Effect of Testicular Germ Cell Tumor Therapy on Renal Function

Cost, Nicholas G.; Adibi, Mehrad; Lubahn, Jessica D.; Romman, Adam; Raj, Ganesh V.; Sagalowsky, Arthur I.; Margulis, Vitaly

doi:10.1016/j.urology.2012.04.064

Cited by 26 publications

(8 citation statements)

References 29 publications

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“…Although most of patients with newly diagnosed TGCT are eventually cured, the treatment-associated morbidity is still significant at higher stages (Feldman et al, 2008;Cost et al, 2012), specifically in patients who have metastatic disease at diagnosis (Sokoloff et al, 2007). The potential morbidity of current therapies is of special concern in this population.…”

Section: Introductionmentioning

confidence: 99%

miRNA-1297 Induces Cell Proliferation by Targeting Phosphatase and Tensin Homolog in Testicular Germ Cell Tumor Cells

Yang¹,

Zhang²,

Tang³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Section: Introductionmentioning

confidence: 99%

miRNA-1297 Induces Cell Proliferation by Targeting Phosphatase and Tensin Homolog in Testicular Germ Cell Tumor Cells

Yang¹,

Zhang²,

Tang³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…For example, renal toxicity of cisplatin limits dose escalation for this anticancer compound, prevents the use of this drug in patients with compromised renal function, and may lead to chronic kidney disease in the treated population. 22 We investigated whether any of the identified genes may affect the response of kidney epithelial cells to cisplatin. Interference with BCL2L14, RHOB and C2ORF42 provided robust protection in HK-2 and HKC-8 cells (Figures 2a and b), whereas interference with TNFAIP6 yields very strong protection in HKC-8 cells only (Figure 2b), indicating that the mechanisms of drug response are not identical between the cell lines.…”

Section: Resultsmentioning

confidence: 99%

Erratum: An RNA interference screen identifies new avenues for nephroprotection

et al. 2016

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Acute kidney injury is a major public health problem, which is commonly caused by renal ischemia and is associated with a high risk of mortality and long-term disability. Efforts to develop a treatment for this condition have met with very limited success. We used an RNA interference screen to identify genes (BCL2L14, BLOC1S2, C2ORF42, CPT1A, FBP1, GCNT3, RHOB, SCIN, TACR1, and TNFAIP6) whose suppression improves survival of kidney epithelial cells in in vitro models of oxygen and glucose deprivation. Some of the genes also modulate the toxicity of cisplatin, an anticancer agent whose use is currently limited by nephrotoxicity. Furthermore, pharmacological inhibition of TACR1 product NK1R was protective in a model of mouse renal ischemia, attesting to the in vivo relevance of our findings. These data shed new light on the mechanisms of stress response in mammalian cells, and open new avenues to reduce the morbidity and mortality associated with renal injury.

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“…Another recent study demonstrated significantly worse glomerular filtration rate after chemotherapy and quantified a 10% increase in the development of chronic Stage 3 kidney disease [70]. A long-term prospective study noted no significant change in nephrotoxicity over time, but severe chronic renal disease did remain stable in 15% of patients 10 years after treatment with cisplatin.…”

Section: Long-term Issuesmentioning

confidence: 97%