<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>10(6)</volume><submitter>Fabbri L</submitter><pubmed_abstract>&lt;b>Rationale&lt;/b>: Renal cell carcinoma (RCC) accounts for about 2% of all adult cancers, and clear cell RCC (ccRCC) is the most common RCC histologic subtype. A hallmark of ccRCC is the loss of the primary cilium, a cellular antenna that senses a wide variety of signals. Loss of this key organelle in ccRCC is associated with the loss of the von Hippel-Lindau protein (VHL). However, not all mechanisms of ciliopathy have been clearly elucidated. &lt;b>Methods&lt;/b>: By using RCC4 renal cancer cells and patient samples, we examined the regulation of ciliogenesis &lt;i>via&lt;/i> the presence or absence of the hypoxic form of the voltage-dependent anion channel (VDAC1-ΔC) and its impact on tumor aggressiveness. Three independent cohorts were analyzed. Cohort A was from PREDIR and included 12 patients wit</pubmed_abstract><journal>Theranostics</journal><pagination>2696-2713</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7052902</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Identification of a new aggressive axis driven by ciliogenesis and absence of VDAC1-ΔC in clear cell Renal Cell Carcinoma patients.</pubmed_title><pmcid>PMC7052902</pmcid><pubmed_authors>Gardie B</pubmed_authors><pubmed_authors>Dufies M</pubmed_authors><pubmed_authors>Viotti J</pubmed_authors><pubmed_authors>Lacas-Gervais S</pubmed_authors><pubmed_authors>Bost F</pubmed_authors><pubmed_authors>Mazure NM</pubmed_authors><pubmed_authors>Contenti J</pubmed_authors><pubmed_authors>Nottet N</pubmed_authors><pubmed_authors>Borchiellini D</pubmed_authors><pubmed_authors>Chamorey E</pubmed_authors><pubmed_authors>Ferrero JM</pubmed_authors><pubmed_authors>Sadaghianloo N</pubmed_authors><pubmed_authors>Pages G</pubmed_authors><pubmed_authors>Fabbri L</pubmed_authors><pubmed_authors>Mograbi B</pubmed_authors><pubmed_authors>Ambrosetti D</pubmed_authors><pubmed_authors>Parola J</pubmed_authors><pubmed_authors>Clavel S</pubmed_authors><pubmed_authors>Rouleau M</pubmed_authors><pubmed_authors>Richard S</pubmed_authors><pubmed_authors>Pouyssegur J</pubmed_authors><pubmed_authors>Craigen WJ</pubmed_authors><pubmed_authors>Gad-Lapiteau S</pubmed_authors><pubmed_authors>Meyenberg Cunha de Padua M</pubmed_authors><pubmed_authors>Mari B</pubmed_authors><pubmed_authors>Leclercq NR</pubmed_authors></additional><is_claimable>false</is_claimable><name>Identification of a new aggressive axis driven by ciliogenesis and absence of VDAC1-ΔC in clear cell Renal Cell Carcinoma patients.</name><description>&lt;b>Rationale&lt;/b>: Renal cell carcinoma (RCC) accounts for about 2% of all adult cancers, and clear cell RCC (ccRCC) is the most common RCC histologic subtype. A hallmark of ccRCC is the loss of the primary cilium, a cellular antenna that senses a wide variety of signals. Loss of this key organelle in ccRCC is associated with the loss of the von Hippel-Lindau protein (VHL). However, not all mechanisms of ciliopathy have been clearly elucidated. &lt;b>Methods&lt;/b>: By using RCC4 renal cancer cells and patient samples, we examined the regulation of ciliogenesis &lt;i>via&lt;/i> the presence or absence of the hypoxic form of the voltage-dependent anion channel (VDAC1-ΔC) and its impact on tumor aggressiveness. Three independent cohorts were analyzed. Cohort A was from PREDIR and included 12 patients wit</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020</publication><modification>2026-04-30T19:50:25.052Z</modification><creation>2020-05-22T13:42:57Z</creation></dates><accession>S-EPMC7052902</accession><cross_references><pubmed>32194829</pubmed><doi>10.7150/thno.41001</doi></cross_references></HashMap>