Expanding our therapeutic options: Beta blockers for breast cancer?

  title={Expanding our therapeutic options: Beta blockers for breast cancer?},
  author={Patricia A. Ganz and Steve W. Cole},
  journal={Journal of clinical oncology : official journal of the American Society of Clinical Oncology},
  volume={29 19},
  • P. GanzS. Cole
  • Published 1 July 2011
  • Medicine
  • Journal of clinical oncology : official journal of the American Society of Clinical Oncology

Figures from this paper

Drug Repurposing for Triple-Negative Breast Cancer

This review specially emphasizes the most relevant research, both at preclinical and clinical settings, aimed at repurposing pre-existing drugs to treat TNBC on the basis of molecular mechanisms and signaling pathways such as androgen receptor, adrenergic receptor, STAT3, nitric oxide synthase, or AXL.

Neurons generated from carcinoma stem cells support cancer progression

It is shown that a fraction of cancer stem cells (CSCs) derived from patients with gastric carcinoma and colorectal carcinoma are capable of producing neurons that are involved in tumor neurogenesis and tumor growth.

β-Adrenergic receptors suppress Rap1B prenylation and promote the metastatic phenotype in breast cancer cells

It is shown that cholera toxin and βAR activation phosphorylate Rap1B and inhibit its prenylation and membrane localization, reducing cell-cell adhesion and promoting cell scattering, and that breast cancer cell migration is decreased by the FDA-approved β-blocker, propranolol.

β2-AR signaling controls trastuzumab resistance-dependent pathway

It is shown that the expression of β2-AR, which mediates most catecholamine-induced effects, negatively correlates with trastuzumab response in the patients with Her2-overexpressing breast cancer, implicating the possibility for combination therapy withtrastuzumsumab plus β-blocker in Her1-ovexpressing Breast cancer.

Sympathetic nervous system regulation of the tumour microenvironment

In addition to identifying a molecular basis for physiologic stress effects on cancer, these findings have also identified new pharmacological strategies to inhibit cancer progression in vivo.

A Her2-let-7-β2-AR circuit affects prognosis in patients with Her2-positive breast cancer

The data suggest that β2-AR may be a new useful biomarker for predicting prognosis in Her2-positive breast cancer and may also be a promising selective therapeutic target for the aggressive subtype of breast cancer.

Long-Term Use of Antihypertensive Agents and Risk of Breast Cancer: A Population-Based Case–Control Study

Long-term use of CCBs or beta-1 selective beta-blockers are likely to be associated with the risk of breast cancer, according to the results of the analysis.



Beta-blocker drug therapy reduces secondary cancer formation in breast cancer and improves cancer specific survival.

This proof-of-principle study showed beta-blocker therapy significantly reduces distant metastases, cancer recurrence, and cancer-specific mortality in breast cancer patients suggesting a novel role for beta- blocker therapy.

The b 2-adrenergic receptor and Her 2 comprise a positive feedback loop in human breast cancer cells

The data indicate that Her2 overexpression and excessive phosphorylation of ERK cause epinephrine autocrine release from breast cancer cells, resulting in up-regulation of b2-AR expression, which supports a model where b 2-AR and Her2 comprise a positive feedback loop in human Breast cancer cells.

Beta-blocker use is associated with improved relapse-free survival in patients with triple-negative breast cancer.

BB intake was associated with improved RFS in all patients with breast cancer and in patients with TNBC, and additional studies evaluating the potential benefits of beta-adrenergic blockade on breast cancer recurrence are warranted.

Epinephrine Protects Cancer Cells from Apoptosis via Activation of cAMP-dependent Protein Kinase and BAD Phosphorylation*

Evidence is provided that epinephrine reduces sensitivity of cancer cells to apoptosis through interaction with β2-adrenergic receptors, which could be one of the mechanisms by which stress promotes tumorigenesis and decreases the efficacy of anti-cancer therapies.

Metformin and pathologic complete responses to neoadjuvant chemotherapy in diabetic patients with breast cancer.

Diabetic patients with breast cancer receiving metformin and neoadjuvant chemotherapy have a higher pCR rate than do diabetics not receiving meetformin, and additional studies to evaluate the potential of met formin as an antitumor agent are warranted.

C-reactive protein levels, variation in the C-reactive protein gene, and cancer risk: the Rotterdam Study.

  • C. SiemesL. Visser B. Stricker
  • Medicine
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • 2006
Baseline CRP levels seem to be a biomarker of chronic inflammation preceding lung cancer, even after subtracting a 5-year latent period, and both chronic inflammation and impaired defense mechanisms resulting in chronic inflammation might explain these results.

Tumor-host interactions: a far-reaching relationship.

  • S. McAllisterR. Weinberg
  • Biology
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • 2010
This review addresses the recent advances in the understanding of the contributions of local and systemic environments to cancer progression, the ability of tumors to actively perturb the host environment, and current therapeutic approaches that are designed to disrupt tumor-host relationships.

Elevated biomarkers of inflammation are associated with reduced survival among breast cancer patients.

Circulating SAA and CRP may be important prognostic markers for long-term survival in breast cancer patients, independent of race, tumor stage, race, and body mass index.