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Genotyping by array of 108 clear cell renal cell carcinoma

ABSTRACT: A Cartes d'Identite des Tumeurs (CIT) project from the french Ligue Nationale Contre le Cancer (http://cit.ligue-cancer.net); Selecting patients with metastatic clear-cell renal cell carcinoma (m-ccRCC) who might benefit from treatment with targeted tyrosine kinase inhibitors (TKIs) is a challenge. Our aim was to identify molecular markers associated with outcome in m-ccRCC patients treated with sunitinib.

ORGANISM(S): Homo sapiens

SUBMITTER: Elarouci Nabila

PROVIDER: E-MTAB-3269 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Prognostic and theranostic impact of molecular subtypes and immune classifications in renal cell cancer (RCC) and colorectal cancer (CRC).

Becht Etienne E Giraldo Nicolas A NA Beuselinck Benoit B Job Sylvie S Marisa Laetitia L Vano Yann Y Oudard Stéphane S Zucman-Rossi Jessica J Laurent-Puig Pierre P Sautès-Fridman Catherine C de Reyniès Aurélien A Fridman Wolf Herman WH

Oncoimmunology 20150807 12

Molecular and immune classifications powerfully predict cancer patient's survival and response to therapies. We herein describe the immune tumor microenvironment of molecular subgroups of colorectal and renal cell cancers, revealing a strong correlation between tumor subtypes and distinct immune profiles. ...[more]

PMID: 26587318

Publication: 1/2

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Project description:VHL mutations are the most common tumorigenic lesions in clear cell renal cell carcinoma (ccRCC) and result in continued activation of the HIF/VEGF pathway and uncontrolled cancer progression. Receptor tyrosine kinase (RTK) inhibitors such as sunitinib have been demonstrated to target tumorigenic signaling pathways, delay tumor progression and improve patient prognosis in metastatic renal cell carcinoma (mRCC). Although several mechanisms of sunitinib resistance have been reported, the solutions to overcome this resistance remain still unclear. In our study, we found that increased expression of YB1 (Y box binding protein 1, a multidrug resistance associated protein) and EphA2 (a member of erythropoietin-producing hepatocellular (Eph) receptors, belonging to the RTK family) mediated sunitinib resistance and mRCC exhibited a large phenotypic dependence on YB1 and EphA2. In addition, our findings confirm that YB1 promotes the invasion, metastasis and sunitinib resistance of ccRCC by regulating the EphA2 signaling pathway. Furthermore, pharmacological inhibition of EphA2 through the small molecule inhibitor ALW-II-41-27 reduced the proliferation of sunitinib-resistant tumor cells and suppressed tumor growth in vivo and restored the sensitivity of sunitinib-resistant tumor cells to sunitinib in vitro and in vivo. Mechanistically, YB1 increases the protein levels of EphA2 by maintaining the protein stabilization of EphA2 through inhibiting the proteasomal degradation pathway. Collectively, our findings provide the theoretical rationale that ccRCC metastasis and RTK-directed therapeutic resistance could be prospectively and purposefully targeted.

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Genotyping by array of human head and neck squamous cell carcinoma.

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