Test-retest would be a good approach in such cases, or having an oppinion from an external lab. HER2 positivity is a marker of aggressiveness, but recent publications point that Hormone Receptor Positive and also HER2 positive are among the Breast Cancers having a longer OS. Lack of Prog receptors may be considered also a marker of tumor aggressiveness that may add factors in the therapy decissions for an individual patient. The subject of dubious HER2 positivity is addresed in several articles an guidelines, I guess.

I intended saying that Breast tumors that are in a simultaneous way HER2 pos and HR pos do behave better, but markers' status can change in time and in space, the figures for this change in positivity of prognostic and predictive markers are known for Breast and ColoRectal Cancers, as far as I know.

Dear Rohan,

I start from these considerations:

1) establish that HER2 is overexpressed remains a gray area even using all the methods currently available (and http://www.ncbi.nlm.nih.gov/pubmed/21990413 http://www.nature.com/modpathol/journal/v26/n1/abs/modpathol2012151a.html);

2) clinical practice shows us cases of HER2 overexpression with estrogen receptors strongly expressed and a low expression of progesterone receptors. (the topic is the difference between the estrogen and progesterone receptors expression).

3) one possibility is that this difference could be due to a non-genomic inhibition of progesterone receptors via mTOR pathway;

4) this hyperactivation of the mTOR pathway should indicate an activation of growth factors (among which there may be, or not, HER2)

5) these data are probably already in the literature, but I can not seem to pull them out in a manner consistent

In a flyover approach, I found some PMID references dealing with subjects related to the question:

23642529, by Brollo J et al

23977244 by Song Q et al

23897954 by Metzger-Filho et al

23747837 by Puig-Vives et al

Hope it's useful as an appetizer, I entered as search words: 'Positive Progesterone Receptor Incidence in Breast Cancer Subtypes'

Thank you very much Jose,

I believe that the recent paper by Brollo (https://www.researchgate.net/publication/236636615_Locoregional_recurrence_in_patients_with_HER2_positive_breast_cancer) establish the current state of knowledges. I transcribe the last lines of the abstract:

“At the multivariate analysis, extensive perivascular invasion, Luminal B HER2/Progesterone Receptor (PgR) negative status and Quadrantectomy followed by Intra-operative radiotherapy with electrons have significantly increased the risk of LRR. Our results suggest that HER2/neu positive breast cancer might have better outcomes when treated simultaneously with external radiotherapy and trastuzumab. Moreover, we underline the importance of PgR and further new stratification of risk among luminal subtypes.”

Article Locoregional recurrence in patients with HER2 positive breast cancer

Biologics. 2012; 6: 289–297.

The molecular profile of luminal B breast cancer

Chad J Creighton

....As luminal B breast cancer expresses ER, the estrogen pathway is regarded as a therapeutic target for this disease, though the case could readily be made that additional targets are needed. According to 2011 St Gallen consensus recommendations, where luminal B could be defined in the clinical setting as ER+/HER2−/Ki67+, standard treatment would include endocrine therapy with or without cytotoxic therapy.15,40 However, a large percentage of ER+ breast cancers, which may be regarded as representing luminal B, do not respond to endocrine therapy.8,41 Where PR (under-expressed in luminal B) has long been studied as a marker of functional ER, therapeutic targets for ER+/PR− disease have been considered.1 Studies suggest that estrogen-independent disease represents a switch from using the estrogen pathway to using an alternative GFR signaling pathway; such candidates including HER2, EGFR, IGF, and Akt/PI3K/mTOR.42–46........

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3430090/pdf/btt-6-289.pdf

New data on the subject

JAMA Surg. 2013 Dec 4. doi: 10.1001/jamasurg.2013.3181. [Epub ahead of print]

Personalizing Breast Cancer Staging by the Inclusion of ER, PR, and HER2.

Bagaria SP, Ray PS, Sim MS, Ye X, Shamonki JM, Cui X, Giuliano AE.

Author information:

Department of Surgery, Mayo Clinic Florida, Jacksonville.

