Sentences with phrase «tumors as oncogenes»

Recent active research in miRNA identified a series of this type of molecules that are involved in tumor progression in various tumors as oncogenes and tumor suppressors (8, 9).

Not exact matches

However, the impact of the two methylation - regulating enzymes was still seen at 10 to 15 months, when scientists found decreased expression of hundreds of genes — many of which are key tumor suppressor genes such as BMP3, SFRP2 and GATA4 — in the smoke - exposed cells and a five - or - more-fold increase in the signaling of the KRAS oncogene that is known to be mutated in smoking - related lung cancers.

«Once this novel tumor - homing agent binds to the EphA2 receptor, the oncogene functions as a cancer - specific molecular Trojan horse for paclitaxel, carrying the drug inside the cancel cell, killing the cell, and thwarting metastasis,» said Maurizio Pellecchia, a professor of biomedical sciences at UCR's School of Medicine who led the research.

«Our study identified miR - 182 as a glioblastoma tumor suppressor that reduces the expression of several oncogenes that promote cancer development,» said senior author of the study Alexander Stegh, an assistant professor in the Ken and Ruth Davee department of neurology and of medicine at Northwestern University Feinberg School of Medicine.

But mutated or dysfunctional Rb is associated with several major cancers and Cyclin D has long been described as an oncogene that promotes cancer because it was believed to inactivate the Rb tumor suppressor function through a process called phosphorylation, which involves phosphate molecules being added to proteins, essentially turning them on or off.

«It wasn't known whether miR - 486 functioned as an oncogene or a tumor - suppressor gene in lung cancer,» says co-corresponding author Patrick Nana - Sinkam, MD, associate professor of medicine and a researcher with the OSUCCC — James Molecular Biology and Cancer Genetics Program.

«This function for BAI1 may have implications for cancer biology, since MDM2 can function as an oncogene by degrading important tumor suppressors like p53.»

That will include validating some of the new predicted tumor suppressors and oncogenes as well as «making some deletions and amplifications and seeing if they have the properties we think they do,» said Elledge.

The authors uncover the cellular and molecular mechanisms, as well as the gene network regulated by Sox9 during the early steps of skin tumor initiation and demonstrates that Sox9 controls the long term maintenance and expansion of oncogene expressing cells by promoting self - renewing division and inhibiting differentiation.

In humans, cancer develops when genes that suppress cancer, known as tumor suppressors, are lost and when mutations or genes that promote cancer, known as oncogenes, are gained or activated.

But the idea fell out of fashion as researchers began to discover that mutations in specific oncogenes and tumor - suppressor genes could set cancer in motion.

In fact, KLF4 blocks senescence and apoptosis by repressing transcription of P53, whereas it can activate P21 - dependent cell - cycle arrest, and therefore, KLF4 can function both as a tumor suppressor and an oncogene (33, 34).

In breast cancer, miR - 21, 155, 27, 96, 182, and 128 were identified as oncogenes, whereas miR - 125, 205, 27, 17, 206, and 145 were found to be tumor suppressor genes, and their corresponding target genes were also defined (10 — 12).

Consequently, these tumor samples were classified as oncogene - positive.

In response to cellular stress such as DNA damage, oncogene activation, transcriptional inhibition, and hypoxia, tumor suppressor p53 is activated and expressed, and acts as a transcription factor to induce its target genes [1], thereby playing a central role in the regulation of DNA repair, cell cycle, apoptosis, senescence, and angiogenesis [2 - 4].

But a puzzle remains: if a drug wipes away methylation indiscriminately, that might turn on an oncogene just as much as it might restore a tumor suppressor gene.

Using a model where K - ras acts as an oncogene and initiates tumor formation, mice that were bred to not have Notch1 function showed an almost uniform distribution of about two cancerous lesions per mouse after 6 weeks, compared with approximately 14 tumors / mouse for those with Notch1 function still remaining.

«The genotoxicity of mainstream smoke carcinogens manifests as mutations occurring in key cancer - related genes, i.e., proto - oncogenes or tumor suppressor genes that control crucial cellular functions, e.g., growth and survival, in lung tumors of active smokers.»