C-reactive protein as a clinically useful biomarker of metastasis of renal cell carcinoma.
ABSTRACT C-reactive protein (CRP) is an acute-phase reactant that can increase dramatically in response to a variety of pathologic states. Elevated pre- and postoperative CRP levels have been associated with an increased tumor burden and metastasis in kidney cancer. We report on a case that serves to highlight a potentially novel use for CRP monitoring in the postoperative management of renal cell carcinoma. Recently, we treated a patient who presented with a localized renal cell carcinoma and an elevated preoperative CRP level. Surgical pathology demonstrated negative surgical margins and absence of nodal metastasis. Postoperatively, the patient's serum CRP levels remained relatively low, consistent with his continued negative staging on CT scans. However, at 6 months postoperatively, the patient's CRP level increased 13-fold. His subsequent CT scan revealed "multiple pulmonary nodules consistent with progression of metastatic disease." This case demonstrates the potential for monitoring CRP in addition to, or instead of, standard restaging imaging.
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ABSTRACT: INTRODUCTION: C-reactive protein (CRP) is an acute-phase reactant with an increasing number of clinical functions. Studies in recent years have identified several social, economic, demographic, and psychological factors that contribute to baseline inflammation. Psychosocial stress represents a significant contributor to baseline inflammation. Given the importance of understanding background drivers of CRP levels, we conducted this review to assess the impact of chronic psychosocial stress on CRP levels. METHODS: Medline was searched through February 2013 for human studies examining CRP levels with respect to chronic psychosocial stress. RESULTS: The initial search identified 587 articles from which 129 potentially appropriate articles were reviewed. Of these 129 articles, 41 articles were included in the review. These studies were published between 2003 and 2013. Of these studies, 6 analyzed employment stress, 2 analyzed unemployment stress, 6 analyzed burnout and vital exhaustion, 6 analyzed caregiver stress, 3 analyzed interpersonal stress, 17 analyzed socioeconomic position, and 2 analyzed discrimination. CONCLUSION: We conclude that psychosocial stress significantly impacts CRP and should be considered when interpreting the meaning of CRP elevations.Molecular Diagnosis & Therapy 04/2013; 17(3). · 2.59 Impact Factor
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ABSTRACT: Despite some controversy, selenomethionine (SeMet) mediated protection against colorectal carcinoma (CRC) might be a very promising non-cytotoxic option. However, responsive molecular targets and underlying mechanisms of SeMet mediated chemoprevention are still unclear. Our aim was to discover new targets of SeMet mediated chemoprevention in CRC using proteomics analysis. We found dietary SeMet supplementation before carcinoma initiation effectively suppressed polyp incidence and dysplastic lesions without any adverse effects. To determine chemopreventive targets of SeMet, we employed 2-dimensional gel electrophoresis based proteomics analysis in CRC mouse model. Pretreatment with SeMet apparently modulated the expression of 30 proteins with functions in major processes like chronic inflammation, oxidative-stress and apoptosis as discovered through pathway analysis with Pathway studio software. We validated four proteins selected from pathway analysis including prohibitin, purine nucleoside phosphorylase, annexin 2 and c-reactive protein by immuno-histochemistry. 8-hydroxy-2'-deoxyguanosine (8-OHdG), a known oxidative stress marker was decreased by SeMet treatment in CRC mice as seen by immunohistochemistry. Further network analysis was done among these new four validated proteins, 8-OHdG and colorectal cancer. These four proteins found by proteomics analysis might be considered as potential chemopreventive biomarkers of SeMet against colon cancer and can help develop and improve approaches in preventive, therapeutic and prognostic aspects.Carcinogenesis 03/2013; · 5.27 Impact Factor
- Molecular Diagnosis & Therapy 12/2011; 16(1):13-4. · 2.59 Impact Factor