Results 11 to 20 of about 373,131 (211)

Tumor RAS Gene Expression Levels Are Influenced by the Mutational Status of RAS Genes and Both Upstream and Downstream RAS Pathway Genes [PDF]

open access: yesCancer Informatics, 2017
The 3 human RAS genes play pivotal roles regulating proliferation, differentiation, and survival in normal cells and become mutated in 15% to 20% of all human tumors and amplified in many others.
Robert M Stephens   +4 more
doaj   +5 more sources

Introduction: Forensic Fail [PDF]

open access: yes, 2014
Background: About 60% of Pheochromocytoma (PCC) and Paraganglioma (PGL) patients have either germline or somatic mutations in one of the 12 proposed disease causing genes; SDHA, SDHB, SDHC, SDHD, SDHAF2, VHL, EPAS1, RET, NF1, TMEM127, MAX and H-RAS ...
Björklund, Peyman   +6 more
core   +9 more sources

The common rejection module in chronic rejection post lung transplantation. [PDF]

open access: yesPLoS ONE, 2018
RATIONALE:Recent studies suggest that similar injury mechanisms are in place across different solid organ transplants, resulting in the identification of a common rejection module (CRM), consisting of 11 genes that are overexpressed during acute and, to ...
Annelore Sacreas   +9 more
doaj   +1 more source

A simplified genomic profiling approach predicts outcome in metastatic colorectal cancer [PDF]

open access: yes, 2019
The response of metastatic colorectal cancer (mCRC) to the first-line conventional combination therapy is highly variable, reflecting the elevated heterogeneity of the disease.
Belardinilli, Francesca   +29 more
core   +2 more sources

A genome-wide Drosophila epithelial tumorigenesis screen identifies Tetraspanin 29Fb as an evolutionarily conserved suppressor of Ras-driven cancer. [PDF]

open access: yesPLoS Genetics, 2018
Oncogenic mutations in the small GTPase Ras contribute to ~30% of human cancers. However, Ras mutations alone are insufficient for tumorigenesis, therefore it is paramount to identify cooperating cancer-relevant signaling pathways.
Tamara Zoranovic   +18 more
doaj   +1 more source

Silenced Expression of NFKBIA in Lung Adenocarcinoma Patients with a Never-smoking History [PDF]

open access: yes, 2013
Nuclear factor of κ-light polypeptide gene enhancer in B cells inhibitor α (NFKBIA), which is a tumor suppressor gene, was found to be silenced in lung adenocarcinomas.
Asano, Hiroaki   +12 more
core   +1 more source

Linking FOXO3, NCOA3, and TCF7L2 to Ras pathway phenotypes through a genome-wide forward genetic screen in human colorectal cancer cells

open access: yesGenome Medicine, 2018
Background The Ras pathway genes KRAS, BRAF, or ERBBs have somatic mutations in ~ 60% of human colorectal carcinomas. At present, it is unknown whether the remaining cases lack mutations activating the Ras pathway or whether they have acquired mutations ...
Snehangshu Kundu   +11 more
doaj   +1 more source

Dominant yeast and mammalian RAS mutants that interfere with the CDC25-dependent activation of wild-type RAS in Saccharomyces cerevisiae [PDF]

open access: yes, 1989
Two mutant alleles of RAS2 were discovered that dominantly interfere with wild-type RAS function in the yeast Saccharomyces cerevisiae. An amino acid substitution which caused the dominant interference was an alanine for glycine at position 22 or a ...
Powers, S.   +2 more
core   +1 more source

Ras-induced changes in H3K27me3 occur after those in transcriptional activity. [PDF]

open access: yesPLoS Genetics, 2013
Oncogenic signaling pathways regulate gene expression in part through epigenetic modification of chromatin including DNA methylation and histone modification.
Masaki Hosogane   +4 more
doaj   +1 more source

ETS1 is a genome-wide effector of RAS/ERK signaling in epithelial cells [PDF]

open access: yes, 2014
The RAS/ERK pathway is commonly activated in carcinomas and promotes oncogenesis by altering transcriptional programs. However, the array of cis-regulatory elements and trans-acting factors that mediate these transcriptional changes is still unclear. Our
Budka, Justin A.   +3 more
core   +1 more source

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