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Hypoxia signature in BIA-ALCL
and metastatic status of clear cell renal cell carcinoma and high preoperative levels are associated with postoperative recurrence.26 We demonstrated that CA9 is readily secret- ed by BIA-ALCL cells in vitro and that significantly elevat- ed CA9 concentrations are present in peri-implant sero- mas involved by BIA-ALCL. Various inflammatory condi- tions can cause peri-implant seromas,46,47 and the diagnosis of BIA-ALCL in seroma fluid can be a significant challenge if neoplastic cells are rare. Hanson et al. recently reported specificity of an enzyme-linked immunosorbent assay for CD30 in seroma specimens involved by BIA-ALCL,48 while Kadin et al. reported that BIA-ALCL cell lines secrete a unique cytokine profile that includes interleukin-13.7 A multi-analyte approach incorporating CA9 that evaluates these proteins in seroma fluid could greatly facilitate the diagnosis of BIA-ALCL when few atypical cells are pres- ent and could potentially guide the decision regarding implant removal in suspicious cases in which definite neo- plastic cells cannot be identified. This prospect should encourage international collaboration and standardized seroma collection protocols to facilitate progress given the rarity of BIA-ALCL. The role of serum CA9 measurement in BIA-ALCL remains unclear because limited samples were available for analysis. However, we identified elevat- ed CA9 concentrations in serum samples from BIA-ALCL xenograft-bearing mice, and the role of serum CA9 as a possible biomarker to predict or monitor disease activity should be evaluated in larger human studies.
Disclosures
No conflicts of interest to disclose.
Contributions
NO performed research, analyzed and interpreted data, and wrote the manuscript. TH, JLP and GH performed research and analyzed and interpreted data. SD performed bioinformatic and statistical analysis and interpreted data. DSV and RH interpret- ed data. MM, HKJ and NHA performed research. SIS, JRC, FV, JS, NNB and LJM provided samples and interpreted data. YS analyzed data. ALE contributed TLBR cell lines and vital reagents. MWC and RNM designed the study, provided sam- ples, and interpreted data. ALF designed the study, analyzed and interpreted data, and wrote the manuscript. All authors approved the final manuscript.
Funding
This work was supported by Award Numbers R01 CA177734 (ALF), P30 CA15083 (Mayo Clinic Cancer Center), P50 CA97274 (University of Iowa/Mayo Clinic Lymphoma SPORE), and UL1 TR002377 (Mayo Clinic Center for Clinical and Translational Science) from the National Institutes of Health; by Award Number CI-48-09 from the Damon Runyon Cancer Research Foundation (ALF); by a grant from the Plastic Surgery Foundation, American Society of Plastic Surgeons (MD Anderson Cancer Center); and by the Department of Laboratory Medicine and Pathology and the Center for Individualized Medicine, Mayo Clinic.
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