scholarly journals Involvement of steroid hormone and growth factor cross-talk in endocrine response in breast cancer.

1999 ◽  
pp. 373-387 ◽  
Author(s):  
R I Nicholson ◽  
R A McClelland ◽  
J F Robertson ◽  
J M Gee
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Cross Talk ◽  
Therapeutic Response ◽  
Steroid Hormone ◽  
Common Element ◽  
Growth Factor Signaling ◽  
Endocrine Response ◽  
Resistant Phenotype ◽  
Lines Of Evidence

Multiple lines of evidence implicate steroid hormone and growth factor cross-talk as a modulator of endocrine response in breast cancer and that aberrations in growth factor signaling pathways are a common element in the endocrine resistant phenotype. Delineation of these relationships is thus an important diagnostic goal in cancer research, while the targeting of aberrant growth factor signaling holds the promise of improving therapeutic response rates.

scholarly journals ZIP7-Mediated Intracellular Zinc Transport Contributes to Aberrant Growth Factor Signaling in Antihormone-Resistant Breast Cancer Cells

Endocrinology ◽  
2008 ◽  
Vol 149 (10) ◽  
pp. 4912-4920 ◽  
Author(s):  
Kathryn M. Taylor ◽  
Petra Vichova ◽  
Nicola Jordan ◽  
Stephen Hiscox ◽  
Rhiannon Hendley ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Growth Factor Signaling ◽  
Zinc Transport ◽  
Intracellular Zinc

Resistance to endocrine therapy in breast cancer: exploiting estrogen receptor/growth factor signaling crosstalk

2006 ◽  
Vol 13 (Supplement_1) ◽  
pp. S15-S24 ◽  
Author(s):  
Suleiman Massarweh ◽  
Rachel Schiff
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Growth Factor ◽  
Endocrine Therapy ◽  
Acquired Resistance ◽  
Growth Factor Signaling ◽  
Breast Cancer Patients ◽  
Signaling Crosstalk ◽  
Receptor Modulator ◽  
Signal Transduction Inhibitors

Targeting the estrogen receptor (ER) is the oldest form of molecular targeted therapy, and the widespread use of the selective estrogen receptor modulator tamoxifen in breast cancer is responsible for major improvements in cure rates, quality of life, and disease prevention in the last 25 years. Newer forms of endocrine therapy now available for the management of endocrine responsive breast cancer include a new generation of aromatase inhibitors, which lower the estrogen ligand for ER, and pure ER antagonists which destroy the receptor. Despite these recent clinical advances, intrinsic and acquired resistance to these endocrine therapies is still a common feature that limits the success of this therapeutic strategy. Recent research into the molecular biology of ER signaling has revealed a remarkably complex interactive signaling with other growth factor signaling pathways in breast cancer cells, potentially explaining some of the reasons behind endocrine therapy action as well as resistance. This view of a more complex ER signaling system has uncovered new molecular targets which, if present in a cancer cell, might be additionally targeted using various signal transduction inhibitors to overcome or prevent resistance to endocrine therapy. In addition, the dynamic inverse relationship between the expression of ER and growth factor receptors brings more excitement to the potential of restoring ER expression in apparently ER-negative cells by inhibition of growth factor signaling. Ongoing clinical trials of endocrine therapy combined with growth factor pathway inhibitors or their downstream signaling elements promise to further improve the present care for breast cancer patients.

scholarly journals Growth factor-driven mechanisms associated with resistance to estrogen deprivation in breast cancer: new opportunities for therapy

2004 ◽  
Vol 11 (4) ◽  
pp. 623-641 ◽  
Author(s):  
R I Nicholson ◽  
C Staka ◽  
F Boyns ◽  
I R Hutcheson ◽  
J M W Gee
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Breast Cancer Cells ◽  
Endocrine Resistance ◽  
Signaling Networks ◽  
Growth Factor Signaling ◽  
Independent Manner ◽  
Estrogen Withdrawal ◽  
Current Article ◽  
The Many

There is an increasing body of evidence demonstrating that elevated growth signaling in breast cancer cells can promote forms of endocrine resistance in either an estrogen receptor-dependent or -independent manner. The current article reviews what is known about such growth factor signaling networks and resistance to estrogen withdrawal and considers the many novel therapeutic opportunities that stem from this knowledge.

scholarly journals Microenvironmental Determinants of Breast Cancer Metastasis: Focus on the Crucial Interplay Between Estrogen and Insulin/Insulin-Like Growth Factor Signaling

2020 ◽  
Vol 8 ◽  
Author(s):  
Veronica Vella ◽  
Ernestina Marianna De Francesco ◽  
Rosamaria Lappano ◽  
Maria Grazia Muoio ◽  
Livia Manzella ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Growth Factor ◽  
Cross Talk ◽  
Cancer Metastasis ◽  
Great Majority ◽  
Breast Cancer Metastasis ◽  
Estrogen Signaling ◽  
Growth Factor Signaling ◽  
Insulin Like Growth Factor ◽  
Breast Cancers

The development and progression of the great majority of breast cancers (BCs) are mainly dependent on the biological action elicited by estrogens through the classical estrogen receptor (ER), as well as the alternate receptor named G-protein–coupled estrogen receptor (GPER). In addition to estrogens, other hormones and growth factors, including the insulin and insulin-like growth factor system (IIGFs), play a role in BC. IIGFs cooperates with estrogen signaling to generate a multilevel cross-communication that ultimately facilitates the transition toward aggressive and life-threatening BC phenotypes. In this regard, the majority of BC deaths are correlated with the formation of metastatic lesions at distant sites. A thorough scrutiny of the biological and biochemical events orchestrating metastasis formation and dissemination has shown that virtually all cell types within the tumor microenvironment work closely with BC cells to seed cancerous units at distant sites. By establishing an intricate scheme of paracrine interactions that lead to the expression of genes involved in metastasis initiation, progression, and virulence, the cross-talk between BC cells and the surrounding microenvironmental components does dictate tumor fate and patients’ prognosis. Following (i) a description of the main microenvironmental events prompting BC metastases and (ii) a concise overview of estrogen and the IIGFs signaling and their major regulatory functions in BC, here we provide a comprehensive analysis of the most recent findings on the role of these transduction pathways toward metastatic dissemination. In particular, we focused our attention on the main microenvironmental targets of the estrogen-IIGFs interplay, and we recapitulated relevant molecular nodes that orientate shared biological responses fostering the metastatic program. On the basis of available studies, we propose that a functional cross-talk between estrogens and IIGFs, by affecting the BC microenvironment, may contribute to the metastatic process and may be regarded as a novel target for combination therapies aimed at preventing the metastatic evolution.

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