The hallmarks of cancer

Article Abstract:

Rules that govern the transformation of normal human cells into malignant cancers are discussed. A small number of molecular, biochemical and cellular traits are shared by most and perhaps all kinds of human cancer. Almost all mammalian cells have similar molecular machinery to regulate proliferation, death and differentiation. A dramatically different kind of science from that of the 25 years just past will likely characterize the future of cancer research with much of the fundamental change conceptual and some of it at the technical level. A small number of underlying principles will be set down. Six essential chnages in cell physiology that as a group dictate malignant growth are given.

Cancer research, Gene mutations, Gene mutation, Genetic aspects, Cancer, Neovascularization, Metabolic regulation, Cancer cells, Metastasis, Cancer invasiveness, Growth (Physiology), Growth regulators, Cancer metastasis

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MMP-9 supplied by bone marrow-derived cells contributes to skin carcinogenesis

Article Abstract:

MMP-9 from cells from bone marrow has been found to contribute to carcinogenesis in skin. The matrix metalloproteinase MMP-9/gelatinase B has been found to be upregulated in angiogenic dysplasias and invasive cancers of the epidermis in mice used to study multistage tumorigenesis brought on by HPV1 oncogenes. Transgenic mice without MMP-9 have lower keratinocyte hyperproliferation at all neoplastic stages and lower rates of invasive tumors. Inflammatory cells can be a factor in carcinogenesis.

Statistical Data Included, Usage, Inflammation, Bone marrow, Keratinocytes, Tumors, Carcinogenesis, Skin cancer, Genetically modified mice

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hSIR2(sup)SIRT1 functions as an NAD-dependent p53 deacetylase

Article Abstract:

Research demonstrates that the human homolog of the Saccharomyces cerevisiae Sir2 protein, encoded by the human Silent Information Regulator family gene hSIR2(sup)SIRT1, binds and deacetylates the p53 protein leading to its activation and function as a transcription factor.

DNA damage, Genetic regulation, Genetic transcription, Transcription (Genetics), Tumor suppressor genes

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