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Journal articles on the topic 'B pr'

Author: Grafiati

Published: 8 November 2023

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1

Yang, F., W. Liu, W. B. Cui, J. N. Feng, and Z. D. Zhang. "Magnetic Properties of Anisotropic Pr–Fe–B/Fe/Pr–Fe–B Films." Journal of Superconductivity and Novel Magnetism 25, no. 6 (April 14, 2012): 2059–62. http://dx.doi.org/10.1007/s10948-012-1563-8.

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2

Wei, L., Y. Zhao, and J. Wang. "The expression of ER, PR, PR-B, PS2 in adenomyosis." Fertility and Sterility 77 (February 2002): S46. http://dx.doi.org/10.1016/s0015-0282(01)03160-0.

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3

Yuane, Erick, Agung Dewanto, and Shofwal Widad. "High Expression of PR-A and Low Expression of PR-B is Correlated with Inflammation in Endometrioma Cases." Indonesian Biomedical Journal 15, no. 1 (February 23, 2023): 85–93. http://dx.doi.org/10.18585/inabj.v15i1.2114.

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BACKGROUND: Progestin therapy has been commonly used in endometriosis. The regulation of progesterone receptors B (PR-B) greatly affects the success rate of therapy in cases of endometriosis. The presence of tumor necrosis factor (TNF)-a in endometriosis triggers PR-B hypermethylation, decreasing PR-B expression and PR-B/A ratio that induce progesterone resistance. It may also occur in endometrioma. Studies regarding the distribution of PR-A and PR-B with TNF-a expression in endometriosis with endometrioma tissue samples has not been elucidated well. Therefore, this study was conducted to measure and compare the distribution of PR-A and PR-B expression, and to assess the effect of PR-B/A ratio on TNF-a in endometrioma and benign cysts.METHODS: A cross-sectional study was conducted by collecting paraffin blocks of endometriomas and benign cysts as controls, from patients undergoing surgery at Dr. Sardjito Hospital, Yogyakarta. Immunohistochemistry was performed to assess the expressions of PR-A, PR-B, TNF-a and PR-B/A ratio, to compared differences between endometriomas and benign cysts.RESULTS: Twenty-three endometrioma and 22 benign cyst tissue samples were collected. The mean PR-B expression and PR-B/A ratio were found to be lower in endometriomas than benign cysts, and mean expression of PR-A and TNF-a in endometriomas was higher than in benign cysts. However, there were no significant correlations between the expression of PR-A, PR-B, PR-B/A ratio, and TNF-a with endometriosis severity.CONCLUSION: In endometrioma cases, the expression of PR-A and TNF-a was higher, while the expression of PR-B and PR-B/A ratio was lower. However, there was no significant relationship between the ratio of PR-B/A and TNF-a.KEYWORDS: progesterone receptor, tumor necrosis factor-alpha, endometriosis, endometrioma, benign cyst, ovarian cyst

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4

Fang, X., S. Wong, and B. F. Mitchell. "Messenger RNA for progesterone receptor isoforms in the late-gestation rat uterus." American Journal of Physiology-Endocrinology and Metabolism 283, no. 6 (December 1, 2002): E1167—E1172. http://dx.doi.org/10.1152/ajpendo.00116.2002.

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The progesterone receptor (PR) has three isoforms, PR-A, PR-B, and PR-C, which have different physiological effects. PR-A may inhibit PR-B-mediated transcription. Parturition requires withdrawal of progesterone (P4). This could occur through decreased P4 concentrations and/or a change in PR isoforms to diminish the effect of P4. We measured mRNA for PR isoforms in rat uterine tissues through late gestation and investigated the effects of antagonists to estrogen (tamoxifen) and P4 (RU-486). Two specific probes were used for ribonuclease protection assays; one (PR-total) measured PR-A, PR-B, and PR-C, and the other recognized only PR-B. PR-total mRNA increased significantly through late gestation, whereas PR-B was unchanged. The ratio of PR-total to PR-B peaked on the day before parturition. Tamoxifen delayed parturition and inhibited the increase in PR-total without affecting PR-B mRNA. RU-486 caused early parturition associated with increased PR-total mRNA, with no change in PR-B. We conclude that there are significant changes in PR isoforms in late-gestation rat uterus. These changes may be regulated by estrogen and P4and may influence the timing of parturition.

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5

Tung, Lin, Hany Abdel-Hafiz, Tianjie Shen, Djuana M. E. Harvell, Lisa K. Nitao, Jennifer K. Richer, Carol A. Sartorius, Glenn S. Takimoto, and Kathryn B. Horwitz. "Progesterone Receptors (PR)-B and -A Regulate Transcription by Different Mechanisms: AF-3 Exerts Regulatory Control over Coactivator Binding to PR-B." Molecular Endocrinology 20, no. 11 (November 1, 2006): 2656–70. http://dx.doi.org/10.1210/me.2006-0105.

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Abstract The two, nearly identical, isoforms of human progesterone receptors (PR), PR-B and -A, share activation functions (AF) 1 and 2, yet they possess markedly different transcriptional profiles, with PR-B being much stronger transactivators. Their differences map to a unique AF3 in the B-upstream segment (BUS), at the far N terminus of PR-B, which is missing in PR-A. Combined mutation of two LXXLL motifs plus tryptophan 140 in BUS, to yield PR-BdL140, completely destroys PR-B activity, because strong AF3 synergism with downstream AF1 and AF2 is eliminated. This synergism involves cooperative interactions among receptor multimers bound at tandem hormone response elements and is transferable to AFs of other nuclear receptors. Other PR-B functions—N-/C-terminal interactions, steroid receptor coactivator-1 coactivation, ligand-dependent down-regulation—also require an intact BUS. All three are autonomous in PR-A, and map to N-terminal regions common to both PR. This suggests that the N-terminal structure adopted by the two PR is different, and that for PR-B, this is controlled by BUS. Indeed, gene expression profiling of breast cancer cells stably expressing PR-B, PR-BdL140, or PR-A shows that mutation of AF3 destroys PR-B-dependent gene transcription without converting PR-B into PR-A. In sum, AF3 in BUS plays a critical modulatory role in PR-B, and in doing so, defines a mechanism for PR-B function that is fundamentally distinct from that of PR-A.

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6

黄, 毅英, 敬魁梁, and 静华田. "Pr-Fe-B三元系." Science in China Series A-Mathematics, Physics, Astronomy & Technological Science (in Chinese) 17, no. 2 (February 1, 1987): 159–69. http://dx.doi.org/10.1360/za1987-17-2-159.

