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A microRNA expression signature of human solid tumors defines cancer gene targets
The results indicate that miRNAs are extensively involved in cancer pathogenesis of solid tumors and support their function as either dominant or recessive cancer genes.
p53 mutations in human cancers.
Transitions predominate in colorectal carcinomas, brain tumors, leukemias, and lymphomas, whereas G:C to T:A transversions are the most frequent substitutions observed in cancers of the lung and liver.
Mutations in the p53 tumor suppressor gene: clues to cancer etiology and molecular pathogenesis.
The p53 tumor suppressor gene has come to the forefront of cancer research because it is commonly mutated in human cancer and the spectrum of p53 mutations in these cancers is providing clues to the
Unique microRNA molecular profiles in lung cancer diagnosis and prognosis.
Results indicate that miRNA expression profiles are diagnostic and prognostic markers of lung cancer.
MicroRNA expression profiles associated with prognosis and therapeutic outcome in colon adenocarcinoma.
expression patterns of microRNAs are systematically altered in colon adenocarcinomas and high miR-21 expression is associated with poor survival and poor therapeutic outcome.
The IARC TP53 database: New online mutation analysis and recommendations to users
Recent developments of the IARC TP53 mutation dataset are described, which include restructuring of the database, which is now patient‐centered, with more detailed annotations on the patient (carcinogen exposure, virus infection, genetic background).
Genetic variation in microRNA networks: the implications for cancer research
In reviewing this new field of cancer biology, the methodological approaches of these studies are described, and recommendations for which strategies will be most informative in the future are made.
Radical causes of cancer
Understanding the association between chronic inflammation and cancer provides insights into the molecular mechanisms involved and highlights the interaction between nitric oxide and p53 as a crucial pathway in inflammatory-mediated carcinogenesis.
Rapid Akt activation by nicotine and a tobacco carcinogen modulates the phenotype of normal human airway epithelial cells.
Redundant Akt activation by nicotine and NNK could contribute to tobacco-related carcinogenesis by regulating two processes critical for tumorigenesis, cell growth and apoptosis.
Centrosome amplification and a defective G2-M cell cycle checkpoint induce genetic instability in BRCA1 exon 11 isoform-deficient cells.
It is shown that mouse embryonic fibroblast cells carrying a targeted deletion of exon 11 of the Brca1 gene maintain an intact G1-S cell cycle checkpoint and proliferate poorly, however, a defective G2-M checkpoint in these cells is accompanied by extensive chromosomal abnormalities.