Prevalence of amplification of the oncogenes c-myc, HER2/neu, and int-2 in one thousand human breast tumours: Correlation with steroid receptors

1992 ◽  
Vol 28 (2-3) ◽  
pp. 697-700 ◽  
Author(s):  
Els M.J.J. Berns ◽  
Jan G.M. Klijn ◽  
Iris L. van Staveren ◽  
Henk Portengen ◽  
Erica Noordegraaf ◽  
...  
Keyword(s):  
Steroid Receptors ◽  
Human Breast ◽  
Breast Tumours

The expression of cytochrome P450 enzymes in human breast tumours and normal breast tissue

2001 ◽  
Vol 70 (1) ◽  
pp. 47-54 ◽  
Author(s):  
Mumtaz Iscan ◽  
Tuula Klaavuniemi ◽  
Tulay Çoban ◽  
Nilgun Kapucuoğlu ◽  
Olavi Pelkonen ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Breast Tissue ◽  
Normal Breast Tissue ◽  
Normal Breast ◽  
Human Breast ◽  
Cytochrome P450 Enzymes ◽  
Breast Tumours

A cross-linking assay allows the detection of receptors for the somatostatin analogue, lanreotide in human breast tumours

1993 ◽  
Vol 29 (11) ◽  
pp. 1589-1592 ◽  
Author(s):  
Grégoire Prévost ◽  
Philippe Provost ◽  
Valérie Sallé ◽  
Monique Lanson ◽  
François Thomas
Keyword(s):  
Cross Linking ◽  
Somatostatin Analogue ◽  
Human Breast ◽  
Breast Tumours

scholarly journals Rapid assay for thein vitro chemosensitivity testing of human breast tumours

1989 ◽  
Vol 11 (6) ◽  
pp. 244-244
Author(s):  
R. F. M. Oude Elferink ◽  
H. M. J. Goldschmidt ◽  
H. J. Majoor ◽  
J. F. Leijten
Keyword(s):  
Human Breast ◽  
Breast Tumours ◽  
Chemosensitivity Testing ◽  
Rapid Assay

Significance of Ca antigen expression in human breast tumours

1985 ◽  
Vol 13 (2) ◽  
pp. 458-458
Author(s):  
DAKSHA P. TRIVEDI ◽  
HAROLD BAUM ◽  
MICHAEL BAUM
Keyword(s):  
Antigen Expression ◽  
Human Breast ◽  
Breast Tumours

scholarly journals Disrupted circadian clocks and altered tissue mechanics in primary human breast tumours

2018 ◽  
Vol 20 (1) ◽  
Author(s):  
Eleanor Broadberry ◽  
James McConnell ◽  
Jack Williams ◽  
Nan Yang ◽  
Egor Zindy ◽  
...  
Keyword(s):  
Tissue Mechanics ◽  
Circadian Clocks ◽  
Human Breast ◽  
Breast Tumours ◽  
Primary Human Breast

Menstrual cycle-dependent variations of breast cyst fluid proteins and sex steroid receptors in the normal human breast

Cancer ◽  
1983 ◽  
Vol 51 (7) ◽  
pp. 1297-1302 ◽  
Author(s):  
John S. Silva ◽  
Gregory S. Georgiade ◽  
William G. Dilley ◽  
Kenneth S. McCarty ◽  
Samuel A. Wells ◽  
...  
Keyword(s):  
Menstrual Cycle ◽  
Steroid Receptors ◽  
Cyst Fluid ◽  
Sex Steroid ◽  
Human Breast ◽  
Breast Cyst Fluid ◽  
Breast Cyst ◽  
Normal Human Breast ◽  
Normal Human ◽  
Cycle Dependent

scholarly journals EMT cells increase breast cancer metastasis via paracrine GLI activation in neighbouring tumour cells

2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Deepika Neelakantan ◽  
Hengbo Zhou ◽  
Michael U. J. Oliphant ◽  
Xiaomei Zhang ◽  
Lukas M. Simon ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Transcription Factor ◽  
Transcription Factors ◽  
Cancer Metastasis ◽  
Breast Cancer Metastasis ◽  
Tumour Cells ◽  
Human Breast ◽  
Breast Tumours ◽  
Cancer Models ◽  
Pdx Models

Abstract Recent fate-mapping studies concluded that EMT is not required for metastasis of carcinomas. Here we challenge this conclusion by showing that these studies failed to account for possible crosstalk between EMT and non-EMT cells that promotes dissemination of non-EMT cells. In breast cancer models, EMT cells induce increased metastasis of weakly metastatic, non-EMT tumour cells in a paracrine manner, in part by non-cell autonomous activation of the GLI transcription factor. Treatment with GANT61, a GLI1/2 inhibitor, but not with IPI 926, a Smoothened inhibitor, blocks this effect and inhibits growth in PDX models. In human breast tumours, the EMT-transcription factors strongly correlate with activated Hedgehog/GLI signalling but not with the Hh ligands. Our findings indicate that EMT contributes to metastasis via non-cell autonomous effects that activate the Hh pathway. Although all Hh inhibitors may act against tumours with canonical Hh/GLI signalling, only GLI inhibitors would act against non-canonical EMT-induced GLI activation.

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