791P - Transcriptomic analysis of collecting duct carcinoma of the kidney

Date 09 October 2016
Event ESMO 2016 Congress
Session Poster display
Topics Renal Cell Cancer
Presenter Anna Tessari
Citation Annals of Oncology (2016) 27 (6): 266-295. 10.1093/annonc/mdw373
Authors A. Tessari1, I. Testa2, E. Verzoni3, G. Nigita4, M. Colecchia5, D. Palmieri4, P. Grassi6, M. Pawlikowski4, C. Maggi3, A. Martinetti2, F. de Braud6, C.M. Croce4, G. Procopio3
  • 1Molecular Virology Immunology And Medical Genetics, Ohio State Univ Medical Center, 43210 - Columbus/US
  • 2Medical Oncology, Fondazione IRCCS - Istituto Nazionale dei Tumori, 44100 - Milano/IT
  • 3Medical Oncology, Fondazione IRCCS - Istituto Nazionale dei Tumori, 20133 - Milano/IT
  • 4Molecular Virology Immunology And Medical Genetics, Ohio State Univ Medical Center, Columbus/US
  • 5Pathology, Fondazione IRCCS Istituto Nazionale dei Tumori, 20133 - Milan/IT
  • 6Medical Oncology, Fondazione IRCCS - Istituto Nazionale dei Tumori, Milano/IT

Abstract

Background

Collecting duct carcinoma (CDC) of the kidney is a rare tumor. It originates from the renal medulla, and it represents less than 2% of all renal tumors. The clinical course of this disease is characterized by aggressive behavior. The locally advanced and/or metastatic presentation, along with the resistance to treatments, confers CDC a poor prognosis. Due to its rarity, little is known about CDC biology, and to date no targeted therapy is available. Here, we aimed to identify deregulated pathways that discriminate between CDC, clear cell carcinoma (CCC) and healthy renal tissue.

Methods

We collected 9 cases of CDC treated at Istituto Nazionale dei Tumori (Milan), together with 7 cases of CCC and 7 healthy normal adjacent renal tissues (NAT). Gene expression profiling was performed by GeneChip® Human Transcriptome Array 2.0 (HTA 2.0 -Affymetrix). 827 coding and 252 non-coding genes were differentially expressed between the three subtypes (p 

Results

Among those genes, we confirmed the differential expression levels of fibronectin 1 (FN1), periostin (POSTN) and stratifin (SFN), by Real Time PCR. The subsequent functional enrichment analyses identified histones modifications, cytoplasmic ribosomal proteins, senescence, autophagy and focal adhesion pathways as the most deregulated in CDC vs both CCC and normal tissues.

Conclusions

Our analysis, in agreement with clinical observations, suggests that CDC genetic basis should be considered distinct from other renal tumors. A better understanding of the specific molecular alterations causally involved in this disease may lead to new prognostic factors and therapeutic approaches for this currently incurable malignancy.

Clinical trial identification

Legal entity responsible for the study

N/A

Funding

Fondazione IRCCS Istituto Nazionale Tumori, Milan, Italy Ohio State University Medical Center, Columbus, Ohio, USA Pelotonia, The Ohio State University, Columbus, Ohio, USA

Disclosure

All authors have declared no conflicts of interest.