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Report on Carcinogens : Carcinogen... 2011
Topics: Animals; Asbestos; Carcinogens; Humans; Neoplasms
PubMed: 21836646
DOI: No ID Found -
Report on Carcinogens : Carcinogen... 2011
Topics: Animals; Carcinogens; Humans; Neoplasms; Phenylenediamines
PubMed: 21850141
DOI: No ID Found -
Report on Carcinogens : Carcinogen... 2011
Topics: Animals; Carcinogens; Chloroform; Humans; Neoplasms; Solvents
PubMed: 21850127
DOI: No ID Found -
Report on Carcinogens : Carcinogen... 2011
Topics: Aminobiphenyl Compounds; Animals; Carcinogens; Humans; Neoplasms
PubMed: 21829249
DOI: No ID Found -
Report on Carcinogens : Carcinogen... 2011
Topics: Animals; Butadienes; Carcinogens; Humans; Neoplasms
PubMed: 21850116
DOI: No ID Found -
Oncogene Mar 2020Insulin-like growth factor (IGF) binding protein 2 (IGFBP2) was discovered and identified as an IGF system regulator, controlling the distribution, function, and... (Review)
Review
Insulin-like growth factor (IGF) binding protein 2 (IGFBP2) was discovered and identified as an IGF system regulator, controlling the distribution, function, and activity of IGFs in the pericellular space. IGFBP2 is a developmentally regulated gene that is highly expressed in embryonic and fetal tissues and markedly decreases after birth. Studies over the last decades have shown that in solid tumors, IGFBP2 is upregulated and promotes several key oncogenic processes, such as epithelial-to-mesenchymal transition, cellular migration, invasion, angiogenesis, stemness, transcriptional activation, and epigenetic programming via signaling that is often independent of IGFs. Growing evidence indicates that aberrant expression of IGFBP2 in cancer acts as a hub of an oncogenic network, integrating multiple cancer signaling pathways and serving as a potential therapeutic target for cancer treatment.
Topics: Gene Expression Regulation, Neoplastic; Humans; Insulin-Like Growth Factor Binding Protein 2; Oncogenes; Signal Transduction
PubMed: 31925333
DOI: 10.1038/s41388-020-1154-2 -
International Journal of Molecular... Nov 2022In the multi-factorial etiology of organ-site cancers by suspect human chemical carcinogens, oncogenic virus, activation of RAS, Myc and HER-2 oncogenes, inactivation of...
In the multi-factorial etiology of organ-site cancers by suspect human chemical carcinogens, oncogenic virus, activation of RAS, Myc and HER-2 oncogenes, inactivation of TP53, RB and APC tumor suppressor genes represent early-occurring genetic events [...].
Topics: Humans; Antineoplastic Agents; Oncogenes; Oncogenic Viruses; Carcinogens; Neoplasms
PubMed: 36430932
DOI: 10.3390/ijms232214457 -
Acta Pharmacologica Sinica Oct 2018Oncogene-induced cellular senescence (OIS) is a complex program that is triggered in response to aberrant activation of oncogenic signaling. Initially, OIS was thought... (Review)
Review
Oncogene-induced cellular senescence (OIS) is a complex program that is triggered in response to aberrant activation of oncogenic signaling. Initially, OIS was thought to be a barrier to malignant transformation because of its suppression on cell proliferation. Later studies showed that senescence induced by oncogenes can also promote the initiation and development of cancer. The opposing effects of OIS occur through different combinations of downstream effectors as well as the interplay of senescent cells and the microenvironment, such as senescence-associated inflammation. Here, we review the common features and molecular mechanisms underlying OIS and the interaction between senescent cells and the microenvironment. We propose that targeting senescent cells may have a beneficial therapeutic effect during the treatment of cancer.
Topics: Animals; Cell Proliferation; Cell Transformation, Neoplastic; Cellular Microenvironment; Cellular Senescence; Humans; Neoplasms; Oncogenes; Signal Transduction
PubMed: 29620049
DOI: 10.1038/aps.2017.198 -
Scandinavian Journal of Work,... 1992It seems increasingly likely that an important mechanism of action of certain workplace carcinogens in contributing to occupational carcinogenesis may be via the... (Review)
Review
It seems increasingly likely that an important mechanism of action of certain workplace carcinogens in contributing to occupational carcinogenesis may be via the activation of cellular oncogenes, which then cause an expression of mutated forms or increased amounts of their oncoprotein products. Two prototypical models of this mechanism may be the ras oncogene and its p21 protein and the neu oncogene and its p185 protein. Both are known to be activated by exposure to common occupational carcinogens, and both are known to occur frequently in human tumors, including those of occupational concern such as lung cancer. Knowledge of their mechanisms of action may lead to new opportunities for preventing occupational cancer.
Topics: Animals; Genes, ras; Humans; Neoplasms; Occupational Diseases; Oncogene Protein p21(ras); Oncogenes; Proto-Oncogene Proteins; Proto-Oncogenes; Receptor, ErbB-2; Retroviridae
PubMed: 1357742
DOI: No ID Found -
The EMBO Journal May 2013Tumour-associated oncogenes induce unscheduled proliferation as well as genomic and chromosomal instability. According to current models, therapeutic strategies that... (Review)
Review
Tumour-associated oncogenes induce unscheduled proliferation as well as genomic and chromosomal instability. According to current models, therapeutic strategies that block oncogene activity are likely to selectively target tumour cells. However, recent evidences have revealed that oncogenes are only essential for the proliferation of some specific tumour cell types, but not all. Indeed, the latest studies of the interactions between the oncogene and its target cell have shown that oncogenes contribute to cancer development not only by inducing proliferation but also by developmental reprogramming of the epigenome. This provides the first evidence that tumorigenesis can be initiated by stem cell reprogramming, and uncovers a new role for oncogenes in the origin of cancer. Here we analyse these evidences and propose an updated model of oncogene function that can explain the full range of genotype-phenotype associations found in human cancer. Finally, we discuss how this vision opens new avenues for developing novel anti-cancer interventions.
Topics: Animals; Cell Biology; Cell Proliferation; Cell Transformation, Neoplastic; Chromosomal Instability; Genetic Association Studies; Humans; Mice; Models, Biological; Mutation; Neoplasms; Neoplastic Stem Cells; Oncogenes
PubMed: 23632857
DOI: 10.1038/emboj.2013.97