Tissue based biomarkers in non-clear cell RCC: Correlative analysis from the ASPEN clinical trial.
Journal
Kidney cancer journal : official journal of the Kidney Cancer Association
ISSN: 1933-0863
Titre abrégé: Kidney Cancer J
Pays: United States
ID NLM: 101299338
Informations de publication
Date de publication:
Oct 2021
Oct 2021
Historique:
entrez:
12
11
2021
pubmed:
13
11
2021
medline:
13
11
2021
Statut:
ppublish
Résumé
Biomarkers are needed in patients with non-clear cell renal cell carcinomas (NC-RCC), particularly papillary renal cell carcinoma, in order to inform on initial treatment selection and identify potentially novel targets for therapy. We enrolled 108 patients in ASPEN, an international randomized open-label phase 2 trial of patients with metastatic papillary, chromophobe, or unclassified NC-RCC treated with the mTOR inhibitor everolimus (n=57) or the vascular endothelial growth factor (VEGF) receptor inhibitor sunitinib (n=51), stratified by MSKCC risk and histology. The primary endpoint was overall survival (OS) and secondary efficacy endpoints for this exploratory biomarker analysis were radiographic progression-free survival (rPFS) defined by intention-to-treat using the RECIST 1.1 criteria and radiographic response rates. Tissue biomarkers (n=78) of mTOR pathway activation (phospho-S6 and -Akt, c-kit) and VEGF pathway activation (HIF-1α, c-MET) were prospectively explored in tumor tissue by immunohistochemistry prior to treatment and associated with clinical outcomes. We found that S6 activation was more common in poor risk NC-RCC tumors and S6/Akt activation was associated with worse PFS and OS outcomes with both everolimus and sunitinib, while c-kit was commonly expressed in chromophobe tumors and associated with improved outcomes with both agents. C-MET was commonly expressed in papillary tumors and was associated with lower rates of radiographic response but did not predict PFS for either agent. In multivariable analysis, both pAkt and c-kit were statistically significant prognostic biomarkers of OS. No predictive biomarkers of treatment response were identified for clinical outcomes. Most biomarker subgroups had improved outcomes with sunitinib as compared to everolimus.
Identifiants
pubmed: 34765076
doi: 10.52733/kcj19n3-a1
pmc: PMC8580377
mid: NIHMS1748706
doi:
Types de publication
Journal Article
Langues
eng
Pagination
64-72Subventions
Organisme : NCI NIH HHS
ID : P30 CA014236
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA021765
Pays : United States
Références
Eur Urol. 2016 May;69(5):866-74
pubmed: 26626617
Clin Cancer Res. 2021 Jun 15;27(12):3503
pubmed: 34117029
J Clin Oncol. 2002 May 1;20(9):2376-81
pubmed: 11981011
Eur Urol. 2015 Jan;67(1):85-97
pubmed: 24857407
Br J Cancer. 2016 Mar 15;114(6):642-9
pubmed: 26908330
Curr Clin Pharmacol. 2011 Aug;6(3):169-80
pubmed: 21861801
Proc Natl Acad Sci U S A. 2006 Oct 17;103(42):15552-7
pubmed: 17028174
JAMA Oncol. 2020 Aug 1;6(8):1247-1255
pubmed: 32469384
J Clin Oncol. 1999 Aug;17(8):2530-40
pubmed: 10561319
Lancet Oncol. 2016 Mar;17(3):378-388
pubmed: 26794930
Clin Cancer Res. 2014 Jul 1;20(13):3411-21
pubmed: 24658158
Clin Cancer Res. 2021 Jun 15;27(12):3317-3328
pubmed: 33593885
Cancer Cell. 2014 Sep 8;26(3):319-330
pubmed: 25155756
JCO Precis Oncol. 2019 Apr 28;3:
pubmed: 32914011
Cancer Cell. 2020 Dec 14;38(6):803-817.e4
pubmed: 33157048
Cancer Cell. 2021 May 10;39(5):649-661.e5
pubmed: 33711272
Lancet. 2021 Feb 20;397(10275):695-703
pubmed: 33592176