Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.7.6 (RNA polymerase)
 34,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

For patients with identical clinical-pathological characteristics or the same stage of lung cancer, great uncertainties remain regarding how some patients will be cured while other patients will have cancer recurrence, metastasis, or death after surgical resection. Identification of patients at high risk of recurrence, those who are unlikely to respond to specific chemotherapeutic agents, is the rationale for measuring specific biochemical markers. Thus, main investigational studies nowadays are focused in identifying molecular markers of recurrence, beyond pathologic stage, after surgical treatment and factors that can predict a benefit from adjuvant chemotherapy in poor prognosis subgroups, to individualize treatments. Advances in genomics and proteomics have generated many candidate markers with potential clinical value. Gene expression profiling (GEP) by microarray or real-time quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR) can be useful in the classification or prognosis of various types of cancer, including lung cancer. A number of prognostic gene expression signatures have been reported to predict survival in non-small cell lung cancer (NSCLC). In this review, we focus on the role of GEP in early-stage NSCLC as predictive and prognostic biomarker and its potential use for a 'personalized' medicine in the years to come.
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PMID:The role of gene expression profiling in early-stage non-small cell lung cancer. 2226 26

Blockade of cell cycle re-entry in quiescent cancer cells is a strategy to prevent cancer progression and recurrence. We investigated the action and mode of action of CPF mixture (Coptis chinensis, Pinellia ternata and Fructus trichosanthis) in impeding a proliferative switch in quiescent lung cancer cells. The results indicated that CPF impeded cell cycle re-entry in quiescent lung cancer cells by reduction of FACT and c-MYC mRNA and protein levels, with concomitant decrease in H3K4 tri-methylation and RNA polymerase II occupancy at FACT and c-MYC promoter regions. Animals implanted with quiescent cancer cells that had been exposed to CPF had reduced tumour volume/weight. Thus, CPF suppresses proliferative switching through transcriptional suppression of FACT and the c-MYC, providing a new insight into therapeutic target and intervention method in impeding cancer recurrence.
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PMID:CPF impedes cell cycle re-entry of quiescent lung cancer cells through transcriptional suppression of FACT and c-MYC. 3196 May 91