IMPORTANCE Nonanatomic factors, such as histologic grade and biomarkers, can

guide breast cancer management but are not included in the current TNM staging

system. OBJECTIVE To use as an example the triple-negative phenotype (TNP)

defined by the absence of estrogen receptor (ER), progesterone receptor (PR), and

human epidermal growth factor 2 (HER2) to examine whether such inclusion improves

the prognostic accuracy of TNM staging for breast cancer. DESIGN, SETTING, AND

PARTICIPANTS Women diagnosed with primary invasive ductal breast cancer from

January 1, 1991, through December 31, 2008, were identified from a prospective

institutional database. Excluded were patients who received neoadjuvant therapy,

those whose staging information was incomplete, or those whose tumor lacked ER,

PR, and HER2 data. Breast cancers were categorized by TNM stage and by the

presence or absence of TNP. MAIN OUTCOMES AND MEASURES Overall survival at 5

years. RESULTS Database review identified 1842 consecutive eligible patients with

breast cancer. When patients were stratified by TNM stage, overall survival

curves for those with TNP breast cancer matched those for patients whose non-TNP

breast cancer was 1 TNM stage higher. Multivariable analysis showed that TNP

status was a powerful prognostic variable, and the likelihood ratio test revealed

that the prognostic accuracy of the TNM staging system that incorporated TNP was

superior to the current TNM staging system (P 

This strudy insists that PgR expression is an independent prognostic factor in Breast ca

Br J Cancer. 2014 Feb 4;110(3):565-72. doi: 10.1038/bjc.2013.756. Epub 2013 Dec

3.

Progesterone receptor expression is an independent prognostic variable in early

breast cancer: a population-based study.

Purdie CA(1), Quinlan P(2), Jordan LB(1), Ashfield A(2), Ogston S(3), Dewar

JA(2), Thompson AM(2).

Author information:

(1)Pathology Department, Ninewells Hospital & Medical School, Dundee DD1 9SY, UK.

(2)Dundee Cancer Centre, University of Dundee, Ninewells Hospital & Medical School,

Dundee DD1 9SY, UK.

(3)Public Health Section, Community Health Sciences University of Dundee, Dundee DD2

4BF, UK.

Background:Progesterone receptor (PR) expression assessment in early invasive

breast cancer remains controversial. This study sought to re-evaluate PR

expression as a potential therapeutic guide in early breast cancer; particularly

in oestrogen receptor (ER)-positive, lymph node (LN)-negative disease.Methods:A

population cohort of 1074 patients presenting to a single Cancer Centre over 4

years (2000-2004) underwent surgery for primary invasive breast cancer with

curative intent. Prospective data collection included patient demographics,

pathology, ER and PR expression, HER2 status, adjuvant chemotherapy and endocrine

therapy. Progesterone receptor expression was compared with (all causes) overall

survival (OS), breast cancer-specific survival (BCSS) and disease-free survival

(DFS).Results:Overall survival was 71.0% and BCSS was 83.0% at median follow-up

of 8.34 years. Absent PR expression was significantly associated with poorer

prognosis for OS, BCSS and DFS (P

Thank you very much Jose, I hope that you continue to follow this issue and that you let me know how things are going in this respect, with gratitude Maurizio

A revised clinico-pathological surrogate definition of Luminal A intrinsic breast cancer subtype.

Patrick Maisonneuve, Davide Disalvatore, Nicole Rotmensz, Giuseppe Curigliano, Marco Colleoni, Silvia Dellapasqua, Giancarlo Pruneri, Mauro G Mastropasqua, Alberto Luini, Fabio Bassi, Gianmatteo Pagani, Giuseppe Viale, Aron Goldhirsch

[more]

Breast cancer research: BCR (Impact Factor: 5.87). 06/2014; 16(3):R65. DOI:10.1186/bcr3679

Source: PubMed

ABSTRACT The 2013 St-Gallen International Expert Panel recognized substantial progress in the pathological characterization of breast cancer subtypes. Useful surrogate definition of Luminal A-like as distinct from Luminal B-like disease could be made using a combination of estrogen receptor (ER), progesterone receptor (PgR) and Ki-67, without requiring molecular diagnostics. Differences depend upon the choice of the threshold value for Ki-67 and the requirement for substantial PgR positivity. We aimed to verify the suitability of the new surrogate definition of luminal subtypes in terms of distant disease control in a large series of patients.

https://www.researchgate.net/publication/263289033_A_revised_clinico-pathological_surrogate_definition_of_Luminal_A_intrinsic_breast_cancer_subtype?ev=pubfeed_overview&trpid=53aaab0cd2fd6454418b45a9_101

http://breast-cancer-research.com/content/pdf/bcr3679.pdf

Article Proposed new clinicopathological surrogate definitions of lu...

