Association of transforming growth factor beta-1 single nucleotide polymorphisms with radiation-induced damage to normal tissues in breast cancer patientsCitation formats

  • External authors:
  • S. Quarmby
  • H. Fakhoury
  • E. Levine
  • J. Barber
  • J. Wylie
  • A. H. Hajeer
  • A. Stewart
  • B. Magee
  • S. Kumar

Standard

Association of transforming growth factor beta-1 single nucleotide polymorphisms with radiation-induced damage to normal tissues in breast cancer patients. / Quarmby, S.; Fakhoury, H.; Levine, E.; Barber, J.; Wylie, J.; Hajeer, A. H.; West, C.; Stewart, A.; Magee, B.; Kumar, S.

In: International Journal of Radiation Biology, Vol. 79, No. 2, 01.02.2003, p. 137-143.

Research output: Contribution to journalArticlepeer-review

Harvard

Quarmby, S, Fakhoury, H, Levine, E, Barber, J, Wylie, J, Hajeer, AH, West, C, Stewart, A, Magee, B & Kumar, S 2003, 'Association of transforming growth factor beta-1 single nucleotide polymorphisms with radiation-induced damage to normal tissues in breast cancer patients', International Journal of Radiation Biology, vol. 79, no. 2, pp. 137-143.

APA

Quarmby, S., Fakhoury, H., Levine, E., Barber, J., Wylie, J., Hajeer, A. H., West, C., Stewart, A., Magee, B., & Kumar, S. (2003). Association of transforming growth factor beta-1 single nucleotide polymorphisms with radiation-induced damage to normal tissues in breast cancer patients. International Journal of Radiation Biology, 79(2), 137-143.

Vancouver

Quarmby S, Fakhoury H, Levine E, Barber J, Wylie J, Hajeer AH et al. Association of transforming growth factor beta-1 single nucleotide polymorphisms with radiation-induced damage to normal tissues in breast cancer patients. International Journal of Radiation Biology. 2003 Feb 1;79(2):137-143.

Author

Quarmby, S. ; Fakhoury, H. ; Levine, E. ; Barber, J. ; Wylie, J. ; Hajeer, A. H. ; West, C. ; Stewart, A. ; Magee, B. ; Kumar, S. / Association of transforming growth factor beta-1 single nucleotide polymorphisms with radiation-induced damage to normal tissues in breast cancer patients. In: International Journal of Radiation Biology. 2003 ; Vol. 79, No. 2. pp. 137-143.

Bibtex

@article{4bdf70a286504eb59273c34e71f05550,
title = "Association of transforming growth factor beta-1 single nucleotide polymorphisms with radiation-induced damage to normal tissues in breast cancer patients",
abstract = "Purpose: To investigate whether transforming growth factor beta-1 (TGFβ1) single nucleotide polymorphisms were associated with the susceptibility of breast cancer patients to severe radiation-induced normal tissue damage. Materials and methods: PCR-RFLP assays were performed for TGFβ1 gene polymorphisms on DNA obtained from 103 breast cancer patients who received radiotherapy. The G-800A, C-509T, T+869C and G+915C polymorphic sites were examined, and genotype and allele frequencies of two subgroups of patients were calculated and compared. Results: The less prevalent -509T and +869C alleles were significantly associated with a subgroup of patients who developed severe radiation-induced normal tissue fibrosis (n=15) when compared with those who did not (n=88) (odds ratio=3.4, p=0.0036, and 2.37, p=0.035, respectively). Furthermore, patients with the -509TT or +869CC genotypes were between seven and 15 times more likely to develop severe fibrosis. Conclusions: These findings imply a role for the -509T and +869C alleles in the pathobiological mechanisms underlying susceptibility to radiation-induced fibrosis. Their predictive value would be limited to patients who are -509TT or +869CC, but if 'fibrosis-associated' polymorphic sites in other genes could be identified, it may be possible to detect fibrosis prone individuals before radiotherapy with greater certainty.",
keywords = "Alleles, Base Sequence, Breast Neoplasms/*genetics/*radiotherapy, DNA, Neoplasm/genetics, Female, Fibrosis, Human, *Polymorphism, Single Nucleotide, Radiation Injuries/*etiology/*genetics/pathology, Radiation Tolerance/genetics, Support, Non-U.S. Gov't, Transforming Growth Factor beta/*genetics",
author = "S. Quarmby and H. Fakhoury and E. Levine and J. Barber and J. Wylie and Hajeer, {A. H.} and C. West and A. Stewart and B. Magee and S. Kumar",
note = "224567080955-3002Journal Article",
year = "2003",
month = feb,
day = "1",
language = "English",
volume = "79",
pages = "137--143",
journal = "International Journal of Radiation Biology",
issn = "0955-3002",
publisher = "Informa Healthcare",
number = "2",

