Factors influencing mutation at the hprt locus in T-lymphocytes: women treated for breast cancer

Cancer Res. 1991 Dec 15;51(24):6603-7.

Abstract

Forty-nine women with breast cancer were enrolled in a prospective, longitudinal study of the genetic damage caused by treatment. Assays of mutant frequency at the hprt locus in peripheral blood lymphocytes were performed at approximately 6-month intervals for 2 years. Treatment consisted of surgery alone or additional tamoxifen, radiotherapy, or chemotherapy in various combinations. At 6 months, there was an elevation of mean mutant frequency compared to initial values (P = 0.004) which persisted for as many as 2 years. A significant elevation at 6 months occurred only in the group of women who received combination chemotherapy (P = 0.005). Within this group, 5 of 15 patients had striking elevations of mutant frequency following chemotherapy (greater than 3 SD). Three of these 5 women had serum folate levels in the deficient range, while only one of 9 patients with lesser responses to chemotherapy were folate deficient. The change in mutant frequency after chemotherapy was inversely related to serum folate levels (P = 0.05) and to the number of years of smoking cigarettes (P = 0.01). We conclude that of the various modalities used to treat breast cancer, only chemotherapy was accompanied by a high risk of somatic mutation. A subset of patients manifested substantial increases in mutant frequency, often in association with low serum folate levels.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Antineoplastic Agents / adverse effects*
  • Breast Neoplasms / therapy*
  • Combined Modality Therapy
  • Female
  • Folic Acid / blood
  • Humans
  • Hypoxanthine Phosphoribosyltransferase / genetics*
  • Mutagenesis*
  • Prospective Studies
  • Radiotherapy / adverse effects*
  • Smoking / adverse effects
  • T-Lymphocytes / physiology*

Substances

  • Antineoplastic Agents
  • Folic Acid
  • Hypoxanthine Phosphoribosyltransferase