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7

Lin, Hao, Kuo-Chung Lan, Yu-Che Ou, Chen-Hsuan Wu, Hong-Yo Kang, I.-Chieh Chuang, and Hung-Chun Fu. "Highly Expressed Progesterone Receptor B Isoform Increases Platinum Sensitivity and Survival of Ovarian High-Grade Serous Carcinoma." Cancers 13, no. 21 (November 8, 2021): 5578. http://dx.doi.org/10.3390/cancers13215578.

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Background: Expression of the progesterone receptor (PR) has been reported to influence survival outcomes in patients with ovarian high-grade serous carcinoma (HGSC). In the present study, we attempted to investigate the association among PR and its isoforms’ expression, platinum sensitivity, and survival in ovarian HGSC. Material and methods: This retrospective study reviewed ovarian HGSC patients who received surgery followed by adjuvant chemotherapy. We analyzed total PR and PR isoform-B (PR-B) expression by immunohistochemical staining and quantified using the H-score. Then, we compared platinum sensitivity and survival outcomes between those patients with weak and strong PR-B expression. Cisplatin viability assays were carried out in ovarian HGSC cell lines (OC-3-VGH and OVCAR-3) with different PR-B expression. Results: Among 90 patients, 49 and 41 patients were considered to have platinum-sensitive and platinum-resistant disease, respectively. Pearson’s correlation model showed that the H-score of total PR correlated positively with PR-B (r = 0.813). The PR-B H-score of tumors was significantly higher in the platinum-sensitive group (p = 0.004). Multivariate analysis revealed that the PR-B H-score and optimal debulking status were independent factors predicting platinum sensitivity. When compared with strong PR-B expression, patients with weak PR-B had significantly poorer progression-free (p = 0.021) and cancer-specific survival (p = 0.046). In a cell model, cisplatin-resistant OC-3-VGH cells expressed a lower level of PR-B than wild-type cells. Overexpression of PR-B or progesterone could increase cisplatin sensitivity in both OC-3-VGH and OVCAR-3 cells via the mechanism of promoting cisplatin-related apoptosis. Conclusions: When compared to weak PR-B, ovarian HGSC patients with a strong PR-B expression had a better chance of platinum sensitivity and survival, and this finding was compatible with our experimental results. Progesterone seemed to be a platinum sensitizer, but the value of adding progesterone in the treatment of ovarian HGSC should be further investigated.

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8

Taylor, Anthony H., Penny C. McParland, David J. Taylor, and Stephen C. Bell. "The Progesterone Receptor in Human Term Amniochorion and Placenta Is Isoform C." Endocrinology 147, no. 2 (February 1, 2006): 687–93. http://dx.doi.org/10.1210/en.2005-0510.

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The mechanism that initiates human parturition has been proposed to be functional progesterone withdrawal whereby the 116-kDa B isoform of the progesterone receptor (PR-B) switches in favor of the 94-kDa A isoform (PR-A) in reproductive tissues. Recently other PR isoforms, PR-S, PR-C, and PR-M generated from the same gene have been identified and partially characterized. Using immunohistochemical, Western blotting, and RT-PCR techniques, evidence is provided that the major PR isoform present in human term fetal membranes (amnion and chorion) and syncytiotrophoblast of the placenta is neither of the classical nuclear PR-B or PR-A isoforms but is the N terminally truncated 60-kDa PR-C isoform. Evidence is also provided that the PR-C isoform resides in the cytoplasm of the expressing cell types. Data are also presented to show that PR-B, PR-A, and PR-S isoforms are essentially absent from the amnion and chorion, whereas PR isoforms A, B, C, and S are all present in the decidua, with PR-A being the major isoform. The syncytiotrophoblast of the placenta contains the cytoplasmic PR-C isoform but not PR-A, PR-B, or PR-S. The major PR isoform in the amnion, chorion, and placenta is PR-C, suggesting that the cytoplasmic PR-C isoform has a specific role in extraembryonic tissues and may be involved in the regulation of human parturition.

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9

Attia, George R., Khaled Zeitoun, Dean Edwards, Alan Johns, Bruce R. Carr, and Serdar E. Bulun. "Progesterone Receptor Isoform A But Not B Is Expressed in Endometriosis1." Journal of Clinical Endocrinology & Metabolism 85, no. 8 (August 1, 2000): 2897–902. http://dx.doi.org/10.1210/jcem.85.8.6739.

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We previously demonstrated that 17β hydroxysteroid dehydrogenase type 2, the enzyme that inactivates estradiol to estrone, is expressed in luteal eutopic endometrium in response to progesterone but not in simultaneously biopsied peritoneal endometriotic tissue. This molecular evidence of progesterone resistance, together with the clinical observation of resistance of endometriosis to treatment with progestins, led us to determine the levels of progesterone receptor (PR) isoforms PR-A and PR-B in eutopic endometrial and extra-ovarian endometriotic tissues. It was proposed that progesterone action on target genes is mediated primarily by homodimers of PR-B, whereas the truncated variant PR-A acts as a repressor of PR-B function. Immunoprecipitation, followed by Western blot analysis, was performed to detect bands specific for PR-A and PR-B in paired samples of endometriotic and eutopic endometrial tissues simultaneously biopsed from 18 women undergoing laparoscopy during various phases of the menstrual cycle. PR-B was present in 17 of 18 eutopic endometrial samples, and its level increased in the preovulatory phase, as expected, whereas PR-A was detected in all samples (n = 18) with a similar, but less prominent, cyclic variation in its levels. In endometriotic samples, however, no detectable PR-B could be demonstrated, whereas PR-A was detected in all samples (n = 18), albeit in much lower levels and without any cyclic variation in contrast with the eutopic endometrium. Levels of PR-A and PR-B in endometriotic and eutopic endometrial tissues were determined and compared after normalization to total protein and estrogen receptor-α levels. Using RNase protection assay, we also demonstrated indirectly that only PR-A transcripts were present in endometriotic tissue samples (n = 8), whereas both PR-A and PR-B transcripts were readily detectable in all eutopic endometrial samples (n = 8). This was indicative that failure to detect PR-B protein in endometriotic tissues is due to the absence of PR-B transcripts. We conclude that progesterone resistance in endometriotic tissue from laboratory and clinical observations may be accounted for by the presence of the inhibitory PR isoform PR-A and the absence of the stimulatory isoform PR-B.

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10

Ilicic, Marina, Tamas Zakar, and Jonathan W. Paul. "Modulation of Progesterone Receptor Isoform Expression in Pregnant Human Myometrium." BioMed Research International 2017 (2017): 1–17. http://dx.doi.org/10.1155/2017/4589214.