}

RIS

TY - JOUR

T1 - Association of transforming growth factor beta-1 single nucleotide polymorphisms with radiation-induced damage to normal tissues in breast cancer patients

AU - Quarmby, S.

AU - Fakhoury, H.

AU - Levine, E.

AU - Barber, J.

AU - Wylie, J.

AU - Hajeer, A. H.

AU - West, C.

AU - Stewart, A.

AU - Magee, B.

AU - Kumar, S.

N1 - 224567080955-3002Journal Article

PY - 2003/2/1

Y1 - 2003/2/1

N2 - Purpose: To investigate whether transforming growth factor beta-1 (TGFβ1) single nucleotide polymorphisms were associated with the susceptibility of breast cancer patients to severe radiation-induced normal tissue damage. Materials and methods: PCR-RFLP assays were performed for TGFβ1 gene polymorphisms on DNA obtained from 103 breast cancer patients who received radiotherapy. The G-800A, C-509T, T+869C and G+915C polymorphic sites were examined, and genotype and allele frequencies of two subgroups of patients were calculated and compared. Results: The less prevalent -509T and +869C alleles were significantly associated with a subgroup of patients who developed severe radiation-induced normal tissue fibrosis (n=15) when compared with those who did not (n=88) (odds ratio=3.4, p=0.0036, and 2.37, p=0.035, respectively). Furthermore, patients with the -509TT or +869CC genotypes were between seven and 15 times more likely to develop severe fibrosis. Conclusions: These findings imply a role for the -509T and +869C alleles in the pathobiological mechanisms underlying susceptibility to radiation-induced fibrosis. Their predictive value would be limited to patients who are -509TT or +869CC, but if 'fibrosis-associated' polymorphic sites in other genes could be identified, it may be possible to detect fibrosis prone individuals before radiotherapy with greater certainty.

AB - Purpose: To investigate whether transforming growth factor beta-1 (TGFβ1) single nucleotide polymorphisms were associated with the susceptibility of breast cancer patients to severe radiation-induced normal tissue damage. Materials and methods: PCR-RFLP assays were performed for TGFβ1 gene polymorphisms on DNA obtained from 103 breast cancer patients who received radiotherapy. The G-800A, C-509T, T+869C and G+915C polymorphic sites were examined, and genotype and allele frequencies of two subgroups of patients were calculated and compared. Results: The less prevalent -509T and +869C alleles were significantly associated with a subgroup of patients who developed severe radiation-induced normal tissue fibrosis (n=15) when compared with those who did not (n=88) (odds ratio=3.4, p=0.0036, and 2.37, p=0.035, respectively). Furthermore, patients with the -509TT or +869CC genotypes were between seven and 15 times more likely to develop severe fibrosis. Conclusions: These findings imply a role for the -509T and +869C alleles in the pathobiological mechanisms underlying susceptibility to radiation-induced fibrosis. Their predictive value would be limited to patients who are -509TT or +869CC, but if 'fibrosis-associated' polymorphic sites in other genes could be identified, it may be possible to detect fibrosis prone individuals before radiotherapy with greater certainty.

KW - Alleles

KW - Base Sequence

KW - Breast Neoplasms/genetics/radiotherapy

KW - DNA, Neoplasm/genetics

KW - Female

KW - Fibrosis

KW - Human

KW - Polymorphism, Single Nucleotide

KW - Radiation Injuries/etiology/genetics/pathology

KW - Radiation Tolerance/genetics

KW - Support, Non-U.S. Gov't

KW - Transforming Growth Factor beta/genetics

M3 - Article

VL - 79

SP - 137

EP - 143

JO - International Journal of Radiation Biology

JF - International Journal of Radiation Biology

SN - 0955-3002

IS - 2

ER -