Surfing the P53 network

Article Abstract:

The p53 tumour-suppressor gene was first thought to be an oncogene, but research revealed it to suppress tumours by slowing growth, DNA replication and division in cells. It was also revealed to function incorrectly in most human tumours, thus being a major catalyst in the development of cancer when it breaks down.

Causes of, Cancer

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APC mutations occur early during colorectal tumorigenesis

Article Abstract:

Mutations to the tumor suppressor gene APC contribute to the growth of colorectal neoplasms and their development into malignant tumors or carcinomas. A genetic sequence analysis of 41 colorectal tumors found that 60% of the carcinomas and 63% of the non-malignant adenomas had a mutated APC gene. Moreover, the mutations were present in the earliest benign tumors on through to highly developed carcinomas.

Health aspects, Development and progression, Colorectal cancer, Genetic aspects, Mutation (Biology), Mutation, Carcinogenesis

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Oncoprotein MDM2 conceals the activation domain of tumour suppressor p53

Article Abstract:

Missense mutations or binding to oncogenic proteins leads to inactivation of tumor suppressor gene p53 in most human malignancies. MDM2 gene amplification is believed to trigger inactivation in human soft tissue sarcomas by binding to p53 and limiting its transcription process. This was shown in a study of Saccharomyces cerevisiae where human MDM2 hindered human p53 transcription ability by binding to a region similar to the acidic activation domain of p53. The inactivation of DNA-binding protein fused to isolated p53 activation domain also confirmed that MDM2 was able to conceal activation domain of p53.

Oncogenes, Tumor proteins

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