This is interesting

J Natl Cancer Inst. 2014 Aug 19;106(8). pii: dju152. doi: 10.1093/jnci/dju152.

Print 2014 Aug.

Molecular features and survival outcomes of the intrinsic subtypes within

HER2-positive breast cancer.

Prat A(1), Carey LA(2), Adamo B(2), Vidal M(2), Tabernero J(2), Cortés J(2),

Parker JS(2), Perou CM(2), Baselga J(2).

Author information:

(1): Breast Cancer Unit (AP, BA, MV, JC), Department of Medical Oncology (AP, BA,

MV, JC, JT), and Translational Genomics Group (AP, MV), Vall d'Hebron Institute

of Oncology Barcelona, Spain; Lineberger Comprehensive Cancer Center (LAC, JSP,

CMP), Department of Genetics (CMP), and Department of Pathology and Laboratory

Medicine (CMP), University of North Carolina, Chapel Hill, NC; Memorial

Sloan-Kettering Cancer Center, New York (JB). [email protected].

(2): Breast Cancer Unit (AP, BA, MV, JC), Department of Medical Oncology (AP, BA,

MV, JC, JT), and Translational Genomics Group (AP, MV), Vall d'Hebron Institute

of Oncology Barcelona, Spain; Lineberger Comprehensive Cancer Center (LAC, JSP,

CMP), Department of Genetics (CMP), and Department of Pathology and Laboratory

Medicine (CMP), University of North Carolina, Chapel Hill, NC; Memorial

Sloan-Kettering Cancer Center, New York (JB).

BACKGROUND: The clinical impact of the biological heterogeneity within

HER2-positive (HER2+) breast cancer is not fully understood. Here, we evaluated

the molecular features and survival outcomes of the intrinsic subtypes within

HER2+ breast cancer.

METHODS: We interrogated The Cancer Genome Atlas (n = 495) and Molecular Taxonomy

of Breast Cancer International Consortium (METABRIC) datasets (n = 1730) of

primary breast cancers for molecular data derived from DNA, RNA and protein, and

determined intrinsic subtype. Clinical HER2 status was defined according to

American Society of Clinical Oncology (ASCO)/College of American Pathologists

(CAP) guidelines or DNA copy-number aberration by single nucleotide polymorphism

arrays. Cox models tested the prognostic significance of each variable in

patients not treated with trastuzumab (n = 1711).

RESULTS: Compared with clinically HER2 (cHER2)-negative breast cancer, cHER2+

breast cancer had a higher frequency of the HER2-enriched (HER2E) subtype (47.0%

vs 7.1%) and a lower frequency of Luminal A (10.7% vs 39.0%) and Basal-like

(14.1% vs 23.4%) subtypes. The likelihood of cHER2-positivity in HER2E, Luminal

B, Basal-like and Luminal A subtypes was 64.6%, 20.0%, 14.4% and 7.3%,

respectively. Within each subtype, only 0.3% to 3.9% of genes were found

differentially expressed between cHER2+ and cHER2-negative tumors. Within cHER2+

tumors, HER2 gene and protein expression was statistically significantly higher

in the HER2E and Basal-like subtypes than either luminal subtype. Neither cHER2

status nor the new 10-subtype copy number-based classification system (IntClust)

added independent prognostic value to intrinsic subtype.

CONCLUSIONS: When the intrinsic subtypes are taken into account, cHER2-positivity

does not translate into large changes in the expression of downstream signaling

pathways, nor does it affect patient survival in the absence of HER2 targeting.

© The Author 2014. Published by Oxford University Press.

PMCID: PMC4151853

PMID: 25139534 [PubMed - indexed for MEDLINE]

This one has some connection to the question:

J Clin Oncol. 2008 Mar 20;26(9):1404-10. doi: 10.1200/JCO.2007.10.6393.

Chemoendocrine compared with endocrine adjuvant therapies for node-negative

breast cancer: predictive value of centrally reviewed expression of estrogen and

progesterone receptors--International Breast Cancer Study Group.

Viale G(1), Regan MM, Maiorano E, Mastropasqua MG, Golouh R, Perin T, Brown RW,

Kovács A, Pillay K, Ohlschlegel C, Braye S, Grigolato P, Rusca T, Gelber RD,

Castiglione-Gertsch M, Price KN, Goldhirsch A, Gusterson BA, Coates AS.

