scholarly journals Targeting TACE-dependent EGFR ligand shedding in breast cancer

2007 ◽  
Vol 117 (2) ◽  
pp. 337-345 ◽  
Author(s):  
P. A. Kenny ◽  
M. J. Bissell
Keyword(s):  
Breast Cancer ◽  
Egfr Ligand ◽  
Ligand Shedding

scholarly journals Substrate Selectivity of Epidermal Growth Factor-Receptor Ligand Sheddases and their Regulation by Phorbol Esters and Calcium Influx

2007 ◽  
Vol 18 (1) ◽  
pp. 176-188 ◽  
Author(s):  
Keisuke Horiuchi ◽  
Sylvain Le Gall ◽  
Marc Schulte ◽  
Takafumi Yamaguchi ◽  
Karina Reiss ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Phorbol Esters ◽  
Calcium Influx ◽  
Growth Factor Receptor ◽  
Egfr Ligands ◽  
Egfr Ligand ◽  
Epidermal Growth ◽  
Ligand Shedding

Signaling via the epidermal growth factor receptor (EGFR), which has critical roles in development and diseases such as cancer, is regulated by proteolytic shedding of its membrane-tethered ligands. Sheddases for EGFR-ligands are therefore key signaling switches in the EGFR pathway. Here, we determined which ADAMs (a disintegrin and metalloprotease) can shed various EGFR-ligands, and we analyzed the regulation of EGFR-ligand shedding by two commonly used stimuli, phorbol esters and calcium influx. Phorbol esters predominantly activate ADAM17, thereby triggering a burst of shedding of EGFR-ligands from a late secretory pathway compartment. Calcium influx stimulates ADAM10, requiring its cytoplasmic domain. However, calcium influx-stimulated shedding of transforming growth factor α and amphiregulin does not require ADAM17, even though ADAM17 is essential for phorbol ester-stimulated shedding of these EGFR-ligands. This study provides new insight into the machinery responsible for EGFR-ligand release and thus EGFR signaling and demonstrates that dysregulated EGFR-ligand shedding may be caused by increased expression of constitutively active sheddases or activation of different sheddases by distinct stimuli.

scholarly journals EGFR-Ligand Signaling in Breast Cancer Metastasis: Recurring Developmental Themes

10.5772/22460 ◽  
2011 ◽  
Author(s):  
Nicole K. ◽  
Jennifer L. ◽  
Kah Tan ◽  
David J. Riese II ◽  
Kenneth P. ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Metastasis ◽  
Breast Cancer Metastasis ◽  
Egfr Ligand

scholarly journals AhR controls redox homeostasis and shapes the tumor microenvironment in BRCA1-associated breast cancer

2019 ◽  
Vol 116 (9) ◽  
pp. 3604-3613 ◽  
Author(s):  
Shawn P. Kubli ◽  
Christian Bassi ◽  
Cecilia Roux ◽  
Andrew Wakeham ◽  
Christoph Göbl ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Microenvironment ◽  
Cancer Cells ◽  
Kinase Inhibitor ◽  
Redox Homeostasis ◽  
Growth Factor Receptor ◽  
Nuclear Accumulation ◽  
Aryl Hydrocarbon ◽  
Egfr Ligand ◽  
Pathway Inhibition

Cancer cells have higher reactive oxygen species (ROS) than normal cells, due to genetic and metabolic alterations. An emerging scenario is that cancer cells increase ROS to activate protumorigenic signaling while activating antioxidant pathways to maintain redox homeostasis. Here we show that, in basal-like and BRCA1-related breast cancer (BC), ROS levels correlate with the expression and activity of the transcription factor aryl hydrocarbon receptor (AhR). Mechanistically, ROS triggers AhR nuclear accumulation and activation to promote the transcription of both antioxidant enzymes and the epidermal growth factor receptor (EGFR) ligand, amphiregulin (AREG). In a mouse model of BRCA1-related BC, cancer-associated AhR and AREG control tumor growth and production of chemokines to attract monocytes and activate proangiogenic function of macrophages in the tumor microenvironment. Interestingly, the expression of these chemokines as well as infiltration of monocyte-lineage cells (monocyte and macrophages) positively correlated with ROS levels in basal-like BC. These data support the existence of a coordinated link between cancer-intrinsic ROS regulation and the features of tumor microenvironment. Therapeutically, chemical inhibition of AhR activity sensitizes human BC models to Erlotinib, a selective EGFR tyrosine kinase inhibitor, suggesting a promising combinatorial anticancer effect of AhR and EGFR pathway inhibition. Thus, AhR represents an attractive target to inhibit redox homeostasis and modulate the tumor promoting microenvironment of basal-like and BRCA1-associated BC.