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Background. Regulation of myometrial progesterone receptor (PR) expression is an unresolved issue central to understanding the mechanism of functional progesterone withdrawal and initiation of labor in women. Objectives. To determine whether pregnant human myometrium undergoes culture-induced changes in PR isoform expression ex situ and, further, to determine if conditions approaching the in vivo environment stabilise PR isoform expression in culture. Methods. Term nonlaboring human myometrial tissues were cultured under specific conditions: serum supplementation, steroids, stretch, cAMP, PMA, PGF2α, NF-κB inhibitors, or TSA. Following 48 h culture, PR-T, PR-A, and PR-B mRNA levels were determined using qRT-PCR. PR-A/PR-B ratios were calculated. Results. PR-T and PR-A expression and the PR-A/PR-B ratio significantly increased in culture. Steroids prevented the culture-induced increase in PR-T and PR-A expression. Stretch blocked the effects of steroids on PR-T and PR-A expression. PMA further increased the PR-A/PR-B ratio, while TSA blocked culture-induced increases of PR-A expression and the PR-A/PR-B ratio. Conclusion. Human myometrial tissue in culture undergoes changes in PR gene expression consistent with transition toward a laboring phenotype. TSA maintained the nonlaboring PR isoform expression pattern. This suggests that preserving histone and/or nonhistone protein acetylation is critical for maintaining the progesterone dependent quiescent phenotype of human myometrium in culture.

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11

Sun, Yu, and Yuguo Sun. "Strong Effect of Process Parameters on the Properties of Boron-Containing Phenolic Resins with High Char Yield." Applied Sciences 10, no. 4 (February 19, 2020): 1408. http://dx.doi.org/10.3390/app10041408.

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This work is focused on the optimization of critical process parameters for preparation of boron-containing phenolic resin (B-containing PR), including the molar ratios of formaldehyde/phenol and potassium borate/phenol, reaction time; and measurement of surface tension of B-containing PR solution and wettability between B-containing PR solution and carbon fibers. The effects of the formaldehyde/phenol and potassium borate/phenol molar ratios on the char yield of the B-containing PR was studied. The highest char yield of B-containing PR could be as high as 71% under optimal conditions (molar ratios of formaldehyde/phenol = 1.8 and potassium borate/phenol = 0.2, and reaction time = 13 h). The effect of concentration and tested temperature on the surface tension of B-containing PR solution was investigated, and the wettability between B-containing PR solution and carbon fibers was evaluated for the first time, providing useful theory and experimental data for the preparation of B-containing PR-based composites.

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12

Truong, Thu H., Amy R. Dwyer, Caroline H. Diep, Hsiangyu Hu, Kyla M. Hagen, and Carol A. Lange. "Phosphorylated Progesterone Receptor Isoforms Mediate Opposing Stem Cell and Proliferative Breast Cancer Cell Fates." Endocrinology 160, no. 2 (December 28, 2018): 430–46. http://dx.doi.org/10.1210/en.2018-00990.

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Abstract Progesterone receptors (PRs) are key modifiers of estrogen receptor (ER) target genes and drivers of luminal breast cancer progression. Total PR expression, rather than isoform-specific PR expression, is measured in breast tumors as an indicator of functional ER. We identified phenotypic differences between PR-A and PR-B in luminal breast cancer models with a focus on tumorsphere biology. Our findings indicated that PR-A is a dominant driver of cancer stem cell (CSC) expansion in T47D models, and PR-B is a potent driver of anchorage-independent proliferation. PR-A+ tumorspheres were enriched for aldehyde dehydrogenase (ALDH) activity, CD44+/CD24−, and CD49f+/CD24− cell populations relative to PR-B+ tumorspheres. Progestin promoted heightened expression of known CSC-associated target genes in PR-A+ but not PR-B+ cells cultured as tumorspheres. We report robust phosphorylation of PR-A relative to PR-B Ser294 and found that this residue is required for PR-A–induced expression of CSC-associated genes and CSC behavior. Cells expressing PR-A S294A exhibited impaired CSC phenotypes but heightened anchorage-independent cell proliferation. The PR target gene and coactivator, FOXO1, promoted PR phosphorylation and tumorsphere formation. The FOXO1 inhibitor (AS1842856) alone or combined with onapristone (PR antagonist), blunted phosphorylated PR, and tumorsphere formation in PR-A+ and PR-B+ T47D, MCF7, and BT474 models. Our data revealed unique isoform-specific functions of phosphorylated PRs as modulators of distinct and opposing pathways relevant to mechanisms of late recurrence. A clear understanding of PR isoforms, phosphorylation events, and the role of cofactors could lead to novel biomarkers of advanced tumor behavior and reveal new approaches to pharmacologically target CSCs in luminal breast cancer.

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13

Wang, C. P., Y. Shi, D. Wang, Y. Lu, D. L. Zhao, and X. J. Liu. "Thermodynamic assessment of the B–Ce and B–Pr systems." Calphad 41 (June 2013): 150–55. http://dx.doi.org/10.1016/j.calphad.2013.03.001.

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14

Qiu, Ming, Abby Olsen, Emily Faivre, Kathryn B. Horwitz, and Carol A. Lange. "Mitogen-Activated Protein Kinase Regulates Nuclear Association of Human Progesterone Receptors." Molecular Endocrinology 17, no. 4 (April 1, 2003): 628–42. http://dx.doi.org/10.1210/me.2002-0378.

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Abstract Breast cancers often have increased MAPK activity; this pathway may drive breast cancer cell growth by targeting steroid hormone receptors. MAPK phosphorylates human progesterone receptors (PRs) on Ser294, thus regulating several aspects of PR activity. To study the role of PR Ser294 phosphorylation on subcellular distribution, we stably expressed wild-type (wt) or S294A (Ser294 to Ala) PR-B in several cell types. PRs phosphorylated on Ser294 were nuclear. Activation of MAPK induced Ser294 phosphorylation and rapid nuclear translocation of wt, but not S294A, PR-B; both receptors concentrated in the nucleus after progestin treatment. The MAPK kinase inhibitor, U0126, blocked epidermal growth factor but not progestin-induced Ser294 phosphorylation and translocation of wt PR, indicating a novel mechanism for nuclear localization. After progestin treatment, wt PR-B underwent ligand-dependent down-regulation, while S294A PR-B persisted in nuclei. Prolonged treatment with U0126 or the nuclear export inhibitor, leptomycin B, promoted nuclear accumulation of wt PR-B and blocked ligand-dependent PR down-regulation, suggesting that PR degradation occurs in the cytoplasm and requires MAPK-dependent nuclear export. Stabilization of PRs by leptomycin B also blocked PR transcriptional activity, indicating a link between nucleocytoplasmic shuttling, receptor stability, and function. These results support a regulatory role for MAPK in nuclear steroid hormone receptor subcellular localization and coupling to multiple PR functions.

