The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
Elevation of cytokine levels in cachectic patients with prostate carcinoma
Abstract
BACKGROUND: Approximately 60–70% of patients with advanced prostate carcinoma (CaP) suffer from cachexia, one of the most devastating conditions associated with advanced malignant disease. The pathophysiology of cachexia is multifactorial, and several cytokines, such as tumor necrosis factor α (TNFα) and interleukin 1 (IL‐1), IL‐6, and IL‐8, may be involved. The objective of the current study was to determine whether cachexia associated with advanced CaP is accompanied by increased serum levels of TNFα, IL‐1β, IL‐6, and IL‐8. METHODS: The levels of TNFα, IL‐1β, IL‐6, IL‐8, and prostate specific antigen (PSA) were examined in serum samples from normal donors (n = 10 donors), from patients with organ‐confined CaP (n = 19 patients), from patients with advanced CaP without cachexia (n = 17 patients), and from patients with cachectic CaP (n = 26 patients). DPC Immulite and Abbott IMx Total‐PSA assays were used to determine cytokine and PSA levels, respectively. RESULTS: Levels of TNFα, IL‐6, and IL‐8 were elevated significantly in the group of patients with advanced, cachectic CaP compared with patients who were without cachexia. In the cachectic patients, levels of TNFα were correlated positively with IL‐8, and there was no correlation between PSA levels and any of the cytokine levels. IL‐1β levels were below the limit of detection in all samples. CONCLUSIONS: The current results show that levels of TNFα, IL‐6, and IL‐8 were increased in CaP patients with cachexia. Increased levels of these cytokines were not correlated with PSA levels, suggesting that they are regulated by a mechanism that is independent of PSA synthesis. Additional fundamental research is needed to determine the mechanisms involved and to identify potential therapeutic targets in patients with cachexia. Cancer 2003;97:1211–6. © 2003 American Cancer Society. DOI 10.1002/cncr.11178
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Tsujinaka, T., Fujita, J., Ebisui, C., Yano, M., Kominami, E., Suzuki, K., Tanaka, K., Katsume, A., Ohsugi, Y., Shiozaki, H., et al. (1996) · Journal of Clinical Investigation · doi:10.1172/jci118398 · Cited by 421 · cited 1×
“reported that IL-6 caused cachexia in an animal model, and recent studies in transgenic mice have demonstrated that IL-6 participates in muscular atrophy.(19) Again, translation from the murine model to humans has not been straightforward, and the evidence of a role for IL-6 in clinical cachexia is mixed.”
BackgroundShariat, S. F., Andrews, B., Kattan, M. W., Kim, J., Wheeler, T. M., & Slawin, K. M. (2001) · Urology · doi:10.1016/s0090-4295(01)01405-4 · Cited by 261 · cited 2×
“Shariat et al.(24) reported increased levels of IL-6 in patients with CaP who had bone metastases, and Wise et al.”
Background
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Self-citationTumor-induced anorexia and weight loss are mediated by the TGF-β superfamily cytokine MIC-1
Johnen, H., Lin, S., Kuffner, T., Brown, D. A., Tsai, V. W.-W., Bauskin, A. R., Wu, L., Pankhurst, G., Jiang, L., Junankar, S., et al. (2007) · Nature Medicine · doi:10.1038/nm1677 · Cited by 612
Self-citationCancer cachexia: Developing multimodal therapy for a multidimensional problem
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Metadata
- Authors
- Pfitzenmaier, J., Vessella, R., Higano, C. S., Noteboom, J. L., Wallace, D., & Corey, E.
- Venue
- Cancer
- Publisher
- Wiley
- Published
- 2003-02-20
- Volume
- 97
- Issue
- 5
- Pages
- 1211-1216
- ISSN
- 0008-543X (ISSN-L)
- 1097-0142
- OpenAlex
- W2027279302
- Cited by
- 167
- References
- 2
- FWCI
- 4.34
- Type
- journal article
- Language
- en
- Open access
- closed
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