Virus-Like Particles in a Human Breast Cancer: Structural Similarity to Previously Reported Particles

1973 ◽  
Vol 31 ◽  
pp. 378-379
Author(s):  
G. Kasnic ◽  
S. E. Stewart ◽  
C. Urbanski
Keyword(s):  
Breast Cancer ◽  
Biological Activity ◽  
Human Breast Cancer ◽  
Osteogenic Sarcoma ◽  
Human Tumor ◽  
Structural Similarity ◽  
Cell Tumor ◽  
Human Breast ◽  
Human Tumor Cell ◽  
Type Particle

We have reported the maturation of an intracisternal A-type particle in murine plasma cell tumor cultures and three human tumor cell cultures (rhabdomyosarcoma, lung adenocarcinoma, and osteogenic sarcoma) after IUDR-DMSO activation. In all of these studies the A-type particle seems to develop into a form with an electron dense nucleoid, presumably mature, which is also intracisternal. A similar intracisternal A-type particle has been described in leukemic guinea pigs. Although no biological activity has yet been demonstrated for these particles, on morphologic grounds, and by the manner in which they develop within the cell, they may represent members of the same family of viruses.

Further Ultrastructural Observations on Metastatic Nodules of Human Breast Cancer

1968 ◽  
Vol 26 ◽  
pp. 224-225
Author(s):  
John L. Swedo ◽  
R. W. Talley ◽  
John H. L. Watson
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
Estrogen Therapy ◽  
Specimen Preparation ◽  
Human Breast ◽  
Autophagic Vacuoles ◽  
Previous Communication ◽  
Linear Profiles ◽  
Metastatic Nodule

Since the report, which described the ultrastructure of a metastatic nodule of human breast cancer after estrogen therapy, additional ultrastructural observations, including some which are correlative with pertinent findings in the literature concerning mycoplasmas, have been recorded concerning the same subject. Specimen preparation was identical to that in.The mitochondria possessed few cristae, and were deteriorated and vacuolated. They often contained particulates and fibrous structures, sometimes arranged in spindle-shaped bundles, Fig. 1. Another apparent aberration was the occurrence, Fig. 2 (arrows) of linear profiles of what seems to be SER, which lie between layers of RER, and are often recognizably continuous with them.It was noted that the structure of the round bodies, interpreted as within autophagic vacuoles in the previous communication, and of vesicular bodies, described morphologically closely resembled those of some mycoplasmas. Specifically, they simulated or reflected the various stages of replication reported for mycoplasmas grown on solid nutrient. Based on this observation, they are referred to here as “mycoplasma-like” structures, in anticipation of confirmatory evidence from investigations now in progress.

The proliferation of breast cancer cells are inhibited by the human intrabody targeting cyclinD1

2010 ◽  
Vol 34 (8) ◽  
pp. S49-S49
Author(s):  
Lei Wang ◽  
Xun Zhou ◽  
Lihong Zhou ◽  
Yong Chen ◽  
Xun Zhu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells

Study of the mechanism responsible for multidrug resistance in breast cancer MCF-7 cell mediated by 14-3-3σ

2010 ◽  
Vol 34 (8) ◽  
pp. S47-S47
Author(s):  
Guopei Zheng ◽  
Sisi Yi ◽  
Yafei Li ◽  
Fangren Kong ◽  
Yanhui Yu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Multidrug Resistance ◽  
Mcf 7

Colorectal cancer knowledge and screening rates are lower than for breast cancer even in individuals at high risk of cancer

2001 ◽  
Vol 120 (5) ◽  
pp. A741-A741
Author(s):  
P ANG ◽  
D SCHRAG ◽  
K SCHNEIDER ◽  
K SHANNON ◽  
J JOHNSON ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Colorectal Cancer ◽  
High Risk ◽  
Cancer Knowledge ◽  
Risk Of Cancer
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