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15

NANAO, Tomohisa, Masato KOIKE, Junji YAMAGUCHI, Mitsuho SASAKI, and Yasuo UCHIYAMA. "Cellular localization and tissue distribution of endogenous DFCP1 protein ." Biomedical Research 36, no. 2 (2015): 121–33. http://dx.doi.org/10.2220/biomedres.36.121.

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16

Jennings, H. J., A. Gamian, and F. E. Ashton. "N-propionylated group B meningococcal polysaccharide mimics a unique epitope on group B Neisseria meningitidis." Journal of Experimental Medicine 165, no. 4 (April 1, 1987): 1207–11. http://dx.doi.org/10.1084/jem.165.4.1207.

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Antibodies induced in mice by the N-propionyl (N-Pr)-group B meningococcal polysaccharide (GBMP)-tetanus toxoid (TT) conjugate were bactericidal for GBM organisms independent of protein serotype. The antisera contained two populations of N-Pr-GBMP-specific antibodies, only one of which crossreacted with the GBMP. Particularly significant was the fact that the bactericidal activity was mainly associated with the population of antibodies that did not crossreact with the GBMP. Therefore it can be inferred from the above evidence that the N-Pr-GBMP mimics a unique epitope on the surface of GBM organisms that is not present on the exogenous GBMP.

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17

Shimoda, Tatsuya. "Hot-Deformed Pr-Fe-B-Cu Magnet." Materia Japan 33, no. 6 (1994): 782–90. http://dx.doi.org/10.2320/materia.33.782.

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18

Shimoda, T., K. Akioka, O. Kobayashi, and T. Yamagami. "High‐energy cast Pr‐Fe‐B magnets." Journal of Applied Physics 64, no. 10 (November 15, 1988): 5290–92. http://dx.doi.org/10.1063/1.342395.

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19

Shimoda, T., K. Akioka, O. Kobayashi, and T. Yamagami. "MICROSTRUCTURE OF CAST Pr-Fe-B MAGNETS." Le Journal de Physique Colloques 49, no. C8 (December 1988): C8–631—C8–632. http://dx.doi.org/10.1051/jphyscol:19888285.

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20

Paik, C. R., M. Okada, and M. Homma. "Anisotropic Pr-Fe-B melt-spun ribbons." IEEE Transactions on Magnetics 26, no. 5 (1990): 1730–32. http://dx.doi.org/10.1109/20.104507.

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21

Layer, Cordula, Gisela Gille, Christine Klapp, and Ulrike Ravens-Sieberer. "Pr�vention der Hepatitis B bei Jugendlichen." Medizinische Klinik 99, no. 12 (December 2004): 703–7. http://dx.doi.org/10.1007/s00063-004-1087-5.

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22

Bethea, Cynthia L., and Andrea A. Widmann. "Differential Expression of Progestin Receptor Isoforms in the Hypothalamus, Pituitary, and Endometrium of Rhesus Macaques*." Endocrinology 139, no. 2 (February 1, 1998): 677–87. http://dx.doi.org/10.1210/endo.139.2.5752.

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Abstract The progestin receptor exists in at least two isoforms: a long form (PR-B) and a short form (PR-A), which can be separated and detected with Western blot analysis. It has been suggested from in vitro transfection experiments that differential expression of the two isoforms may provide one mechanism for tissue specific actions of progesterone (P). However, more information from in vivo experimentation is needed. It has been reported that P down-regulates the expression of PR in the endometrium and pituitary of E primed macaques. However, PR protein and PR messenger RNA expression in the hypothalamus is maintained with P treatment of E-primed macaques. Thus, there is tissue-specific regulation of PR by its cognate ligand in the nonhuman primate. To gain insight into the tissue-specific regulation of PR by P, we questioned whether differential expression of the isoforms of PR exists in the endometrium, pituitary, and hypothalamus of rhesus monkeys. The expression of PR-A and PR-B was examined after E (28–30 days) and E + P (14 days E + 14 days E + P) treatment in the primate endometrium, pituitary, and hypothalamus. After E or E + P treatment, the levels of PR-A were 5 times higher than PR-B in the endometrium. PR-A was 1.6-fold higher than PR-B in the pituitary. In the hypothalamus, the ratio of A to B ranged from less than 1 (B exceeds A) to unity (A and B equimolar). There was no difference in the ratio of A to B between E-treated and E + P-treated groups in any tissue examined. These observations (a) provide further support of the hypothesis that differential expression of the isoforms of PR may subserve the tissue specific actions of P and (b) also suggest that P does not differentially affect the expression of the isoforms of its cognate receptor in the endometrium, pituitary, or hypothalamus.

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23

Setiawan, Arief, Ruswana Anwar, Mas Rizky Anggun Adipurna Syamsunarno, Johanes Cornelius Mose, Budi Santoso, Ani Melani Maskoen, Wiryawan Permadi, Budi Setiabudiawan, Meita Dhamayanti, and Yudi Mulyana Hidayat. "Epigenetic Regulation Interplays with Endometriosis Pathogenesis in Low-Birth-Weight Patients via the Progesterone Receptor B–VEGF-DNMT1 Axis." Diagnostics 13, no. 12 (June 16, 2023): 2085. http://dx.doi.org/10.3390/diagnostics13122085.

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Background: Low birth weight (LBW) is a risk factor associated with endometriosis. Our study aimed to analyze the risk of endometriosis in women with a LBW history and the relationships of progesterone receptor B (PR-B) gene promoter methylation, DNA methyltransferase-1 (DNMT1) expression, PR-B expression, and vascular endothelial growth factors (VEGF) with endometriosis. Methods: This study was conducted in two stages, a retrospective case-control design and a cross-sectional design, with 52 cases of endometriosis and 30 controls, which were further subdivided into LBW and non-LBW groups, at Hasan Sadikin General Hospital and its hospital networks from October 2017 to August 2021. Menstrual blood was taken from subjects and analyzed using pyrosequencing techniques to assess DNA methylation, while q-RT PCR was used to assess gene expression. Results: There were significant differences in PR-B methylation, DNMT1 expression, PR-B expression, and VEGF expression (p < 0.001) between the case and control groups. There was a significant negative correlation between PR-B methylation and PR-B expression (r = −0.558; p = 0.047). Based on a multiple logistic analysis, the most dominant factor affecting endometriosis incidence is PR-B (OR 10.40, 95% CI 3.24–33.4, R2 = 45.8). We found that patients with a low birth weight history had a 1.41-times-higher risk of developing endometriosis (95% CI 0.57–3.49, p = 0.113), although the relationship was not statistically significant. Conclusion: Endometriosis is associated with PR-B gene promoter hypermethylation, decreased PR-B expression, and increased DNMT1 and VEGF expression. The methylation of PR-B is the most dominant factor affecting endometriosis incidence.

