suPAR as a biomarker for cancer
Various cancers cause an elevated plasma suPAR level. The more serious and advanced disease, the higher the suPAR level. suPAR is therefore also a prognostic marker predicting mortality in cancer patients. Cancer patients with a low suPAR level have a better chance of a progression-free outcome.
The suPAR level is elevated in cancer patients compared to healthy individuals, and a high suPAR level is associated with:
- Advanced disease
- High TNM (Tumor Node, Metastasis) staging, which is a system used to describe the amount and spread of cancer
- Aggressive and invasive tumor growth
- Metastatic disease
- Poor prognosis
This applies to various types of cancer, among others:
- Acute leukemia1
- Colorectal cancer2–4
- Hepatic cancer5
- Cervical cancer6
- Lung cancer (small cell and non-small cell)7
- Ovarian cancer9
- Pancreatic cancer10
- Prostate cancer11
- Esophageal cancer3
- Gastric cancer3,12
In the general population, an elevated suPAR level is associated with an increased risk of lung cancer and other cancers. Among smokers, the risk of lung cancer is also higher in individuals with an elevated suPAR level compared to those with lower suPAR levels13.
Examples of SuPAR in various cancers
In prostate cancer patients, the suPAR level is higher than in patients with benign prostatic hyperplasia11.
In neurologic patients with paraneoplastic cerebellar syndromes or carcinomatous meningitis, the suPAR level is also elevated in plasma and in cerebrospinal fluid14.
In patients with gastrointestinal cancers, the suPAR level is higher in patients with esophageal cancer than in patients with colorectal cancer3.
“it is essential to have the help of biomarkers, such as suPAR, which can support the discharge decision”
Juan González del Castillo,
Dr PhD, Hospital Clínico San Carlos, Spain
suPAR News Vol. 1, April 2019
suPAR in relation to cancer diagnostics and other biomarkers
In patients with liver diseases, an elevated suPAR level has proved to be an early predictor of future development of hepatocellular carcinoma, and the suPAR level may be elevated as early as 1-7 years prior to appearance of imaging signs of hepatic cancer. In this study, suPAR was statistically stronger than alpha-fetoprotein5.
In patients with ovarian tumors, a combination of suPAR and CA-125 is able to discriminate benign tumors from malignant tumors (AUC 0.94; 95% CI 0.90-0.98)9.
suPAR in cancer treatment
In patients in with resectable colorectal cancer, the suPAR level is lower than in patients with unresectable disease receiving palliative treatment3,4. Furthermore, suPAR might help to guide preoperative treatment decisions regarding patients’ outcome and to identify patients particularly susceptible to acute kidney injury16.
In women with cervical cancer, the suPAR level decreases significantly following surgery6.
In patients with acute leukemia, the suPAR plasma level correlates with the number of circulating tumor cells, and following treatment with chemotherapy, the suPAR level decreases to a normal level in parallel with a reduction in the number of tumor cells1.
In patients without known cancer but with serious nonspecific symptoms and signs of cancer referred to a diagnostic outpatient clinic for an accelerated cancer diagnostic program, elevated suPAR levels were significantly associated with newly diagnosed cancer during follow-up15. Thus, a high suPAR level is associated with increased risk of finding cancer patients15. In cancer patients, elevated suPAR levels are associated with a poor prognosis and a shorter survival4,10–12.
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2. Lomholt, a F., Høyer-Hansen, G., Nielsen, H. J. & Christensen, I. J. Br. J. Cancer 101, 992–7 (2009).
3. Usnarska-Zubkiewicz, L., Strutyńska-Karpińska, M., Zubkiewicz-Kucharska, A., Zarębski, P. & Grabowski, K. Adv. Clin. Exp. Med. 23, 959–967 (2014).
4. Tarpgaard, L. S. et al. Int. J. Cancer 1, n/a–n/a (2015).
5. Chounta, A. et al. Liver Int. 35, 601–607 (2015).
6. Jing, J. et al. J. Clin. Lab. Anal. 26, 16–21 (2012).
7. Cobos, E., Jumper, C. & Lox, C. Clin. Appl. Thromb. 9, 241–246 (2003).
8. Rubio-Jurado, B. et al. Clin. Lymphoma Myeloma Leuk. 15, 621–626 (2015).
9. Henic, E., Borgfeldt, C., Christensen, I. J., Casslén, B. & Høyer-Hansen, G. Clin. Cancer Res. 14, 5785–93 (2008).
10. Sorio, C. et al. BMC Cancer 11, 448 (2011).
11. Miyake, H. et al. Prostate 39, 123–9 (1999).
12. Fidan, E. et al. Med. Oncol. 30, 540 (2013).
13. Langkilde, A. et al. Cancer Epidemiol. biomarkers Prev. 20, 609–18 (2011).
14. Garcia-Monco, J. C., Coleman, J. L. & Benach, J. L. J. Neuroimmunol. 129, 216–223 (2002).
15. Rasmussen LJH, et al. Int J Cancer. 2017 Jul 1;141(1):191-199.
16. Loosen SH et al, Oncotarget. 2018 Jun 5;9(43):27027-27038.