Author information:

(1)Division of Pathology and Laboratory Medicine, European Institute of Oncology,

University of Milan, Milan, Italy. [email protected]

Comment in

J Clin Oncol. 2008 Mar 20;26(9):1397-9.

PURPOSE: To centrally assess estrogen receptor (ER) and progesterone receptor

(PgR) levels by immunohistochemistry and investigate their predictive value for

benefit of chemo-endocrine compared with endocrine adjuvant therapy alone in two

randomized clinical trials for node-negative breast cancer.

PATIENTS AND METHODS: International Breast Cancer Study Group Trial VIII compared

cyclophosphamide, methotrexate, and fluorouracil (CMF) chemotherapy for 6 cycles

followed by endocrine therapy with goserelin with either modality alone in pre-

and perimenopausal patients. Trial IX compared three cycles of CMF followed by

tamoxifen for 5 years versus tamoxifen alone in postmenopausal patients. Central

Pathology Office reviewed 883 (83%) of 1,063 patients on Trial VIII and 1,365

(82%) of 1,669 on Trial IX and determined ER and PgR by immunohistochemistry.

Disease-free survival (DFS) was compared across the spectrum of expression of

each receptor using the Subpopulation Treatment Effect Pattern Plot methodology.

RESULTS: Both receptors displayed a bimodal distribution, with substantial

proportions showing no staining (receptor absent) and most of the remainder

showing a high percentage of stained cells. Chemo-endocrine therapy yielded DFS

superior to endocrine therapy alone for patients with receptor-absent tumors, and

in some cases also for those with low levels of receptor expression. Among

patients with ER-expressing tumors, additional prediction of benefit was

suggested in absent or low PgR in Trial VIII but not in Trial IX.

CONCLUSION: Low levels of ER and PgR are predictive of the benefit of adding

chemotherapy to endocrine therapy. Low PgR may add further prediction among pre-

and perimenopausal but not postmenopausal patients whose tumors express ER.

PMID: 18349391 [PubMed - indexed for MEDLINE]

This reference has some connection to your question, I guess

 Breast Cancer Res Treat. 2012 Oct;135(3):849-55. doi: 10.1007/s10549-012-2183-5.

Epub 2012 Aug 19.

Estrogen receptor, progesterone receptor, and HER2-neu expression in first

primary breast cancers and risk of second primary contralateral breast cancer.

Saltzman BS(1), Malone KE, McDougall JA, Daling JR, Li CI.

Author information:

(1)Division of Public Health Sciences, Fred Hutchinson Cancer Research Center,

Seattle, WA, USA. [email protected]

Breast cancer survivors have a 60 % higher risk of developing a second primary

asynchronous contralateral breast cancer (CBC) compared to women's risk of

developing a first primary breast cancer (FBC). However, little is known about

how expression of tumor markers in first breast cancers influences CBC risk. We

conducted a population-based nested case-control study among women 20-74 years of

age diagnosed with a first breast cancer between 1996 and 2008 in western

Washington State to evaluate the association between their tumor's estrogen

receptor (ER), progesterone receptor (PR) and HER2-neu (HER2) expression, and

risk of CBC. The study included 482 cases diagnosed with both a FBC and a CBC and

1,506 control women diagnosed only once with breast cancer identified through our

local Surveillance, Epidemiology and End Results (SEER) cancer registry. Compared

to the women whose FBC was ER+/PR+, those with ER-/PR- first tumors had a

1.6-fold (95 % confidence interval (CI): 1.2-2.3) increased risk of developing a

CBC. When evaluated by joint ER/PR/HER2 status, compared to women with ER+/HER2-

first cancers, those with HER2-overexpressing (ER-/HER2+) and triple-negative

disease (ER-/PR-/HER2-) had 2.0-fold (95 % CI: 1.1-3.8) and 1.4-fold (95 % CI:

0.9-2.3) elevated risks of developing CBC, respectively. Beyond the known higher

risks of mortality among patients diagnosed with more aggressive BC subtypes,

here, we observe that they may also have increased risks of developing CBC.