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24

Lim, Sooyeun, Yoojin Lee, Jungbin Kim, Hyunjin Cho, Keunho Yang, Kyeongmee Park, Jiyoung Kim, Youngjoo Sin, Yeyoung Seo, and Geumhee Gwak. "Progesterone Receptor Expression as a Prognostic Factor in Luminal B Breast Cancer." Journal of Breast Disease 10, no. 1 (June 30, 2022): 46–52. http://dx.doi.org/10.14449/jbd.2022.10.1.46.

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Purpose: The luminal subtype of breast cancer has heterogeneous biological characteristics with respect to the expression of estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor-2 (HER2), and Ki-67. We analyzed luminal B breast cancer subcategorized by PR expression and identified clinically relevant prognostic factors.Methods: We collected the clinical and pathologic data of 247 breast cancer patients (stage 1-4) who were diagnosed with luminal B subtype, defined as ER- and/or PR-positive and/or HER2-positive and with a high Ki-67 proliferation index (>14%). We classified them into PR intact and PR low groups according to PR expression pattern. We also analyzed the clinical and pathological data of each group, including age at diagnosis, tumor size, node metastasis, breast and axillary operative method, margin involvement, tumor-node-metastasis (TNM) stage, histological grade, nuclear grade, number of tumors, and expression of ER, PR, Ki-67, and Bcl-2; evaluated recurrence or metastatic characteristics; and analyzed disease-free survival (DFS) and overall survival (OS) in both groups.Results: Among the 247 luminal B breast cancer patients (stage 1-4), 141 were classified into the PR intact group (57.1%) and 106 into the PR low group (42.9%). The PR low group was associated with age >50 years (p=0.001), low Bcl-2 expression (p<0.001), and high proportion of mastectomies (p<0.001). DFS and OS were significantly lower in the PR low group (p=0.025 and 0.024, respectively).Conclusion: This study showed that decreased in PR expression (PR low group) in luminal B breast cancer was related to poor prognosis compared to normal PR expression (PR intact group).

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25

OKUMA, Tomotake, Makoto HIRATA, Fumiko YANO, Daisuke MORI, Hiroshi KAWAGUCHI, Ung-il CHUNG, Sakae TANAKA, and Taku SAITO. "Regulation of mouse chondrocyte differentiation by CCAAT/enhancer-binding proteins ." Biomedical Research 36, no. 1 (2015): 21–29. http://dx.doi.org/10.2220/biomedres.36.21.

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26

Lehtinen, Sanna. "B. Janz, Place, space and hermeneutics." Phenomenological Reviews 4, no. 1 (2018): 35. http://dx.doi.org/10.19079/pr.4.1.35.

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27

Gabor, Octavian. "B. Butcher, Liturgical theology after Schmemann." Phenomenological Reviews 5 (2019): 7. http://dx.doi.org/10.19079/pr.5.7.

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Shimada, M., Y. Yamashita, J. Ito, T. Okazaki, K. Kawahata, and M. Nishibori. "Expression of two progesterone receptor isoforms in cumulus cells and their roles during meiotic resumption of porcine oocytes." Journal of Molecular Endocrinology 33, no. 1 (August 1, 2004): 209–25. http://dx.doi.org/10.1677/jme.0.0330209.

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The present study aimed to investigate progesterone receptor (PR) gene expression in cumulus cells and their roles during meiotic resumption of porcine oocytes. The amount of PR-A or PR-B mRNA was analyzed by RT-PCR using primer sets for the PR-B region or the PR-A/B common region. The level of PR-B mRNA in cumulus cells was up-regulated by FSH and LH during the first 8 h of cultivation but the level significantly decreased at 12 h. However, a high level of total PR mRNA was maintained up to a cultivation period of 20 h. The level of PR-B protein in cumulus cells reached its maximum at 4 to 12 h, whereas PR-A predominated in cumulus cells of cumulus-oocyte complexes (COCs) at 20 h. Accompanying the shift in expression of PR isoforms, progesterone production in cumulus cells was significantly increased, and both the proliferative activity of cumulus cells during a 10- to 20-h cultivation period and the level of connexin-43, a major component of the gap junction, in cumulus cells significantly decreased. When COCs were cultured with FSH and LH for 10 h and then further cultured with additional RU486, there was a significant suppression in the shift in PR isoforms and in progesterone production, a loss of proliferative activity, and a decrease in connexin-43 mRNA in cumulus cells. Moreover, treatment with RU486 after 10-h cultivation of COCs inhibited the meiotic resumption of oocytes and cumulus cell expansion. These results suggest that the induction of PR isoforms in cumulus cells and their binding to progesterone appear to impact on proliferation and differentiation in a time-dependent manner, and the shift from PR-B to PR-A may help mediate certain events.

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Gracanin, Ana, Monique E. van Wolferen, Carol A. Sartorius, Arjan B. Brenkman, Willem G. Schoonen, and Jan A. Mol. "Canid Progesterone Receptors Lack Activation Function 3 Domain-Dependent Activity." Endocrinology 153, no. 12 (December 1, 2012): 6104–13. http://dx.doi.org/10.1210/en.2012-1793.

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Abstract Progesterone regulates multiple behavioral, physiological, and pathological aspects of female reproductive biology through its two progesterone receptors (PRs), PR-B and the truncated PR-A. PR-B is necessary for mammary gland development in mice and, compared with PR-A, is overall a stronger transactivator of target genes due to an additional activation function 3 (AF3) domain. In dogs, known for their high sensitivity to progesterone-induced mammary cancer, the PR-B function was studied. Canine PR (cPR)-B appeared to contain multiple mutations within AF3 core sequence motifs and lacks N-terminal ligand-independent posttranslational modifications. Consequently, cPR-B has a weak transactivation potential on progesterone-responsive mouse mammary tumor virus-luc and progesterone response element 2-luc reporters transiently transfected in hamster, human, or canine cells and also on known target genes FKBP5 and SGK in doxycycline-inducible, stable transfected cPR-B in canine mammary cells. The cPR-B function was restored to the level of human PR-B by the replacement of canine AF3 domain with the human one. The lack of AF3 domain-dependent transcriptional activity was unique for canids (gray wolf, red fox, and raccoon dog) and not present in closely related caniform species (brown bear, gray seal, and domestic ferret). Despite the limited transactivation potential, canids develop normal mammary glands and frequently mammary tumors. Therefore, these results question the role of PR-B in breast cancer development and may explain unique features of canid reproduction.

