scholarly journals FOXA1 is an essential determinant of ER  expression and mammary ductal morphogenesis

Development ◽  
2010 ◽  
Vol 137 (12) ◽  
pp. 2045-2054 ◽  
Author(s):  
G. M. Bernardo ◽  
K. L. Lozada ◽  
J. D. Miedler ◽  
G. Harburg ◽  
S. C. Hewitt ◽  
...  
Keyword(s):  
Ductal Morphogenesis ◽  
Er Expression

Estrogenrezeptor-(ER-)Expression auf disseminierten Tumorzellen von Mammakarzinompatientinnen

2008 ◽  
Vol 68 (S 01) ◽  
Author(s):  
NH Krawczyk ◽  
M Banys ◽  
EF Solomayer ◽  
D Wallwiener ◽  
S Duerr-Stoerzer ◽  
...  
Keyword(s):  
Er Expression

Reply to: Hippo signalling maintains ER expression and ER+ breast cancer growth

Nature ◽  
2021 ◽  
Vol 591 (7848) ◽  
pp. E11-E12
Author(s):  
Adrian Britschgi ◽  
Joana Pinto Couto ◽  
Mohamed Bentires-Alj
Keyword(s):  
Breast Cancer ◽  
Cancer Growth ◽  
Breast Cancer Growth ◽  
Er Expression ◽  
Hippo Signalling

scholarly journals CITED1 homozygous null mice display aberrant pubertal mammary ductal morphogenesis

Oncogene ◽  
2005 ◽  
Vol 25 (10) ◽  
pp. 1532-1542 ◽  
Author(s):  
J Howlin ◽  
J McBryan ◽  
S Napoletano ◽  
T Lambe ◽  
E McArdle ◽  
...  
Keyword(s):  
Ductal Morphogenesis

scholarly journals Stromal Cells Are Critical Targets in the Regulation of Mammary Ductal Morphogenesis by Parathyroid Hormone-Related Protein

1998 ◽  
Vol 203 (1) ◽  
pp. 75-89 ◽  
Author(s):  
Maureen E. Dunbar ◽  
Peter Young ◽  
Jian-Ping Zhang ◽  
James McCaughern-Carucci ◽  
Beate Lanske ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Stromal Cells ◽  
Related Protein ◽  
Ductal Morphogenesis ◽  
Parathyroid Hormone Related Protein

Abstract LB-194: AhR Arg554Lys impacts tumor ER expression and endocrine treatment response in breast cancer

2016 ◽  
Author(s):  
Maria Simonsson ◽  
Andrea Markkula ◽  
Carsten Rose ◽  
Christian Ingvar ◽  
Helena C. Jernström
Keyword(s):  
Breast Cancer ◽  
Treatment Response ◽  
Endocrine Treatment ◽  
Er Expression

Phenotypic plasticity of ER+ breast cancer in the bone microenvironment

2020 ◽  
Author(s):  
Igor L. Bado ◽  
Hai Wang ◽  
Poonam Sarkar ◽  
Jun Liu ◽  
William Wu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Phenotypic Plasticity ◽  
Clonal Selection ◽  
Endocrine Resistance ◽  
Bone Microenvironment ◽  
Pdgf Signaling ◽  
Stable Memory ◽  
Epigenomic Reprogramming ◽  
Er Expression ◽  
Therapeutic Responses

SummaryER+ breast cancer exhibits a strong bone-tropism in metastasis. How the bone microenvironment impacts the ER signaling and endocrine therapies remains poorly understood. Here, we discover that the osteogenic niche transiently reduces ER expression and activities specifically in bone micrometastases (BMMs), leading to endocrine resistance. This is mediated by gap junctions and paracrine FGF/PDGF signaling, which together generate a stable “memory”: cancer cells extracted from bone remain resistant to endocrine therapies for several generations. Using single cell-derived populations (SCPs), we demonstrated that this process is independent of clonal selection, and represents an EZH2-mediated epigenomic reprogramming. EZH2 drives ER+ BMMs toward a basal and stem-like state. EZH2 inhibition reverses endocrine resistance. Our data demonstrates how epigenomic adaptation to the bone microenvironment drives phenotypic plasticity of metastatic seeds and alters their therapeutic responses together with clonal selection, and provides insights into the clinical enigma of ER+ metastatic recurrences despite endocrine therapies.

Muss der ER-Grenzwert neu definiert werden?

2018 ◽  
Vol 50 (02) ◽  
pp. 82-84
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Clinical Oncology ◽  
Primary Breast Cancer ◽  
Estrogen Receptor Positivity ◽  
American Society ◽  
Definition Of ◽  
Er Expression

Fujii T, Kogawa T, Dong W et al. Revisiting the definition of estrogen receptor positivity in HER2-negative primary breast cancer. Ann Oncol 2017; 28: 2420–2428 Gemäß den Empfehlungen der „American Society of Clinical Oncology“ sowie der Fachgesellschaft der US-Pathologen werden Mammakarzinome mit einer ER-Expression < 1% als rezeptornegativ bewertet. Wissenschaftliche Untersuchungen deuten jedoch darauf hin, dass diese Tumoren in molekulargenetischer und prognostischer Hinsicht Karzinomen mit einer ER-Expression zwischen 1 und 9% ähneln. Sollte der Grenzwert angehoben werden?

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