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A Hypothetical Model Suggesting Some Possible Ways That the Progesterone Receptor May Be Involved in Cancer
Jerome H Check1,2, Diane L Check2
1Department of Obstetrics and Gynecology, Division of Reproductive Endocrinology & Infertility, Cooper Medical School of Rowan University, Camden, NJ 08103, USA.
Abstract:
Cancer and the fetal-placental semi-allograft share certain characteristics, e.g., rapid proliferation, the capacity to invade normal tissue, and, related to the presence of antigens foreign to the host, the need to evade immune surveillance. Many present-day methods to treat cancer use drugs that can block a key molecule that is important for one or more of these characteristics and thus reduce side effects. The ideal molecule would be one that is essential for both the survival of the fetus and malignant tumor, but not needed for normal cells. There is a potential suitable candidate, the progesterone induced blocking factor (PIBF). The parent 90 kilodalton (kDa) form seems to be required for cell-cycle regulation, required by both the fetal-placental unit and malignant tumors. The parent form may be converted to splice variants that help both the fetus and tumors escape immune surveillance, especially in the fetal and tumor microenvironment. Evidence suggests that membrane progesterone receptors are involved in PIBF production, and indeed there has been anecdotal evidence that progesterone receptor antagonists, e.g., mifepristone, can significantly improve longevity and quality of life, with few side effects.
Insights
The progesterone induced blocking factor (PIBF) is crucial for both fetal development and tumor growth, offering a potential target for cancer therapy. Blocking PIBF may improve cancer patient outcomes with minimal side effects.
Area of Science:
- Immunology
- Oncology
- Reproductive Biology
Background:
- Cancer and the fetal-placental unit share traits like rapid proliferation, invasion, and immune evasion.
- Current cancer treatments target key molecules, aiming to reduce side effects.
- An ideal therapeutic target would be essential for both fetal survival and tumor growth, but not normal cells.
Purpose of the Study:
- To investigate the progesterone induced blocking factor (PIBF) as a potential therapeutic target for cancer.
- To explore the role of PIBF in cell-cycle regulation and immune evasion in both fetal and tumor microenvironments.
Main Methods:
- Review of existing literature on PIBF, cancer biology, and fetal-placental immunology.
- Analysis of the proposed role of PIBF in cell-cycle regulation and immune surveillance.
- Consideration of evidence linking membrane progesterone receptors and PIBF production.
Main Results:
- The 90 kDa form of PIBF is essential for cell-cycle regulation in both fetal-placental units and tumors.
- PIBF splice variants may facilitate immune evasion in fetal and tumor microenvironments.
- Progesterone receptor antagonists, like mifepristone, show anecdotal promise in improving cancer patient longevity and quality of life with few side effects.
Conclusions:
- PIBF is a promising candidate for cancer therapy due to its dual role in fetal and tumor survival.
- Targeting PIBF, potentially via progesterone receptor antagonists, could offer a novel treatment strategy with reduced toxicity.
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