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Wu, Yan, Estil Strawn, Zainab Basir, Gloria Halverson, and Sun-Wei Guo. "Promoter Hypermethylation of Progesterone Receptor Isoform B (PR-B) in Endometriosis." Epigenetics 1, no. 2 (April 2006): 106–11. http://dx.doi.org/10.4161/epi.1.2.2766.

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Gordon, Ana, José C. Garrido-Gracia, Rafaela Aguilar, and José E. Sánchez-Criado. "Understanding the regulation of pituitary progesterone receptor expression and phosphorylation." REPRODUCTION 149, no. 6 (June 2015): 615–23. http://dx.doi.org/10.1530/rep-14-0592.

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Administration of human FSH (hFSH) during the diestrus phase in cyclic rats is followed by a reduction in the preovulatory LH surge. This inhibitory action of FSH involves a decrease in the stimulatory effect of gonadotrope progesterone receptor (PR) activation, in a ligand-dependent (progesterone) and -independent (GNRH) manner. PR activation and action are mandatory for LH surge, and are dependent on the phosphorylation of serine (Ser) residues. Together with this post-translational modification, PR is marked for downregulation by proteasome machinery. These experiments used the western blotting technique to measure pituitary expression of PR-A and PR-B isoforms and phosphorylation levels of Ser294 and Ser400 PR-B in rats bearing i) hFSH treatment or ii) PR downregulation. Treatment with hFSH reduced LH secretion and increased that of estradiol in proestrus afternoon. hFSH injections, without altering PR-A and PR-B content or ratio, caused a reduction in phosphorylation of Ser294 and Ser400 but only when pituitaries were previously challenged with progesterone or GNRH for 2 h. However, while pSer294 levels increased after 2 h of pituitary incubation with progesterone or GNRH, those of pSer400 were not modified by thesein vitrotreatments. Finally, progesterone had a biphasic effect: in 2-h incubations increased pituitary PR-A and PR-B content, but after 8 h caused downregulation and altered PR-A:PR-B ratio. The results provide a potential mechanism through which LH levels are decreased by hFSH administration and better understanding of the control of PR expression and phosphorylation in rat pituitaries.

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Zhang, Xun, M. Jeyakumar, Sergei Petukhov, and Milan K. Bagchi. "A Nuclear Receptor Corepressor Modulates Transcriptional Activity of Antagonist-Occupied Steroid Hormone Receptor." Molecular Endocrinology 12, no. 4 (April 1, 1998): 513–24. http://dx.doi.org/10.1210/mend.12.4.0089.

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Abstract Synthetic steroid hormone antagonists are clinically important compounds that regulate physiological responses to steroid hormones. The antagonists bind to the hormone receptors, which are ligand-inducible transcription factors, and modulate their gene-regulatory activities. In most instances, a steroid receptor, such as progesterone receptor (PR) or estrogen receptor (ER), is transcriptionally inactive when complexed with an antagonist and competitively inhibits transactivation of a target steroid-responsive gene by the cognate hormone-occupied receptor. In certain cellular and promoter contexts, however, antagonist-occupied PR or ER acquires paradoxical agonist-like activity. The cellular mechanisms that determine the switch from the negative to the positive mode of transcriptional regulation by an antagonist-bound steroid receptor are unknown. We now provide strong evidence supporting the existence of a cellular inhibitory cofactor that interacts with the B form of human PR (PR-B) complexed with the antiprogestin RU486 to maintain it in a transcriptionally inactive state. In the presence of unliganded thyroid hormone receptor (TR) or ER complexed with the antiestrogen 4-hydroxytamoxifen, which presumably sequesters a limiting pool of the inhibitory cofactor, RU486-PR-B functions as a transcriptional activator of a progesterone-responsive gene even in the absence of hormone agonist. In contrast, hormone-occupied TR or ER fails to induce transactivation by RU486-PR-B. Recent studies revealed that a transcriptional corepressor, NCoR (nuclear receptor corepressor), interacts with unliganded TR but not with liganded TR. Interestingly, coexpression of NCoR efficiently suppresses the partial agonistic activity of antagonist-occupied PR-B but fails to affect transactivation by agonist-bound PR-B. We further demonstrate that RU486-PR-B interacts physically with NCoR in vitro. These novel observations suggest that the inhibitory cofactor that associates with RU486-PR-B and represses its transcriptional activity is either identical or structurally related to the corepressor NCoR. We propose that cellular mechanisms that determine the switch from the antagonistic to the agonistic activity of RU486-PR-B involve removal of the corepressor from the antagonist-bound receptor so that it can effect partial but significant gene activation.

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Tetel, Marc J., Paloma H. Giangrande, Susan A. Leonhardt, Donald P. McDonnell, and Dean P. Edwards. "Hormone-Dependent Interaction between the Amino- and Carboxyl-Terminal Domains of Progesterone Receptor in Vitro and in Vivo." Molecular Endocrinology 13, no. 6 (June 1, 1999): 910–24. http://dx.doi.org/10.1210/mend.13.6.0300.

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Abstract Full transcriptional activation by steroid hormone receptors requires functional synergy between two transcriptional activation domains (AF) located in the amino (AF-1) and carboxyl (AF-2) terminal regions. One possible mechanism for achieving this functional synergy is a physical intramolecular association between amino (N-) and carboxyl (C-) domains of the receptor. Human progesterone receptor (PR) is expressed in two forms that have distinct functional activities: full-length PR-B and the amino-terminally truncated PR-A. PR-B is generally a stronger activator than PR-A, whereas under certain conditions PR-A can act as a repressor in trans of other steroid receptors. We have analyzed whether separately expressed N- (PR-A and PR-B) and C-domains [hinge plus ligand-binding domain (hLBD)] of PR can functionally interact within cells by mammalian two-hybrid assay and whether this involves direct protein contact as determined in vitro with purified expressed domains of PR. A hormone agonist-dependent interaction between N-domains and the hLBD was observed functionally by mammalian two-hybrid assay and by direct protein-protein interaction assay in vitro. With both experimental approaches, N-C domain interactions were not induced by the progestin antagonist RU486. However, in the presence of the progestin agonist R5020, the N-domain of PR-B interacted more efficiently with the hLBD than the N-domain of PR-A. Coexpression of steroid receptor coactivator-1 (SRC-1) and the CREB binding protein (CBP), enhanced functional interaction between N- and C-domains by mammalian two-hybrid assay. However, addition of SRC-1 and CBP in vitro had no influence on direct interaction between purified N- and C-domains. These results suggest that the interaction between N- and C-domains of PR is direct and requires a hormone agonist-induced conformational change in the LBD that is not allowed by antagonists. Additionally, coactivators are not required for physical association between the N- and C-domains but are capable of enhancing a functionally productive interaction. In addition, the more efficient interaction of the hLBD with the N-domain of PR-B, compared with that of PR-A, suggests that distinct interactions between N- and C-terminal regions contribute to functional differences between PR-A and PR-B.

