|1.||Esteller, Manel: 2 articles (06/2015 - 08/2013)|
|2.||Pinyol, Roser: 1 article (06/2015)|
|3.||Méndez-González, Jesús: 1 article (06/2015)|
|4.||HEPTROMIC Consortium: 1 article (06/2015)|
|5.||Cornella, Helena: 1 article (06/2015)|
|6.||Portela, Anna: 1 article (06/2015)|
|7.||Llovet, Josep M: 1 article (06/2015)|
|8.||Imbeaud, Sandrine: 1 article (06/2015)|
|9.||Fuster, Josep: 1 article (06/2015)|
|10.||Zucman-Rossi, Jessica: 1 article (06/2015)|
02/18/2015 - "Some of these switches occur in known tumor drivers, including PPARG, CCND3, RALGDS, MITF, PRDM1, ABI1 and MYH11, for which the switch implies a change in the protein product. "
03/01/2005 - "Experiments performed in cells isolated from skin tumors suggest that RalGDS mediates cell survival through the activation of the JNK/SAPK pathway. "
03/01/2005 - "Lack of RalGDS results in reduced tumor incidence, size, and progression to malignancy in multistage skin carcinogenesis, and reduced transformation by Ras in tissue culture. "
03/01/2005 - "RalGDS is required for tumor formation in a model of skin carcinogenesis."
03/01/2005 - "The hunt for a clear role for RalGDS activation in human cancer is on."
|2.||Cardiomegaly (Heart Hypertrophy)
04/01/2003 - "Although a number of studies indicate that Ras induces cardiac hypertrophy, the functional role of Ral-GDS/Ral signaling pathway is as yet unknown in cardiac myocytes. "
06/01/2013 - "Together, these data implicate RalGDS-mediated induction of autophagy and exocyst function as a critical feature of load-induced cardiac hypertrophy."
03/01/2007 - "Such pathways include Ras/MEK/ERK and Ral/RalGDS cascades, which can lead to cardiac hypertrophy. "
04/01/2003 - "Our data provide evidence that the Ral-GDS/Ral signaling pathway is a link to the process of cardiac hypertrophy."
04/01/2003 - "We investigated the role of the Ral-GDS/Ral pathway in cardiac hypertrophy. "
|3.||Adenomatous Polyposis Coli (Familial Adenomatous Polyposis)
06/01/2015 - "The study confirmed a high prevalence of genes known to be deregulated by aberrant methylation in HCC (e.g., Ras association [RalGDS/AF-6] domain family member 1, insulin-like growth factor 2, and adenomatous polyposis coli) and other solid tumors (e.g., NOTCH3) and describes potential candidate epidrivers (e.g., septin 9 and ephrin B2). "
12/01/2004 - "As changes in methylation of the following genes occurred marginally, their impact on the formation of colorectal cancer were trivial: adenomatous polyposis coli (APC) (8%, 5/65), Ras association (RalGDS/AF-6) domain family 1A (RASSF1A) (3%, 2/65) and cyclin-dependent kinase inhibitor 2A, alternated reading frame (p14(ARF)) (6%, 4/65). "
|4.||Squamous Cell Carcinoma (Epidermoid Carcinoma)
08/01/2002 - "We have previously identified the oncogene rgr (ralGDS related) in DNA derived from a rabbit squamous cell carcinoma. "
08/25/2011 - "Our laboratory has previously identified the RalGDS-related (Rgr) oncogene in a DMBA (7,12-dimethylbenz[α]anthracene)-induced rabbit squamous cell carcinoma and its human orthologue, hRgr. "
01/01/2008 - "A set of 4 genes, including CDH1 (E-cadherin), SFN (stratifin), RARB (retinoic acid receptor, beta) and RASSF1A (Ras association (RalGDS/AF-6) domain family 1), had their methylation patterns evaluated by MSP (Methylation-Specific Polymerase Chain Reaction) analysis in 49 fresh urinary bladder carcinoma tissues (including 14 cases paired with adjacent normal bladder epithelium, 3 squamous cell carcinomas and 2 adenocarcinomas) and 24 cell sediment samples from bladder washings of patients classified as cancer-free by cytological analysis (control group). "
|5.||Breast Neoplasms (Breast Cancer)
01/01/2015 - "Our data suggest that RILP suppresses the invasion of breast cancer cells by interacting with RalGDS to inhibit its GEF activity for RalA. "
01/01/2015 - "RILP suppresses invasion of breast cancer cells by modulating the activity of RalA through interaction with RalGDS."
07/01/2014 - "BMI showed a positive association with the methylation of extracellular superoxide dismutase (r = 0.21, p < 0.05), Ras-association (RalGDS/AF-6) domain family member 1 (RASSF1A) (r = 0.31, p < 0.001), and breast cancer type 1 susceptibility protein (r = 0.19, p < 0.05); and inverse association with methylation of BNIP3 (r = -0.48, p < 0.0001). "
12/01/2004 - "In comparison with the normal mucosa of the non-cancer patients, the following 14 genes displayed no tumor associated changes: breast cancer 1, early onset (BRCA1), cadherin 1, type 1, E-cadherin (epithelial) (CDH1), death-associated protein kinase 1 (DAPK1), DNA (cytosine-5-)-methyltransferase 1 (DNMT1), melanoma antigen, family A, 1 (directs expression of antigen MZ2-E) (MAGEA1), tumor suppressor candidate 3 (N33), cyclin-dependent kinase inhibitor 1A (p21, Cip1) (p21(WAF1)), cyclin-dependent kinase inhibitor 1B (p27, Kip1) (p27(KIP1)), phosphatase and tensin homolog (mutated in multiple advanced cancers 1) (PTEN), retinoic acid receptor, beta (RAR- , Ras association (RalGDS/AF-6) domain family 1 C (RASSF1C), secreted frizzled-related protein 1 (SFRP1), tissue inhibitor of metalloproteinase 3 (Sorsby fundus dystrophy, pseudoinflammatory) (TIMP3), and von Hippel-Lindau syndrome (VHL). "
|1.||Cyclin-Dependent Kinase Inhibitor p16
|2.||retinoic acid receptor beta
|4.||Estrogen Receptor alpha
|5.||Ephrin-B2 (Ephrin B2)
|6.||Monomeric GTP-Binding Proteins
|7.||Progesterone Receptors (Progesterone Receptor)
|9.||GTP Phosphohydrolases (GTPases)