Purpose: To assess the extent of variation in radiosensitivity between individuals, gender-related dissimilarity and impact on the association with single nucleotide polymorphisms (SNPs).
Materials And Methods: Survival curves of 152 fibroblast cell strains derived from both gender were generated. Individual radiosensitivity was characterized by the surviving fraction at 2Gy (SF2).
Gemcitabine (2',2'-difluoro-2'-deoxycytidine; dFdCyd) is one of the anti-metabolites drugs that target DNA replication. We evaluated dFdCyd cytotoxicity and its radiosensitizing ability in human breast cancer cell lines, MCF-7 (wild-type p53) and MDA-MB-231 (mutant-type p53) along with normal mammary epithelial cell line (MCF-12) for comparison. Radiosensitivity and cytotoxicity were measured by the clonogenic survival assays.
View Article and Find Full Text PDFJ Egypt Natl Canc Inst
September 2008
Background: It has been hypothesized that patient to patient variation in normal tissue reactions to radiotherapy is associated with the presence of polymorphic variations in genes involved in DNA repair.
Purpose: To test for a possible association between two single-nucleotide polymorphisms (SNPs), XRCC1 399 G>A Arg/Gln and XRCC3 241 C>T Thr/Met and late reactions to radiotherapy.
Patients And Methods: In this case control study, 50 Head and Neck cancer patients were retrospectively recruited.
Purpose: Genetic predictive markers of radiosensitivity are being sought for stratifying radiotherapy for cancer patients and risk assessment of radiation exposure. We hypothesized that single nucleotide polymorphisms in susceptible genes are associated with, and the number of risk alleles has incremental effect on, individual radiosensitivity.
Methods And Materials: Six amino acid substitution variants (ATM 1853 Asp/Asn G>A, p53 72 Arg/Pro G>C, p21 31 Ser/Arg C>A, XRCC1 399 Arg/Gln G>A, XRCC3 241 Thr/Met C>T, and TGFbeta1 10 Leu/Pro T>C) were genotyped by direct sequencing in 54 fibroblast strains of different radiosensitivity.
Int J Radiat Oncol Biol Phys
February 2004
Purpose: To test the hypothesis that breast cancer patients could have a predisposing defect in the induction of TP53 tumor suppressor protein (known as p53) that could be a marker of genetic instability and increased cancer susceptibility. The accumulation of p53 was triggered by ionizing radiation, and its transcriptional activity was estimated from the induction of CDKN1A (known as p21).
Methods And Materials: Using Western blot, we studied the radiation induction of p53 and p21 proteins in 28 fibroblast cell strains derived from 7 healthy donors (Control), 3 ataxia telangiectasia (AT), 3 AT heterozygous, and 15 breast cancer patients.