منابع مشابه
Oncogene activation and tumor progression.
25 years ago (1) Leslie Foulds formulated a number of 'rules' for tumor progression, the process whereby 'tumors go from bad to worse', in Peyton Rous' original description (2). These rules are equally pertinent today and accessible to analysis by the powerful tools of modem biology. Foulds dissected the malignant phenotype into 'unit characteristics', such as growth rate, invasiveness, metasta...
متن کاملTumor dormancy and oncogene addiction.
Cancer is caused by genetic changes that activate oncogenes or inactivate tumor suppressor genes. The repair or inactivation of mutant genes may be effective in the treatment of cancer. Indeed, drugs that target oncogenes can be effective in the treatment of cancer. However, it is still unclear why the inactivation of a single cancer-associated gene would ever result in the elimination of tumor...
متن کاملMechanisms of Oncogene Activation
The main modifications that characterize cancer are represented by alterations in onco‐ genes, tumor-suppressor genes, and non-coding RNA genes. Most of these alterations are somatic and the process is a multistep one. Tumors often arise from an initial trans‐ formed cell, and after subsequent genetic alterations different cytogenetically clones lead to tumor heterogeneity. Oncogenes encode pro...
متن کاملTumor Cell Instability, Diversification, and Progression to the Metastatic Phenotype: From Oncogene to Oncofetal Expression1
valid today. We seem to be closer, however, at least to defining the wide range of characteristics that exemplify different cancer cells and their host environments, particularly those properties that contribute to the malignant phenotypes of tumor cells, clearly an important problem (2-5). Assembling these data into grandiose hypotheses that might explain the complex, dynamic nature of cancers...
متن کاملInk4a/Arf and oncogene-induced senescence prevent tumor progression during alternative colorectal tumorigenesis.
Colonic cancers with a serrated morphology have been proposed to comprise a molecularly distinct tumor entity following an alternative pathway of genetic alterations independently of APC mutations. We demonstrate that intestinal epithelial cell specific expression of oncogenic K-ras(G12D) in mice induces serrated hyperplasia, which is characterized by p16(ink4a) overexpression and induction of ...
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ژورنال
عنوان ژورنال: Carcinogenesis
سال: 1984
ISSN: 0143-3334,1460-2180
DOI: 10.1093/carcin/5.4.429