2*1100delC confers an increased risk of breast cancer and that this risk is apparent in women unselected for family history. The results are consistent with the hypothesis that CHEK2*1100delC multiplies the risks associated with susceptibility alleles in other genes to increase the risk of breast cancer