Медицинская иммунология (Dec 2018)

IMMUNOLOGICAL IMBALANCE IN BREAST CANCER AND LUNG CANCER IN POSTMENOPAUSAL WOMEN

  • A. N. Glushkov,
  • E. G. Polenok,
  • L. A. Gordeeva,
  • S. A. Mun,
  • M. V. Kostyanko,
  • A. V. Antonov,
  • V. A. Titov,
  • N. E. Verzhbitskaya,
  • I. A. Vafin

DOI
https://doi.org/10.15789/1563-0625-2018-6-927-934
Journal volume & issue
Vol. 20, no. 6
pp. 927 – 934

Abstract

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Previous studies reported some associations between class A antibodies specific for benzo[a]pyrene (IgA-Bp), estradiol (IgA-Es) and progesterone (IgA-Pg) and breast cancer (BC) in women like as with lung cancer (LC) in men. It was suggested that IgA-Bp and IgA-Es may stimulate tumor initiation and promotion, whereas IgA-Pg may inhibit the in vivo human carcinogenesis.The purpose of this study was to identify the suggested associations of such immunological imbalance with BC and LC in postmenopausal women.The serum A-class antibodies specific to benzo[a]pyrene, estradiol and progesterone (IgA-Bp, IgA-Es, IgA- Pg) were studied in 335 healthy women, 824 breast cancer (BC) patients and 127 cases of lung cancer (LC) by means of non-competitive solid phase immunoassay. The following results were obtained: Increased ratio of IgA-Bp and IgA-Es amounts exceeding the IgA-Pg levels was associated with a higher risk of breast cancer (OR = 2.8 and 2.4 respectively, p < 0.0001), and higher risk of LC (OR = 2.9 and 2.8, respectively, p < 0.0001). Conversely, the OR values decreased to 0.3-0.4 for BC and LC if IgA-Pg levels were higher than IgA-Bp and IgA-Es levels (p < 0.0001). These findings confirm the hypothesis that IgA-Bp and IgA-Es are capable to stimulate, and IgA-Pg, to inhibit the BC and LC occurrence n postmenopausal women. The balance between IgA-Bp and IgA-Es, on the one hand, and IgA-Pg, on the other hand, is much more important than individual contents of these antibodies.In conclusion, the phenomenon of “immunological interference” is revealed, i.e., the mutual enhancement of IgA-Bp and IgA-Es effects, thus, probably, stimulating the initial and subsequent events of carcinogenesis initiation and promotion, with a weak anticancer effect of IgA-Pg, and by weakening the mutual procarcinogenic effects of IgA-Bp and IgA-Es by the marked effect of IgA-Pg.

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