Cancer predisposition in Bloom's syndrome

Article Abstract:

Constitutive elevation of c-myc protein level of Epstein Barr virus immortalized B cells derived from Bloom's syndrome (BS) cell lines correlate with reduction of DNA ligase I activity. BS is characterized by reduced DNA synthesis rates, high sister chromatid exchange and spontaneous chromosomal rearrangements. The time required for c-myc elevation corresponds to the kinetics of repair of DNA strand breaks by poly (ADP-ribose) polymerase. Low doses of radiation also induce activation of this potent oncogene. These factors and others contribute to cancer predisposition.

User Contributions:

Comment about this article or add new information about this topic:

Comment:  (50-4000 characters)

Name:

E-mail:

Security Code:

Mutation rates

Article Abstract:

Studies on microbes demonstrate that mean mutation rate is invariably constant at 0.0003 despite correction for detection inefficiencies. This is inversely related genome size and the evolution of antimutagenic mechanisms among these organisms. However, defects in deoxyribonucleic acid polymerease function increase the generation of genetic mutants which intensifies transition, transversion and frameshift mutation rates.

User Contributions:

Comment about this article or add new information about this topic:

Comment:  (50-4000 characters)

Name:

E-mail:

Security Code:

Methylation, mutation and cancer

Article Abstract:

Carcinogenesis in humans is associated with the presence of 5-methylcytosine that causes transition mutations in deoxyribonucleic acids. This occurs despite the infrequent occurence of the DNA methyltransferase substrate, CpG, and the efficient cellular repair mechanisms that exist. Mutations due to cystosine methylation also occur in p53 tumor suppressor genes predominatly involved in colonic tumors.

User Contributions:

Comment about this article or add new information about this topic:

Comment:  (50-4000 characters)

Name:

E-mail:

Security Code: