Breast cancer: Current and future endocrine therapies

Palmieri, Carlo; Patten, Darren K.; Januszewski, Adam; Zucchini, G; Howell, Sacha J.

doi:10.1016/j.mce.2013.08.001

Cited by 87 publications

(53 citation statements)

References 230 publications

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“…The tyrosine kinase inhibitors have revolutionized the treatment of not only leukemia, but also renal cell carcinoma, neuroendocrine tumors, and GI stromal tumors. Other examples of targeted enzyme therapy for cancer include the mammalian target of rapamycin inhibitors for breast and renal cell cancers (everolimus, temsirolimus) (2,55), the tyrosine kinase inhibitor regorafenib for colorectal cancer (33), and aromatase inhibitors, which decrease the production of estrogen and are used to treat estrogen receptor (ER)-positive breast cancer (61). Examples of monoclonal antibodies used to target a specific protein include bevacizumab, which targets vascular endothelial growth factor (VEGF), cetuximab and panitumumab, which bind epidermal growth factor receptor (EGFR) (colorectal cancer) (83), and trastuzamab, which targets human EGFR-2 and is used in HER-2 positive breast cancer (75).…”

Section: The Cancer Problemmentioning

confidence: 99%

The Emerging Role of QSOX1 in Cancer

Lake

Faigel

2014

Antioxidants & Redox Signaling

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Significance: Quiescin sulfhydryl oxidase 1 (QSOX1) is an enzyme that oxidizes thiols during protein folding, reducing molecular oxygen to hydrogen peroxide. Tumor cells may take advantage of oxidative environments at different stages of tumorigenesis, but QSOX1 may also serve additional functions in tumors. Recent Advances: Several groups have reported the over-expression of QSOX1 in breast, pancreas, and prostate cancers. A consensus is building that QSOX1 over-expression is important during tumor cell invasion, facilitating tumor cell migration at the tumor-stroma interface. As such, QSOX1 may be considered a prognostic indicator of metastatic potential or even indicate that cancer is present in a host. Critical Issues: However, some controversy exists between QSOX1 as a marker of poor or favorable outcome in breast cancer. More studies are required to reveal what advantage QSOX1 provides to breast and other types of cancer. More specifically, it is critical to learn which tumor types over-express QSOX1 and use its enzymatic activity to their advantage. Future Directions: As interest increases in understanding the mechanisms of tumorigenesis within the extracellular matrix and how tumor cells influence fibroblasts and other stromal cells, QSOX1 may be revealed as an important player in cancer detection and prognosis. Defining the mechanism(s) of QSOX1 activity in tumors and in in vivo models will provide important insights into how to target QSOX1 with anti-neoplastic agents. Antioxid. Redox Signal. 21, 485-496.

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Section: The Cancer Problemmentioning

confidence: 99%

The Emerging Role of QSOX1 in Cancer

Lake

Faigel

2014

Antioxidants & Redox Signaling

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“…However, all patients eventually experience disease progression, requiring alternative therapies. Resistance to endocrine therapies has been extensively studied, in order to decipher its mechanisms and to generate a rationale for targeted therapies which might circumvent endocrine resistance and/or exert significant clinical activity per se [2,3]. Among those mechanisms, activation of the PI3K/mTOR pathway has been repeatedly demonstrated as a key endocrine resistance factor [4].…”

Section: Introductionmentioning

confidence: 99%

Efficacy and tolerance of everolimus in 123 consecutive advanced ER positive, HER2 negative breast cancer patients. A two center retrospective study

et al. 2015

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“…Le SERM le plus utilisé est le tamoxifène, mais on a recours également au raloxifène. Des mécanismes de résistance tumorale à ces traitements apparaissent dans environ la moitié des cas [4,5]. La recherche de nouveaux SERM est par conséquent nécessaire pour le traitement de la ménopause, mais également pour le cancer du sein.…”

Section: Le Récepteur Alpha Des Oestrogènes (Era) : Un Récepteur Nuclunclassified

“…Des données préliminaires indiquent clairement que dans le foie, la régulation de l'expression des gènes par ER repose à la fois sur les effets nucléaires et membranaires du récepteur. Le découplage des effets membranaires et nucléaires par l'E4 pourrait donc, selon notre hypothèse, permettre d'atténuer les effets hépatiques des oestrogènes et donc présenter un profil liver friendly 4 , caractéristique unique pour un SERM.…”

Section: Référencesunclassified