PMCID: PMC4144411

PMID: 22903686  [PubMed - indexed for MEDLINE]

Two from the same team

Clin Transl Oncol. 2015 Mar;17(3):238-46. doi: 10.1007/s12094-014-1220-8. Epub

2014 Oct 1.

Differential patterns of recurrence and specific survival between luminal A and

luminal B breast cancer according to recent changes in the 2013 St Gallen

immunohistochemical classification.                                                                            García Fernández A(1), Chabrera C, García Font M, Fraile M, Lain JM, Gónzalez S,  Barco I, González C, Torres J, Piqueras M, Cirera L, Veloso E, Pessarrodona A, Giménez N.

Author information:

(1)Breast Unit, Department of Gynecology, CTD, University Hospital of Mútua

Terrassa, Research Foundation Mútua Terrassa, University of Barcelona, Barcelona,

Spain, [email protected].

INTRODUCTION: In 2011, the St Gallen panel introduced several changes in breast cancer classification, thereby creating the luminal B Her2- subtype. In 2013, the panel also included Ki67 overexpression and PR

I have the trunk plenty of news!

Endocr Relat Cancer. 2015 Apr 21. pii: ERC-15-0129. [Epub ahead of print]

TFF3 is a valuable predictive biomarker of endocrine response in metastatic

breast cancer.

May FE(1), Westley BR(2).

Author information:

(1)F May, Northern Institute for Cancer Research, University of Newcastle,

Newcastle upon Tyne, NE2 4HH, United Kingdom [email protected]. (2)B Westley,

Pathology, University of Newcastle,, Newcastle upon Tyne, United Kingdom.

Stratification of breast cancer patients for endocrine therapies by oestrogen or

progesterone receptor expression is effective but imperfect. Study aims were to:

validate microarray studies that demonstrate TFF3 regulation by oestrogen and

association with oestrogen receptor in breast cancer, evaluate TFF3 as a

biomarker of endocrine response, and investigate TFF3 function. Microarray data

were validated by quantitative RT-PCR, northern and western transfer analyses.

TFF3 was induced by oestrogen and its induction inhibited by antioestrogens,

tamoxifen, 4-hydroxytamoxifen and fulvestrant in oestrogen-responsive breast

cancer cells. Expression of TFF3 and oestrogen receptor mRNAs was associated in

breast tumours (Pearson's coefficient=0.762; p=0.000). Monoclonal antibodies

raised against TFF3 protein detected TFF3 by immunohistochemistry in oesophageal

submucosal glands, intestinal goblet and neuroendocrine cells, Barrett's

metaplasia and intestinal metaplasia. TFF3 protein expression was associated with

oestrogen receptor, progesterone receptor and TFF1 expression in malignant breast

cells. TFF3 is a specific and sensitive predictive biomarker of response to

endocrine therapy, degree and duration of response in unstratified metastatic

breast cancer patients (p=0.000; p=0.002; p=0.002). Multivariate binary logistic

regression analysis demonstrated that TFF3 is an independent biomarker of

endocrine response and of degree of response and was confirmed in a validation

cohort. TFF3 stimulated migration and invasion of breast cancer cells. In

conclusion, TFF3 expression is associated with response to endocrine therapy and

outperforms oestrogen receptor, progesterone receptor and TFF1 as an independent

biomarker possibly because it mediates malign effects of oestrogen on invasion

and metastasis.

PMID: 25900183 [PubMed - as supplied by publisher]

Salut †

HER-2 positivity is alway a high-rosk marker, in Hormone Receptor postive Breast Cancer, the lack of Progesterone Receptor is considered a marker of a more aggressive tumor than when both ER and PR are present, interactions of Hormone Receptors, crosstalk between it, and with other anti-apoptotic, or pathways promoting proliferation and invasion are complex

Cancer Res. 2007 Sep 15;67(18):8942-51.

Progestins reinitiate cell cycle progression in antiestrogen-arrested breast

cancer cells through the B-isoform of progesterone receptor.

McGowan EM(1), Russell AJ, Boonyaratanakornkit V, Saunders DN, Lehrbach GM,

Sergio CM, Musgrove EA, Edwards DP, Sutherland RL.

Author information:

(1)Cancer Research Program, Garvan Institute of Medical Research, Sydney, New

South Wales, Australia.

Estrogen treatment of MCF-7 human breast cancer cells allows the reinitiation of

synchronous cell cycle progression in antiestrogen-arrested cells. Here, we

report that progestins also reinitiate cell cycle progression in this model.

