Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P43146 (tumour suppressor)
 5,935 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Darwinian medicine is the treatment of disease based on evolution. The underlying assumption of Darwinian medicine is that traits are coded by genes, which are often assumed to be sequences of DNA nucleotides. The quantitative genetic ramification of this perspective is that traits, including disease susceptibility, are either caused by genes or by the environment, with genotype-by-environment interactions usually considered statistical artefacts. I emphasize also examining those epigenetic signals that can be altered by environmental perturbations and then transmitted to subsequent generations. Although seldom studied, environmentally-alterable meiotically-heritable epigenetic signals exist and provide a mechanism underlying genotype-by-environment interactions. Environment of a parent can affect its descendants by heritably altering epigenetic signals. Neo-Lamarckian medicine is the application of these evolutionary epigenetic notions to diseases and could have enormous public health and environmental policy implications. If industrial contaminants adversely affect organisms by meiotically-heritably altering their epigenetic signals, then cleaning up these contaminants will not remedy the problem. Once contaminants have adversely altered an individual's epigenetic signals, this harm will be transmitted to future generations even if they are not exposed to the contaminant. Exposure to environmental shocks such as free radicals or other carcinogens can alter cytosine methylation patterns on regulatory genes. This can cause cancer by up-regulating genes for cell division or by down-regulating tumour suppressor genes. Environmentally-alterable meiotically-heritable epigenetic signals could also underlie other diseases, such as diabetes, Prader-Willi syndrome, and many complex diseases. If environmentally-altered meiotically-heritable epigenetic effects are widespread - which is an important open empirical question - they have the potential to alter paradigmatic views of evolutionary medicine and the putative dichotomy of nature versus nurture. Neo-Lamarckian medicine would thereby shift emphasis from cure to prevention of diseases.
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PMID:Neo-Lamarckian medicine. 1496 44

Cancer can be defined as a genetic disease, resulting as a consequence of multiple events associated with initiation, promotion and metastatic growth. Cancer results from the loss of control of cellular homeostasis. Cell homeostasis is the result of the balance between proliferation and cell death, while cellular transformation can be viewed as a loss of relationship between these events. Oncogenes and tumour suppressor genes act as modulators of cell proliferation, while the balance of apoptotic and anti-apoptotic genes controls cell death. All cancer cells acquire similar sets of functional capacities: (1) independence from mitogenic/growth signals; (2) loss of sensitivity to "anti-growth" signals; (3) evade apoptosis; (4) Neo-angiogenic conversion; (5) release from senescence; and (6) invasiveness and metastasis. One of the goals of molecular biology is to elucidate the mechanisms that contribute to the development and progression of cancer. Such understanding of the molecular basis of cancer will provide new possibilities for: (1) earlier detection as well as better diagnosis and staging of disease with detection of minimal residual disease recurrences and evaluation of response to therapy; (2) prevention; and (3) novel treatment strategies. We feel that increased understanding of ETS-regulated biological pathways will directly impact these areas. ETS proteins are transcription factors that activate or repress the expression of genes that are involved in various biological processes, including cellular proliferation, differentiation, development, transformation and apoptosis. Identification of target genes that are regulated by a specific transcription factor is one of the most critical areas in understanding the molecular mechanisms that control transcription. Furthermore, identification of target gene promoters for normal and oncogenic transcription factors provides insight into the regulation of genes that are involved in control of normal cell growth, and differentiation, as well as provide information critical to understanding cancer development. This review will highlight the current understanding of ETS genes and their role in cancer.
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PMID:ETS transcription factors and their emerging roles in human cancer. 1621 4