Endocrine-responsive breast cancer and strategies for combating resistance

By Simak Ali, R. Coombes. Nature Reviews. Cancer, 2002

939 citations recorded by the source corpus.

Subfields: Cancer Research, Genetics, Oncology

View Paper: https://www.semanticscholar.org/paper/215e360122ca5feedd88c2fa38de395b9eee4ad3

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. W. Vanden Berghe
2. G. Haegeman
3. K. De Bosscher
4. N. Perkins

In Genetics

1. Jan-Ake Gustafsson

In Oncology

1. N. Hynes
2. Jan-Ake Gustafsson
3. R. Sutherland
4. E. Musgrove
5. G. Haegeman
6. J. Baselga
7. N. Perkins

Citations in the corpus

• ERBB receptors and cancer: the complexity of targeted inhibitors (2005, background): “Furthermore, the converse occurs: AKT, MAPK and p38 MAPK phosphorylate ER on key residues that are involved in the induction of ligand-independent activation by growth-factor receptors (reviewed in Ref”
• The interplay between the glucocorticoid receptor and nuclear factor-kappaB or activator protein-1: molecular mechanisms for gene repression. (2003, background): “NR mutations affecting ligand binding or cofactor affinities, changed cofactor expression levels, NF- B-dependent expression of the multidrug resistance protein MDR1, oncogenic activation of growth factorsignaling pathways, and altered circuitry in nongenomic NR pathways (549, 720, 721).”
• The emerging roles of forkhead box (Fox) proteins in cancer (2007, background): “The expression of ERα is a marker for favourable prognosis and endocrine responsiveness in breast cancer, as the success of endocrine treatment is dependent on a functional ER&alpha”
• The different roles of ER subtypes in cancer biology and therapy (2011, background): “The cytoplasmic localization of proline, glutamate and leucine-rich protein 1 (PELP1) and the expression of the truncated ERα variant ERα-36 have been reported to promote constitutive ERα-mediated transcription, which also decreases sensitivity in vitro and is associated with reduced responsivenes”
• Biological determinants of endocrine resistance in breast cancer (2009, background): “Many of the broad concepts discussed will probably also apply to resistance to aromatase inhibitors and other anti-oestrogens, although the lack of clinical cross-resistanc”
• Mechanisms of tamoxifen resistance: increased estrogen receptor-HER2/neu cross-talk in ER/HER2-positive breast cancer. (2004, background): “The resulting ER phosphorylation in the N-terminal region, which can also be induced by estrogen binding, increases transcription arising from the AF-1 domain of the ER; the resulting phosphorylation of AIB1, which is not directly induced by estrogen, augments its coactivator activity (9, 10 ).”