Using clonal cell lines derived from progesterone receptor (PR)-negative MCF-7M13

cells expressing wild-type or mutant forms of PRA and PRB, we show that this

effect is mediated via PRB, not PRA. Cell cycle progression did not occur with a

DNA-binding domain mutant of PRB but was unaffected by mutation in the

NH(2)-terminal, SH3 domain interaction motif, which mediates rapid progestin

activation of c-Src. Thus, the progestin-induced proliferative response in

antiestrogen-inhibited cells is mediated primarily by the transcriptional

activity of PRB. Analysis of selected cell cycle targets showed that progestin

treatment induced levels of cyclin D1 expression and retinoblastoma protein (Rb)

phosphorylation similar to those induced by estradiol. In contrast, progestin

treatment resulted in only a 1.2-fold induction of c-Myc compared with a 10-fold

induction by estradiol. These results support the conclusion that progestin, in a

PRB-dependent manner, can overcome the growth-inhibitory effects of antiestrogens

in estrogen receptor/PR-positive breast cancer cells by the induction of cyclin

D1 expression. The mediation of this effect by PRB, but not PRA, further suggests

a mechanism whereby abnormal regulation of the normal expression ratios of PR

isoforms in breast cancer could lead to the attenuation of antiestrogen-mediated

growth arrest.

PMID: 17875737 [PubMed - indexed for MEDLINE]

This one is brand new, not yet in EntrezPubMed:

Progesterone receptor modulates ERα action in breast cancer

Hisham Mohammed, et al -Nature 2015   doi:10.1038/nature14583

This is related, although not fully addressing your question

Nature. 2015 Jul 16;523(7560):313-7. doi: 10.1038/nature14583. Epub 2015 Jul 8.

Progesterone receptor modulates ERα action in breast cancer.

Mohammed H(1), Russell IA(1), Stark R(1), Rueda OM(1), Hickey TE(2), Tarulli

GA(2), Serandour AA(1), Birrell SN(2), Bruna A(1), Saadi A(1), Menon S(1),

Hadfield J(1), Pugh M(1), Raj GV(3), Brown GD(1), D'Santos C(1), Robinson JL(1),

Silva G(4), Launchbury R(1), Perou CM(4), Stingl J(1), Caldas C(5), Tilley WD(2),

Carroll JS(1).

Author information:

(1)Cancer Research UK Cambridge Institute, University of Cambridge, Robinson Way,

Cambridge CB2 0RE, UK. (2)Dame Roma Mitchell Cancer Research Laboratories and the

Adelaide Prostate Cancer Research Centre, School of Medicine, Hanson Institute

Building, University of Adelaide, Adelaide, South Australia 5005, Australia.

(3)Department of Urology, University of Texas, Southwestern Medical Center at

Dallas, Dallas, Texas 75390, USA. (4)Lineberger Comprehensive Cancer Center,

University of North Carolina at Chapel Hill, 450 West Drive, CB7295, Chapel Hill,

North Carolina 27599, USA. (5)1] Cancer Research UK Cambridge Institute,

University of Cambridge, Robinson Way, Cambridge CB2 0RE, UK [2] Cambridge Breast

Unit, Addenbrooke's Hospital, Cambridge University Hospital NHS Foundation Trust

and NIHR Cambridge Biomedical Research Centre, Cambridge CB2 2QQ, UK [3]

Cambridge Experimental Cancer Medicine Centre, Cambridge CB2 0RE, UK.

Progesterone receptor (PR) expression is used as a biomarker of oestrogen

receptor-α (ERα) function and breast cancer prognosis. Here we show that PR is

not merely an ERα-induced gene target, but is also an ERα-associated protein that

modulates its behaviour. In the presence of agonist ligands, PR associates with

ERα to direct ERα chromatin binding events within breast cancer cells, resulting

in a unique gene expression programme that is associated with good clinical

outcome. Progesterone inhibited oestrogen-mediated growth of ERα(+) cell line

xenografts and primary ERα(+) breast tumour explants, and had increased

anti-proliferative effects when coupled with an ERα antagonist. Copy number loss

of PGR, the gene coding for PR, is a common feature in ERα(+) breast cancers,

explaining lower PR levels in a subset of cases. Our findings indicate that PR

functions as a molecular rheostat to control ERα chromatin binding and

transcriptional activity, which has important implications for prognosis and

therapeutic interventions.

PMID: 26153859 [PubMed - in process]