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Medical Science Monitor 2002-Jun

Does the negative correlation found in breast cancer patients between plasma melatonin and insulin-like growth factor-I concentrations imply the existence of an additional mechanism of oncostatic melatonin influence involved in defense?

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Dariusz Kajdaniuk
Bogdan Marek
Beata Kos-Kudła
Krystyna Zwirska-Korczala
Zofia Ostrowska
Barbara Buntner
Jan Szymszal

Mots clés

Abstrait

BACKGROUND

Insulin-like growth factor-I (IGF-I) is probably involved in promoting both normal and neoplastic cell growth, neoplastic transformation processes, angiogenesis, and neoplasma progression. On the other hand, one possible mechanism of the oncostatic action of melatonin is its influence on the action and/or release of the growth factors that stimulate neoplastic cell growth. Quantitative changes in melatonin and IGF-I, as well as an imbalance between melatonin and IGF-I, may affect the growth of breast cancer cells and exacerbate the disease. The aim of our research was to study the interactions between plasma melatonin and IGF-I concentrations in pre-menopausal breast cancer patients.

METHODS

Our research involved 24 breast cancer patients (mean age 43 +/-6) with stage II breast cancer (Bloom and Richardson classification), confirmed by histological studies, and were 4 weeks after radical mastectomy. The control group consisted of 16 healthy women volunteers (mean age 44 +/- 5).

RESULTS

No statistically significant relations were found between mean plasma melatonin and IGF-I concentrations in the two study groups. In the breast cancer group the correlation coefficient between IGF-I concentration in plasma and melatonin was r = -0.392 (p = 0.058).

CONCLUSIONS

The negative correlation between the plasma melatonin and IGF-I concentrations in the breast cancer patients we studied could reach statistical significance in a larger population. The presence of such a negative correlation between plasma melatonin and IGF-I concentrations in patients with neoplastic disease may imply the existence of an additional defense mechanism based on the oncostatic influence of melatonin.

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