Cancer genes and the pathways they control

By Bert Vogelstein, Kenneth W. Kinzler. Nature Medicine, 2004

4,411 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/4cdda994eb54b7591da9e1b2dcda661502056451

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In Oncology

Citations in the corpus

Global survey of phosphotyrosine signaling identifies oncogenic kinases in lung cancer. (2007, neutral): “One such strategy involves analysis of the cellular signaling pathways corrupted in cancer (Vogelstein and Kinzler , 2004).”
miR-34a repression of SIRT1 regulates apoptosis (2008, background): “P53 is a transcription factor that inhibits cell growth in response to DNA damage, and inactivation of p53 pathways is a common feature of many cancers (55, 56).”
The impact of translocations and gene fusions on cancer causation (2007, background): “There is now a general agreement that cancer is, in essence, a genetic disease at the cellular leve”
Intratumor heterogeneity: the Rosetta stone of therapy resistance (2020, background): “Despite mounting challenges, gene and mutation-centric focus remains at the core of molecular oncology, and the majority of cancer researchers would probably still agree with the famous statement by Bert Vogelstein: “The revolution in cancer research can be summed up in a single sentence: cancer is,”
Dual role of hydrogen peroxide in cancer: possible relevance to cancer chemoprevention and therapy. (2007, background): “There is evidence that the most important oncogenes and tumor-suppressor gene pathways may culminate in HIF-1 activation [15] and that HIF-1 activation plays an important role in apoptosis resistance, invasion/metastasis, angiogenesis and immortalization [5,40–43].”
Acidic extracellular pH promotes experimental metastasis of human melanoma cells in athymic nude mice. (2006, background): “genomic alterations during growth, resulting in the development of an increasing number of aggressive phenotypic traits with time, a process termed malignant progression (1, 2).”
Paul Ehrlich's magic bullet concept: 100 years of progress (2008, background): “The discovery of oncogenes and tumour suppressor genes in the 1970s and 1980s, and the subsequent deciphering of the cellular signal transduction pathways, helped define the biological hallmarks of cance”
Glycine decarboxylase activity drives non-small cell lung cancer tumor-initiating cells and tumorigenesis. (2012, positive): “Despite numerous advances in our knowledge of cancer (Vogelstein and Kinzler, 2004; Hanahan and Weinberg, 2011), our ability to develop clinically effective therapies based on this understanding has met with limited success.”
ERK promotes tumorigenesis by inhibiting FOXO3a via MDM2-mediated degradation (2008, neutral): “dtd" [ ]> The constitutive activation of certain signal transduction cascades leads to the development of tumours and the resistance of tumours to clinical therap”
Interferons, immunity and cancer immunoediting (2006, background): “These pathways coordinately defend cells from the oncogenic and/or genotoxic stimuli that can lead to malignant transformatio”
Tenets of PTEN tumor suppression. (2008, background): “Regulating the PTEN Message Genetic loss or mutation of tumor suppressor genes is a frequent event initiating and/or promoting tumorigenesis (Vogelstein and Kinzler, 2004).”
Cancer: a Systems Biology disease. (2006, background): “The vast majority of these genes function in signal transduction processes within or between cells, govern cell cycle progression, apoptosis, angiogenesis, and infiltration (Vogelstein and Kinzler, 2004).”
Algorithms for Detecting Significantly Mutated Pathways in Cancer (2010, neutral): “Moreover, it is well known that there is crosstalk between different pathways (Vogelstein and Kinzler, 2004; McCormick, 1999), and dividing genes into discrete pathway groupings limits the ability to detect whether this crosstalk is itself a target of mutations.”
Distribution and biological activities of the flavonoid luteolin. (2009, background): “According to the most accepted theory of cancer (the somatic mutation theory of cancer), tumorigenesis is caused by DNA alterations in oncogen, tumor-suppressor genes and stability genes [130].”