Alterations in RCAS1 serum concentration levels during the normal menstrual cycle and the lack of analogical changes in ovarian endometriosis

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Abstract

PROBLEM: The selective suppression phenomenon of the cytotoxic immune response may be brought about by an increase in sRCAS1 blood serum concentration. Such an increase has been observed during cancer progression and decidualization. The aim of this study has been to evaluate alterations in RCAS1 blood serum concentration in women during normal menstrual cycle (NMC) phases and to compare the levels found with those in patients with ovarian endometriosis. METHOD OF STUDY: The sRCAS1 blood serum concentration level was determined for both 147 patients with ovarian endometriosis and a healthy control group. RESULTS: Fluctuations in sRCAS1 blood serum concentration levels correlating with the NMC phases were demonstrated. The highest level of sRCAS1 was found during menstruation and the lowest during the proliferative cycle phase. However, no such fluctuations correlating with menstrual cycle phases were observed in the patients with endometriosis. The level of sRCAS1 in patients with endometriosis remained almost constant. Moreover, the sRCAS1 blood serum concentration level has been shown to increase, as ovarian endometriosis progresses. CONCLUSION: RCAS1 blood serum concentration may be a useful indicator of the selective suppression of the immune cytotoxic cell phenomenon associated with the development of endometriosis.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Antigens, Neoplasm Endometriosis Menstrual Cycle Ovarian Diseases Antigens, Neoplasm Antigens, Neoplasm Disease Progression Endometriosis Endometriosis Enzyme-Linked Immunosorbent Assay Female Humans Immune Tolerance Menstrual Cycle Menstrual Cycle Ovarian Diseases Ovarian Diseases

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europepmc
last seen: 2026-06-04T01:30:01.192114+00:00
pubmed
last seen: 2026-05-13T22:14:36.758325+00:00
unpaywall
last seen: 2026-06-02T02:00:03.124865+00:00
License: public-domain-us · commercial use OK · attribution required
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