ArticleClinical cancer research : an official journal of the American Association for Cancer Research2011
Adaptive changes result in activation of alternate signaling pathways and acquisition of resistance to aromatase inhibitors.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 34 citations in OpenAlex.
- Impact of adding the multikinase inhibitor sorafenib to endocrine therapy in metastatic estrogen receptor-positive breast cancer.Future oncology (London, England) · 2014Trial
- Advances in the intrinsic signaling pathway interactions and clinical translation of HR+/HER2+ breast cancer.Breast cancer (Tokyo, Japan) · 2025Review
- Anoikis resistance in Cancer: Mechanisms, therapeutic strategies, potential targets, and models for enhanced understanding.Cancer letters · 2025Review
- Hi-C profiling in tissues reveals 3D chromatin-regulated breast tumor heterogeneity informing a looping-mediated therapeutic avenue.Cell reports · 2025Article
- ESR1 gene amplification and MAP3K mutations are selected during adjuvant endocrine therapies in relapsing Hormone Receptor-positive, HER2-negative breast cancer (HR+ HER2- BC).PLoS genetics · 2023Article
- Review
- The 3D genomic landscape of differential response to EGFR/HER2 inhibition in endocrine-resistant breast cancer cells.Biochimica et biophysica acta. Gene regulatory mechanisms · 2020Article
- Effect of neoadjuvant therapy on breast cancer biomarker profile.BMC cancer · 2020Article
- Cancer stem-like properties of hormonal therapy-resistant breast cancer cells.Breast cancer (Tokyo, Japan) · 2019Article
- Overcoming endocrine resistance in hormone receptor-positive breast cancer.Current oncology (Toronto, Ont.) · 2018Review
- FOXA1 overexpression mediates endocrine resistance by altering the ER transcriptome and IL-8 expression in ER-positive breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- The impact of low-dose carcinogens and environmental disruptors on tissue invasion and metastasis.Carcinogenesis · 2015Review
- Bidirectional Crosstalk between the Estrogen Receptor and Human Epidermal Growth Factor Receptor 2 Signaling Pathways in Breast Cancer: Molecular Basis and Clinical Implications.Breast care (Basel, Switzerland) · 2013Review
- Mechanisms of resistance to endocrine therapy in breast cancer: focus on signaling pathways, miRNAs and genetically based resistance.International journal of molecular sciences · 2012Review
- Models and Mechanisms of Acquired Antihormone Resistance in Breast Cancer: Significant Clinical Progress Despite Limitations.Hormone molecular biology and clinical investigation · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Hormone therapy is an effective approach for the treatment of breast cancer. Although the antiestrogen tamoxifen has had a major impact on the treatment of the disease, aromatase inhibitors (AIs), which reduce estrogen synthesis, have recently proved to be more effective. These agents are now used as first-line therapy for postmenopausal breast cancer. Nevertheless, despite the efficacy of these agents, resistance to treatment eventually may occur in some patients. In an effort to overcome this resistance and extend the benefits of AIs, investigators have studied the mechanisms involved in resistance to AIs. Adaptive changes that result in activation of alternate signaling pathways in AI-resistant tumors have been identified in xenograft and cell line models. Expression of estrogen receptor α and aromatase was shown to be decreased in tumors after long-term treatment with AIs. In contrast, increased expression was observed in tyrosine kinase receptors such as Her-2 and insulin-like growth factor receptor, as well as in downstream signaling proteins such as mitogen-activated protein kinase. Functional activation of the mitogen-activated protein kinase pathway and dependency on growth factor receptor signaling have been observed in AI-resistant cells and tumors.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.