It is important to recognize that most of the mutation described above arise in a somatic cell and are not transmitted to the patient’s offspring. Nevertheless, some human families are genetically prone to cancer. One group of cancer patients, exemplified by xeroderma pigmentosum (XP) and the hereditary non-polyposis colon cancer (HNPCC) families, have defects ion DNA repair enzymes (See. Figure 1.7) so that they accumulate mutations at faster rate. More commonly, individuals in cancer-prone families inherit of a mutation in a particular oncogene, essentially reducing the number of additional mutations a cell from that person requires to become neoplastic. The two-hit model explains why even in theses cancer-prone families Tumours may require many years to develop. The inherited oncogene may be particularly relevant for a certain cell type, predisposing to a particular form of tumor (e.g. N-Ras and neurological Tumours), or be able to deregulate growth in a variety of different cell types (e.g. p53 mtations in Li-Fraumeni families which are particularly prone to early-onset leukaemias, sarcomas, and breast and brain malignancies).
from the Book of :
DAVIDSON’S
Principles and Practice of Medicine
Eighteenth Edition 
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