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Models and mechanisms in malignant melanoma.

Mol Carcinog 2007 Aug;46(8):671-8

Department of Immunology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA.

Human melanoma represents the fastest growing malignancy in the US. The etiology of melanoma is highly debated as is the role of ultraviolet (UV) radiation in the initiation and progression of melanoma. This article discusses data from UV exposure and its relationship to the development of melanoma from various models of melanoma as well as various genetic alterations seen in oncogenic transformation of melanocytes. Genetic alterations such as the p16(INK4a) deletion, melanocortin 1 receptor (MC1R), RAS, and v-raf murine sarcoma viral oncogene homolog B1 (BRAF) may be indicative of a predisposition to melanoma development. Historical research as well as current data on the significance of the hot spot mutation in BRAF is discussed in its relative potential to the activating mutation in RAS.

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Prostate Cancer Clinical Research Unit, Spanish National Cancer Research Centre, Madrid, Spain; Genitourinary Cancer Translational Research Group, Instituto de Investigación Biomédica de Málaga, Spain; Medical Oncology, UGCI, Hospitales Universitarios Virgen de la Victoria y Regional de Málaga, Málaga, Spain. Electronic address:

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[Prion induced spongiform encephalopathy of Creutzfeldt-Jakob disease].

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The infectious protein or prion (PrPSC) is a transmissible and replicable polypeptide, which arises from an abnormal folding of the PrP protein, by unknown mechanisms and without changes in the primary sequence of its amino acids. Its new spatial disposition arises from the substitution of its alpha helices by beta bands, which increase its structural stability, avoiding its complete proteolysis, resulting in a residual accumulation of prions. These prions induce the misfolding of normal PrP protein, generating their exponential increase, leading to a disturbance of neuronal homeostasis which results in the development of the fatal spongiform encephalopathy of the Creutzfeldt-Jakob disease (CJD). Read More

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Genetically determined hypercholesterolaemia results into premature leucocyte telomere length shortening and reduced haematopoietic precursors.

Eur J Prev Cardiol 2020 Nov 17. Epub 2020 Nov 17.

Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Via Balzaretti 9, 20133 Milan, Italy.

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J Neurosci 2021 Feb 22. Epub 2021 Feb 22.

Department of Developmental, Molecular and Chemical Biology, Tufts University School of Medicine, Boston, MA 02111

Reversible modification of AMPARs with ubiquitin regulates receptor levels at synapses and controls synaptic strength. The conserved deubiquitinating enzyme (DUB) USP-46 removes ubiquitin from AMPARs and protects them from degradation in both and mammals. Although DUBs are critical for diverse physiological processes, the mechanisms that regulate DUBs, especially in the nervous system, are not well understood. Read More

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