These reagents could serve as noninvasive ccRCC markers for regression.
📌 3 Key Takeaways
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Objective & Hypothesis:Objective: Analyzing protein kinase C (PKC) alpha, iota, and zeta as well as levels of Mxi-2 and Vim3 in regressive clear cell renal carcinomas (ccRCCs) and urine samples.
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Key Findings & Data:Material and methods: Fresh samples of ccRCCs (predominantly pT1a/b) with different degrees of regression ( 50%),while PKC isoformalpha was significantly increased by advanced regression rate.
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Conclusion & Impact:These reagents could serve as noninvasive ccRCC markers for regression.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters
Özet
Objective: Analyzing protein kinase C (PKC) alpha, iota, and zeta as well as levels of Mxi-2 and Vim3 in regressive clear cell renal carcinomas (ccRCCs) and urine samples. Material and methods: Fresh samples of ccRCCs (predominantly pT1a/b) with different degrees of regression ( 50%),while PKC isoformalpha was significantly increased by advanced regression rate. PKC iota in patients’ urine was overexpressed in oncocytoma and reduced in all ccRCC urines. Conclusion: Tumor regression in ccRCC tissue shows strong nuclear overexpression of Mxi-2, Vim3, and PKC alpha and iota. In respective urines, PKC alpha was overexpressed; PKC iota was decreased. Mxi-2 and Vim3 decreased with increasing regression rates. These reagents could serve as noninvasive ccRCC markers for regression.
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Cite This Article
KÖDİTZ, B., BRADENSTEİN, M. V., ARANA, M. H., HEIDENREICH, A., FRİES, J. W. U. (2022). Novel noninvasive marker of regression of clear cell renal cell carcinoma (ccRCC). Turkish Journal of Urology, Cilt: 48 - Sayı: 1, 49–57. https://ajindex.com/articles/413239
National Cancer Institute, Center for Cancer Research: Clear cell renal carcinoma. Website. March 2020. 2. von Brandenstein M, Bernhart SH, Pansky A, et al. Beyond the 3’UTR binding-microRNA-induced protein truncation via DNA binding. Oncotarget. 2018;9:32855-32867. [CrossRef] 3. von Brandenstein M, Pandarakalam JJ, Kroon L, et al. MicroRNA 15a, inversely correlated to PKCalpha, is a potential marker to differentiate between benign and malignant renal tumors in biopsy and urine samples. Am J Pathol. 2012;180:1787-1797. [CrossRef] 4. von Brandenstein M, Schlosser M, Richter C, Depping R, Fries JW. ETS-dependent p16INK4a and p21waf1/cip1 gene expression upon endothelin-1 stimulation in malignant versus and nonmalignant proximal tubule cells. Life Sci. 2012;91:562-571. [CrossRef] 5. Ikuerowo SO, Kuczyk MA, von Wasielewski R, et al. p16INK4a expression and clinicopathologic parameters in renal cell carcinoma. Eur Urol. 2007;51:732-737. [CrossRef] 6. Lowery J, Kuczmarski ER, Herrmann H, Goldman RD. Intermediate filaments play a pivotal role in regulating cell architecture and function. J Biol Chem. 2015;290:17145-17153. [CrossRef] 7. von Brandenstein M, Puetz K, Schlosser M, et al. Vimentin 3, the new hope, differentiating RCC versus oncocytoma. Dis Markers. 2015;2015:368534. [CrossRef] 8. von Brandenstein M, Herden J, Ko¨ditz B, et al. Non-invasive urine markers for the differentiation between RCCs and oncocytoma. J Clin Lab Anal. 2021;35:e23762. [CrossRef] 9. Nishizuka Y. Protein kinase C and lipid signaling for sustained cellular responses. FASEB J. 1995;69:484-496. [CrossRef] 10. Tickon SK, Vankalakunit M, Reuter VE. Renal cell carcinoma. In Aman MR (ed.): Diagnostic Pathology: Genitourinary. Salt Lake City, UT: Amirsis Publ., 2010: 1-24-1-46
Bradford MM. A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Anal Biochem. 1976;72:248-254. [Cross- Ref] 13. Ko¨ditz B, Fries JWU, Go¨bel H, et al. Mxi-2 dependent regulation of p53 in prostate cancer. Anticancer Res. 2020;40:5539-5544. [CrossRef] 14. Ko¨ditz B, Stog A, Go¨bel H, et al. Vimentin 3 expression in prostate cancer cells. Anticancer Res. 2021;41:169-174. [CrossRef] 15. Gerstung von Brandenstein M, Abety AN, Depping R, et al. A p38-p65 transcription complex induced by endothelin-1 mediates si