Prognostic value of expression of intracellular and extracellular domains of HER2 in patients with HER2-possitive breast cancer

Dębska, Sylwia; Kusińska, Renata; Czernek, Urszula; Szydłowska-Pazera, Katarzyna; Błasińska-Morawiec, Maria; Dowgier-Witczak, Izabela; Olas, Elżbieta; Kulig, Andrzej; Jakubiak-Wielganowicz, Magdalena; Potemski, Piotr

doi:10.5114/wo.2011.25654

2011

DOI: 10.5114/wo.2011.25654

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Prognostic value of expression of intracellular and extracellular domains of HER2 in patients with HER2-possitive breast cancer

Sylwia Dębska¹,

Renata Kusińska²,

Urszula Czernek³

et al.

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Cited by 2 publications

(1 citation statement)

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“…Breast cancer is one of the most common female malignant tumors, with morbidity increasing year by year and age of onset tending to be younger, so its harm cannot be neglected. The HER2/neu gene (also called c-erbB2) coding transmembrane receptor tyrosine protein kinase has an overexpression rate of up to 30% in breast cancer and is closely related to adverse prognosis and low sensitivity to radiotherapy and chemotherapy [ 1 , 2 ]; therefore targeted therapy against HER-2/neu has become a research hotspot in recent years. Trastuzumab (trade name: Herceptin) is a kind of humanized monoclonal antibody resisting the HER-2/neu gene.…”

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Research on drug resistance mechanism of trastuzumab caused by the activation of PI3K/Akt signaling pathway

Chen¹,

Han²,

Ouyang³

et al. 2013

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Aim of the studyTo discuss the activation of the signal transduction pathway of phosphatidylinositol 3’-kinase/serine-threonine kinase (PI3K/Akt), one of the important targets of drug resistance of trastuzumab, which provides a theoretical basis for the targeted therapy of drug resistance of trastuzumab in breast cancer.Material and methodsEstablish the drug-resistance sub-strain BT-HerR of trastuzumab for the continuous treatment of human breast cancer cell strain BT474, conduct Her-2 phenotype analysis on the drug-resistance cell strain BT-HerR with the FISH method, detect the proliferation inhibition in vitro of trastuzumab to BT474 and BT-HerR cells with the MTT method, detect the apoptosis variation after interference of trastuzumab with a flow cytometer and detect p-Akt and apoptosis-related protein expression with Western blot after PI3K/Akt inhibitor LY294002 interferes with the cells.ResultsThe gene expression of drug-resistance cell strain BT-HerR Her-2 is strongly positive; 72 hours after interference of trastuzumab, the proliferation in vitro of the BT474 and BT-HerR cells is inhibited, which is strengthened with the increase of concentration, showing a significant difference (p < 0.01); after treatment of trastuzumab, comparison of the cell apoptosis rate of BT474 and BT-HerR shows a significant difference (p < 0.01); trastuzumab can only inhibit the Akt protein phosphorylation of BT474, while LY294002 can inhibit the BT-HerR and BT474 Akt protein phosphorylation simultaneously.ConclusionsAkt protein phosphorylation of trastuzumab drug-resistance cells is activated; LY294002, a PI3K/Akt inhibitor, can obviously inhibit Akt protein phosphorylation of trastuzumab drug-resistance cells and there is a clear association between the PI3K/Akt signal transduction pathway and trastuzumab resistance.

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mentioning

confidence: 99%

Research on drug resistance mechanism of trastuzumab caused by the activation of PI3K/Akt signaling pathway

Chen¹,

Han²,

Ouyang³

et al. 2013

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Mechanistic Insight of Drug Resistance with Special Focus on Iron in Estrogen Receptor Positive Breast Cancer

Mittal¹,

Chaudhry²,

Pathania³

et al. 2014

CPB

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Estrogens along with their receptors are required for the normal physiological development of women. However, in altered physiological conditions a high level of estrogens acts either as initiator or progressor of breast cancer. Approximately in 75% of estrogen dependent breast cancer cases estrogen receptors (ERs) are held responsible. Recent studies indicate that estrogens along with iron (Fe) concomitantly involved in the proliferation of ER(+) breast cancer cells. While a number of antiestrogen/anti-ER drugs including selective estrogen receptor modulators (SERMs), aromatase inhibitors (AIs) and selective estrogen receptor down regulators (SERDs) are used to eradicate breast cancer but their action on Fe dependent breast cancer complication is not yet explored. Moreover, many of the ER(+) breast cancer patients receiving anti-estrogen drugs relapsed within a couple of years and become resistant to antiestrogen therapy. Mutation and loss of affinity to the target molecule (ERs), loss or overexpression of ERs, along with activation of growth promoting pathways alternative to estrogen-ER pathways are the major reasons of drug resistance. Combinational therapy may be best alternative to antiestrogen relapsed patients. Some of the widely studied drug combinations are roscovitine (ROSC) and tamoxifen, metformin and tamoxifen, tamoxifen and RAD001. While in all these drug combinations anti-ER compound tamoxifen may be one of the major content, anti-Fe compounds are yet to be used as drug combination. The present review article describes all the currently studied drugs/drug combinations in ER(+) breast cancer cells and future drug possibilities including anti-Fe compounds.

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Prognostic value of expression of intracellular and extracellular domains of HER2 in patients with HER2-possitive breast cancer

Cited by 2 publications

References 29 publications

Research on drug resistance mechanism of trastuzumab caused by the activation of PI3K/Akt signaling pathway

Research on drug resistance mechanism of trastuzumab caused by the activation of PI3K/Akt signaling pathway

Mechanistic Insight of Drug Resistance with Special Focus on Iron in Estrogen Receptor Positive Breast Cancer

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