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34

Kablov, E. N., O. G. Ospennikova, V. P. Piskorsky, I. I. Rezchikova, R. A. Valeev, and E. A. Davydova. "Phase composition of the Pr–Dy–Fe–Co–B sintered materials." «Aviation Materials and Technologies», S2 (2015): 5–10. http://dx.doi.org/10.18577/2071-9170-2015-0-s2-5-10.

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Chen, Zhongmin, Yong Keat Lim, and David Brown. "Substitution of Ce for (Nd,Pr) in Melt-Spun (Nd,Pr)–Fe–B Powders." IEEE Transactions on Magnetics 51, no. 11 (November 2015): 1–4. http://dx.doi.org/10.1109/tmag.2015.2437376.

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36

Rump, Jacob. "B. Stawarska, Saussure's linguistics, structuralism, and phenomenology." Phenomenological Reviews 6 (2020): 54. http://dx.doi.org/10.19079/pr.6.54.

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37

González-Orozco, Juan Carlos, Aylin Del Moral-Morales, and Ignacio Camacho-Arroyo. "Progesterone through Progesterone Receptor B Isoform Promotes Rodent Embryonic Oligodendrogenesis." Cells 9, no. 4 (April 14, 2020): 960. http://dx.doi.org/10.3390/cells9040960.

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Oligodendrocytes are the myelinating cells of the central nervous system (CNS). These cells arise during the embryonic development by the specification of the neural stem cells to oligodendroglial progenitor cells (OPC); newly formed OPC proliferate, migrate, differentiate, and mature to myelinating oligodendrocytes in the perinatal period. It is known that progesterone promotes the proliferation and differentiation of OPC in early postnatal life through the activation of the intracellular progesterone receptor (PR). Progesterone supports nerve myelination after spinal cord injury in adults. However, the role of progesterone in embryonic OPC differentiation as well as the specific PR isoform involved in progesterone actions in these cells is unknown. By using primary cultures obtained from the embryonic mouse spinal cord, we showed that embryonic OPC expresses both PR-A and PR-B isoforms. We found that progesterone increases the proliferation, differentiation, and myelination potential of embryonic OPC through its PR by upregulating the expression of oligodendroglial genes such as neuron/glia antigen 2 (NG2), sex determining region Y-box9 (SOX9), myelin basic protein (MBP), 2′,3′-cyclic-nucleotide 3′-phosphodiesterase (CNP1), and NK6 homeobox 1 (NKX 6.1). These effects are likely mediated by PR-B, as they are blocked by the silencing of this isoform. The results suggest that progesterone contributes to the process of oligodendrogenesis during prenatal life through specific activation of PR-B.

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KIMURA, Shunsuke, Junko NIO-KOBAYASHI, Ayuko KISHIMOTO, and Toshihiko IWANAGA. "The broad distribution of GP2 in mucous glands and secretory products ." Biomedical Research 37, no. 6 (2016): 351–58. http://dx.doi.org/10.2220/biomedres.37.351.

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39

Christodoulou, C. N., W. E. Wallace, and T. B. Massalski. "Magnetic hardening of Pr‐Co‐B sintered magnets." Journal of Applied Physics 66, no. 6 (September 15, 1989): 2749–51. http://dx.doi.org/10.1063/1.344197.

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40

Kablov, E. N., R. A. Valeev, V. P. Piskorskii, and A. V. Buzenkov. "Sintering of Pr-Dy-Fe-Co-B materials." Russian Metallurgy (Metally) 2014, no. 5 (May 2014): 406–11. http://dx.doi.org/10.1134/s0036029514050048.

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Gabay, A. M., Y. Zhang, and G. C. Hadjipanayis. "Die-upset hybrid Pr–Fe–B nanocomposite magnets." Applied Physics Letters 85, no. 3 (July 19, 2004): 446–48. http://dx.doi.org/10.1063/1.1773931.

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42

Sultana, D., M. Marinescu, Y. Zhang, and G. C. Hadjipanayis. "Isotropic nanocomposite Pr–Fe–Co–B ribbons with." Physica B: Condensed Matter 384, no. 1-2 (October 2006): 306–9. http://dx.doi.org/10.1016/j.physb.2006.06.018.

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Laufs, A. "B. Schlink , Aktuelle Fragen des pr�natalen Lebensschutzes." MedR Medizinrecht 21, no. 2 (February 1, 2003): 1. http://dx.doi.org/10.1007/s00350-003-0871-1.

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44

Kuz’ma, Yurii B., and S. I. Mikhalenko. "Phase Equilibria in the Pr - Re - B System." Powder Metallurgy and Metal Ceramics 44, no. 1-2 (January 2005): 35–39. http://dx.doi.org/10.1007/s11106-005-0054-x.

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Neiva, A. C., A. P. Tschiptschin, and F. P. Missell. "Phase diagram of the PrFeB system." Journal of Alloys and Compounds 217, no. 2 (February 1995): 273–82. http://dx.doi.org/10.1016/0925-8388(94)01356-x.

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46

Conway, Jay. "B. Fondane, Existential Monday." Phenomenological Reviews 2 (2016): 59. http://dx.doi.org/10.19079/pr.2016.7.con.

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47

Facco, M., P. E. Cogo, M. Simonato, G. Lamonica, E. Santacatterina, E. Baraldi, and A. Baritussio. "Surfactant Proteins A and B (SP-A and SP-B) in Bronchoalveolar Lavages of Children with Chronic Lung Disease." Pediatric Research 70 (November 2011): 512. http://dx.doi.org/10.1038/pr.2011.737.

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48

Faivre, Emily J., and Carol A. Lange. "Progesterone Receptors Upregulate Wnt-1 To Induce Epidermal Growth Factor Receptor Transactivation and c-Src-Dependent Sustained Activation of Erk1/2 Mitogen-Activated Protein Kinase in Breast Cancer Cells." Molecular and Cellular Biology 27, no. 2 (October 30, 2006): 466–80. http://dx.doi.org/10.1128/mcb.01539-06.

