Systemic treatment of <scp>HER</scp>2‐positive metastatic breast cancer: A systematic review

Wilcken, Nicholas; Zdenkowski, Nicholas; White, Michelle; Snyder, Ray; Pittman, Ken; Mainwaring, Paul N.; Green, Michael; Francis, Prudence A.; Boer, Richard de; Colosimo, Maree; Chua, S.L.; Chirgwin, Jacquie; Beith, Jane

doi:10.1111/ajco.12206

Cited by 15 publications

(17 citation statements)

References 69 publications

(68 reference statements)

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“…Several factors contribute to initiation and progression of breast cancer [2][3][4]. Sustaining proliferative signaling, escaping growth inhibition and resisting cell death are hallmarks of cancers.…”

Section: Breast Cancermentioning

confidence: 99%

The role of E-cadherin - 160C/A polymorphism in breast cancer

Luo

Huang

Tao³

et al. 2016

Open Life Sciences

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Open Life Sci. 2016; 11: 110-115 invasion and metastases. These characteristics are results of genetic deregulation. Accumulation of genetic mutations results in increasingly aggressive phenotypes [5]. E-cadherin in Breast Cancer Structure and Functions of E-CadherinThe CDH1 gene is located on human chromosome 16q22.1 and encodes for the E-cadherin protein [6]. The E-cadherin glycoprotein is composed of three major structural domains: a single transmembrane domain, connected with a cytoplasmic domain, and an extracellular domain comprising five tandemly repeated domains called EC1-EC5, which are exclusive to cadherins [7]. The extracellular domain of E-cadherin is essential for cell to cell adhesion, as well as for the correct folding and homo/hetero dimerisation of the proteins. The cytoplasmic domain of E-cadherin interacts with the catenins (α-, β-, γ-and p120 catenin) anchored to the actin cytoskeleton, establishing cadherin-catenin complexes [8]. Conformation of E-cadherin is only stable upon Ca 2+ binding to its highly conserved, negatively charged extracellular motifs [9]. Its stabilization at the cell membrane and accurate function occur by association to cytoplasmic p120-catenin [10]. E-cadherin forms adherens junction with its binding partner β-catenin and actin filaments. This complex is critical to inhibit individual epithelial cell motility and to provide homeostatic tissue architecture [11,12] (Figure 1). Signaling Pathways Regulated by E-CadherinIn addition to its role in cell to cell adhesion, E-cadherin is involved in a number of signaling pathways in carcinogenesis [13]. For the Wnt/β-catenin pathway, free β-catenins may accumulate in the cytoplasm attributed Abstract: Breast cancer is the most prevalent cancer in women worldwide. Numerous studies have suggested that the E-cadherin adhesion system is dysregulated in cancer cells. These impaired functions of E-cadherin contribute to releasing cancer cells from the primary lesion to cell dedifferentiation. Some studies have shown that polymorphism may affect E-cadherin expression, and then play a role in susceptibility to breast cancer. However, the results remained controversial. In this short review, we summarize the functions of E-cadherin and the signaling pathways it regulates, and assess the association between CDH1 polymorphisms and breast cancer susceptibility. This study suggests that genetic variation in CDH1 and -160C/A polymorphism may have an association with breast cancer risk. The assessment of CDH1 polymorphisms may be used for the identification of patients suitable for anti-CDH1 therapy.

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Section: Breast Cancermentioning

confidence: 99%

The role of E-cadherin - 160C/A polymorphism in breast cancer

Luo

Huang

Tao³

et al. 2016

Open Life Sciences

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“…Based on these pivotal studies, clinicians have recommended the use of dual anti‐HER2 blockade pertuzumab and trastuzumab in combination with taxane chemotherapy in the first‐line setting as the new international standard of care . There are a large number of ongoing interventional studies of pertuzumab in adults with breast cancer.…”

Section: Clinical Efficacy and Safety Of Pertuzumabmentioning

confidence: 99%

“…The development of targeted biological therapies for women with HER2‐positive metastatic breast cancers has improved progression‐free survival (PFS), overall survival (OS) and overall response rate (ORR) compared with traditional chemotherapy, especially in the first‐line setting . The development of HER2‐targeted therapy in the first‐line setting; specifically trastuzumab, both internationally and within our Australian population, significantly extended survival beyond previously used chemotherapy regimens .…”

Section: Introductionmentioning

confidence: 99%

“…More recently, pertuzumab was developed, and it has been trialed in combination with trastuzumab and chemotherapy for women with HER2‐positive metastatic breast cancer . This combination of pertuzumab with trastuzumab and docetaxel has shown significant improvements in ORRs, PFS and OS in women with HER2‐positive metastatic breast cancer …”

Section: Introductionmentioning

confidence: 99%

“…As a result of these highly effective anti‐HER2 agents, patients with HER2‐positive metastatic breast cancer are now surviving longer . The treatment paradigm is evolving and requires management of not only metastatic HER2‐positive disease, but also acute and chronic treatment‐related toxicities.…”

Section: Introductionmentioning

confidence: 99%

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Management of patients treated with pertuzumab in the Australian clinical practice setting

Woodward

White

Pugliano³

et al. 2016

Asia-Pac J Clncl Oncology

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Aim: Treatment with pertuzumab-trastuzumab-taxane combinations has become the international standard of care for patients with HER2-positive metastatic breast cancer. In this paper we discuss the practicalities of treating patients with this combination with a particular focus on treatment in the Australian setting. Method: An expert panel was convened to discuss practical aspects for use of pertuzumab in the Australian clinical setting. The findings of this panel are reported in this article. Results:The combination of pertuzumab-trastuzumab-docetaxel has established efficacy in patients with HER2-positive metastatic breast cancer, prolonging progression-free and overall survival compared to trastuzumab-taxane combinations. In Australia, combinations of pertuzumab and trastuzumab with docetaxel or paclitaxel are reimbursed. Management of treatment related side-effects such as diarrhea, febrile neutropenia and neuropathy typically include dose reduction or switching taxane. Specific patients with poorer tolerance of chemotherapy such as the elderly or those from Asian backgrounds may require particular management strategies. Conclusions:The advent of targeted therapies for women with metastatic HER2-positive breast cancer has markedly improved survival. Combinations of pertuzumab-trastuzumab and a taxane are the standard of care in patients with good performance status. Given prolongation of survival and the importance of quality of life endpoints, the treatment paradigm for patients with metastatic HER2-positive breast cancer is changing rapidly. Careful management of toxicities is required, and dose reduction or switching taxane may be necessary. Further research is required on the efficacy of pertuzumab combinations in patients with brain metastases, and on those who relapse quickly following adjuvant therapy.

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