Oops, you're using an old version of your browser so some of the features on this page may not be displaying properly.

MINIMAL Requirements: Google Chrome 24+Mozilla Firefox 20+Internet Explorer 11Opera 15–18Apple Safari 7SeaMonkey 2.15-2.23

ePoster Display

684P - Molecular underpinnings of glandular tropism in metastatic clear cell renal cell carcinoma

Date

16 Sep 2021

Session

ePoster Display

Topics

Tumour Site

Renal Cell Cancer

Presenters

Eduard Roussel

Citation

Annals of Oncology (2021) 32 (suppl_5): S678-S724. 10.1016/annonc/annonc675

Authors

E. Roussel1, L. Kinget2, A.T.L. Verbiest3, J. Zucman-Rossi4, G. Couchy4, S. Caruso4, M. Baldewijns5, S. Joniau1, H. Van Poppel1, M. Albersen1, B. Beuselinck2

Author affiliations

  • 1 Urology, University Hospitals Leuven - Campus Gasthuisberg, 3000 - Leuven/BE
  • 2 General Medical Oncology, University Hospitals Leuven - Campus Gasthuisberg, 3000 - Leuven/BE
  • 3 General Medical Oncology Department, University Hospitals Leuven - Campus Gasthuisberg, 3000 - Leuven/BE
  • 4 Medical Oncology, UMR1138 Centre de recherche des Cordeliers, Université Paris-5, Paris/FR
  • 5 Pathology, University Hospitals Leuven - Campus Gasthuisberg, 3000 - Leuven/BE

Resources

Login to get immediate access to this content.

If you do not have an ESMO account, please create one for free.

Abstract 684P

Background

The presence of glandular metastases (GM) is associated with improved survival in metastatic clear cell renal cell carcinoma (m-ccRCC), but underlying molecular mechanisms remain to be elucidated.

Methods

We performed whole transcriptome RNA sequencing of 47 primary tumors of patients with at least one GM (pancreas, thyroid or adrenal) and 113 primary tumors of patients who did not, as well as 32 metastatic lesions in glandular organs and 258 metastatic lesions in non-glandular organs. We calculated the IMmotion 150 Angio, Teff and Myeloid gene expression signatures (GES) and the JAVELIN RENAL 101 Angio and Immuno GES, which correlate with outcome on therapy. Differences in GES were tested using Mann-Withney U tests with Bonferroni correction. Overall (OS) and progression-free survival (PFS) was studied using Kaplan-Meier survival analysis and Cox regression models.

Results

Primary tumors of patients with GM had higher IMmotion Angio (p=0.0001) and JAVELIN Angio (p=0.004) GES than those without GM. Metastatic lesions in glandular organs had higher IMmotion Angio (p=0.003) and JAVELIN Angio (p=0.007) GES, compared to lesions in non-glandular organs. Immune-related GES were not different between either primary tumors or metastatic lesions. Patients with GM had better OS (HR 0.46, 95% CI 0.30-0.70, p=0.0003) and PFS on first-line vascular endothelial growth factor receptor tyrosine kinase inhibitors (VEGFR-TKIs) (HR 0.64, 95% CI 0.41-0.98, p=0.04) than patients with non-GM. PFS on first- or later line immunotherapy (IO) was not different. IMmotion Angio and JAVELIN Angio GES were associated with better OS and PFS on first-line VEGFR-TKIs, but not PFS on first-line IO.

Conclusions

Patients with m-ccRCC who develop GM have higher angiogenesis-related GES in both primary tumors and metastatic lesions, while differences in immune-related GES are not apparent. Patients with GM have longer OS and PFS on first-line VEGFR-TKIs but no different PFS on first- or later line IO. Glandular tropism is thus likely to be an indicator of heightened angiogenesis, better prognosis, and better outcomes on VEGFR-TKIs. Therefore, the preferential first-line therapy for m-ccRCC patients with GM would be a VEGFR/IO combination rather than ipilimumab/nivolumab.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

BMS.

Disclosure

All authors have declared no conflicts of interest.

This site uses cookies. Some of these cookies are essential, while others help us improve your experience by providing insights into how the site is being used.

For more detailed information on the cookies we use, please check our Privacy Policy.

Customise settings
  • Necessary cookies enable core functionality. The website cannot function properly without these cookies, and you can only disable them by changing your browser preferences.