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ABSTRACT Progesterone receptor (PR) ligand binding induces rapid and transient (5- to 10-min) activation of cytosolic c-Src-Ras-Erk1/2 mitogen-activated protein kinase (MAPK) signaling that is independent of PR functioning as transcription factors. Here, we have explored the integration of PR-dependent transcription and rapid signaling events in breast cancer cells. PR-B, but not PR-A, induced robust and sustained (6- to 72-h) Erk1/2 activation that was required for elevated cyclin D1 protein but not mRNA levels. Sustained Erk1/2 activation in response to progestins occurred via a novel mechanism distinct from rapid signaling initiated by PR/c-Src interactions and required the PR-B DNA-binding domain (DBD). PR/progestin upregulated epidermal growth factor receptor (EGFR) and Wnt-1. In response to PR-induced Wnt-1 signaling, matrix metalloprotease (MMP)-mediated membrane-proximal shedding of EGFR ligands transactivated EGFR and induced persistent downstream c-Src and Erk1/2 activities. T47D cell anchorage-independent growth was stimulated by progestins and blocked by inhibition of Erk1/2, c-Src, EGFR, or RNA interference of Wnt-1. Similarly, cell growth in soft agar required the PR DBD but was sensitive to disruption of PR/c-Src interactions, suggesting that both PR-B-induced rapid signaling events and nuclear actions contribute to this response. Our discovery that progestins are capable of robust autocrine activation of EGFR and sustained Erk1/2 signaling provides further support for the physiological linkage of growth factor and steroid hormone signaling. PR-B-induced sustained MAPK signaling may provide prosurvival or proliferative advantages to early breast cancer lesions.

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Leonhardt, Susan A., Magda Altmann, and Dean P. Edwards. "Agonist and Antagonists Induce Homodimerization and Mixed Ligand Heterodimerization of Human Progesterone Receptors in Vivo by a Mammalian Two-Hybrid Assay." Molecular Endocrinology 12, no. 12 (December 1, 1998): 1914–30. http://dx.doi.org/10.1210/mend.12.12.0210.

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Abstract This study utilizes the mammalian two-hybrid system to examine the role of ligand in the dimerization of human progesterone receptor (hPR). The GAL4 DNA-binding domain and the herpes simplex virus VP16 transactivation domain were fused to the amino terminus of full-length hPR (both the A and B isoforms) to produce chimeric proteins. PR dimerization was detected by the ability of cotransfected GAL4/PR and VP16/PR chimeras in COS cells to induce expression of a reporter gene under the control of GAL4-binding sites (pG5CAT). Hormone agonist-dependent interactions were observed between the two like isoforms of PR (A-A and B-B) and between PR-A and PR-B (A-B), indicating that hormone can stimulate the formation of the three possible dimeric forms of PR within cells. In contrast, neither type I (ZK98299) nor type II (RU486, ZK112993) progestin antagonists stimulated interaction between these same hybrid PR proteins. However, activation of the VP16/PR chimera by antagonists on a progesterone response element-controlled reporter gene (DHRE-E1b-CAT) was only a fraction (4–13%) of that stimulated by agonist R5020. One possibility for the failure to detect an induction in the two-hybrid assay is antagonist-induced repression of the activity of the VP16/PR fusion protein rather than a failure of antagonists to stimulate interaction between the hybrid proteins. To test this idea, an UP-1 carboxyl-terminal truncation mutant of PR was used to construct the two-hybrid proteins. PR-UP-1 selectively binds antagonists, but not agonists, and is fully activated in response to antagonists. Both types of progestin antagonists stimulated interactions between GAL4/PR(UP-1) and VP16/PR(UP-1) hybrid proteins, indicating that antagonists are capable of stimulating PR dimerization in cells and do not function by disrupting or preventing dimerization. To determine whether PR bound to an antagonist can dimerize in whole cells with PR bound to agonist, GAL4/PR(UP-1) was paired in the two- hybrid assay with a VP16/PR fusion protein harboring a point mutation in PR at amino acid 722 (Gly-Cys) that specifically binds progestin agonist but not antagonist. Neither R5020 nor RU486 alone stimulated interaction between these ligand-specific PR hybrid proteins. However, strong interaction was detected by addition of both agonist and antagonists, indicating the formation of mixed ligand heterodimers and that both PR partners require ligand for dimerization to occur. Based on electrophoretic gel mobility shift assays (EMSAs), these heterodimers appear to have substantially reduced DNA binding activity. Progestin antagonists inhibit agonist activation of PR at concentrations that are too low to be accounted for by a simple competition mechanism for binding to PR. We propose that antiprogestin inactivation of PR in trans by heterodimerization contributes to the biological potency of these compounds.

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Zhao, Meng, Jianying Zhang, Janette S. Laubacher, Maria-Teresa Ramirez, and Charles L. Shapiro. "The role of adjuvant chemotherapy in luminal B breast cancer." Journal of Clinical Oncology 32, no. 26_suppl (September 10, 2014): 156. http://dx.doi.org/10.1200/jco.2014.32.26_suppl.156.

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156 Background: Luminal B breast cancer is a heterogeneous subtype characterized by higher grade, increased proliferation rates and overall poorer prognosis. We conducted a retrospective study on the associations between adjuvant chemotherapy, HER2 overexpression, progesterone receptor (PR) and treatment outcomes. Methods: The characteristics of 1,372 patients (pts) with ER positive (ER+) breast cancer (stages 1-3) diagnosed between 1998 and 2005 were reviewed. 432 (31%) were phenotypically defined as luminal B: (2011 St. Gallen’s consensus criteria): ER+, HER2-negative (HER2-) and histological grade 3, or ER+ and HER2-positive (HER2+). ER and PR was positive if nuclear staining was > 1%. HER2 was positive if IHC = 3+ or gene amplification was confirmed by FISH. Statistical analyses were performed using Kaplan-Meier estimate and multivariable cox regression. Results: Among the 432 luminal B pts, 179 cases (41%) were HER2+ and 93 (22%) were PR negative (PR-). Tumor characteristics were similar (see Table). With a median follow-up of 105 months the overall recurrence rate was 56/432 (13%) pts and the median disease-free survival (DFS) and overall survival (OS) have not been reached. No differences were observed in DFS or OS between HER2+ and HER2- groups or between PR+ and PR- groups. In multivariate analysis, Pts who received adjuvant chemotherapy had better DFS (HR = 0.3, p = 0.034) and OS (HR = 0.2, p = 0.013) and the benefit of adjuvant chemotherapy was not dependent on HER2 overexpression (DFS: HR = 1.65, p = 0.37; OS: HR = 1.65, p = 0.39) or PR status (DFS: HR = 1.8, p = 0.37; OS: HR = 2.3, p = 0.25). HER2+ in pts ≥ age of 60 (presumed postmenopausal) was associated with worse DFS (HR = 3.23, p = 0.017) and OS (HR = 3.06, p = 0.027). Conclusions: In patients with luminal B subtype adjuvant chemotherapy significantly improved OS and DFS irrelevant of HER2 or PR status. HER2+ was a poor prognostic factor in postmenopausal pts, however, the vast majority of them did not receive adjuvant trastuzumab. [Table: see text]

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