We are analyzing https://link.springer.com/article/10.1186/bcr2625.

Title:
Anti-tumor effects of retinoids combined with trastuzumab or tamoxifen in breast cancer cells: induction of apoptosis by retinoid/trastuzumab combinations | Breast Cancer Research
Description:
Introduction HER2 and estrogen receptor (ER) are important in breast cancer and are therapeutic targets of trastuzumab (Herceptin) and tamoxifen, respectively. Retinoids inhibit breast cancer growth, and modulate signaling by HER2 and ER. We hypothesized that treatment with retinoids and simultaneous targeting of HER2 and/or ER may have enhanced anti-tumor effects. Methods The effects of retinoids combined with trastuzumab or tamoxifen were examined in two human breast cancer cell lines in culture, BT474 and SKBR3. Assays of proliferation, apoptosis, differentiation, cell cycle distribution, and receptor signaling were performed. Results In HER2-overexpressing/ER-positive BT474 cells, combining all-trans retinoic acid (atRA) with tamoxifen or trastuzumab synergistically inhibited cell growth, and altered cell differentiation and cell cycle. Only atRA/trastuzumab-containing combinations induced apoptosis. BT474 and HER2-overexpressing/ER-negative SKBR3 cells were treated with a panel of retinoids (atRA, 9-cis-retinoic acid, 13-cis-retinoic acid, or N-(4-hydroxyphenyl) retinamide (fenretinide) (4-HPR)) combined with trastuzumab. In BT474 cells, none of the single agents except 4-HPR induced apoptosis, but again combinations of each retinoid with trastuzumab did induce apoptosis. In contrast, the single retinoid agents did cause apoptosis in SKBR3 cells; this was only modestly enhanced by addition of trastuzumab. The retinoid drug combinations altered signaling by HER2 and ER. Retinoids were inactive in trastuzumab-resistant BT474 cells. Conclusions Combining retinoids with trastuzumab maximally inhibits cell growth and induces apoptosis in trastuzumab-sensitive cells. Treatment with such combinations may have benefit for breast cancer patients.
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Keywords {🔍}

cells, cancer, breast, trastuzumab, pubmed, google, scholar, cas, cell, atra, article, retinoids, tamoxifen, combinations, phase, treatment, growth, apoptosis, figure, acid, skbr, retinoic, single, agents, patients, hpr, activity, combination, receptor, cycle, treated, retinoid, drugs, analysis, differentiation, effect, effects, pbs, res, human, inhibition, trial, clin, estrogen, fenretinide, μgml, proliferation, oncol, results, drug,

Topics {✒️}

her2-overexpressing/er-positive bt474 cells her2-overexpressing/er-negative skbr3 cells nuclear steroid/thyroid/retinoid receptors cmv-renilla luciferase vectors er-negative/her2-overexpressing cells mitogen-activated protein kinase possess anti-tumor activity anti-p185her2 monoclonal antibodies p27kip1-cdk2 complex formation endocrine-responsive breast cancer consulting/advisory board roles mediates transcriptional cross-talk exert anti-estrogenic effects her2-positive breast cancer article download pdf shown anti-tumor activity epidermal growth factor enhanced anti-tumor effects estrogen receptor-negative model anti-p185her2 antibody receptor-selective ligand lgd1069 retinoic acid receptor-alpha c-erbb-2 signaling pathways atra/trastuzumab/tamoxifen combination induced full size image neutral lipid production er-positive t47d cells 9-cis-ra caused decreases inhibit estrogen-induced growth humanized tumor mice propidium iodide-positive cells tumor necrosis factor humanized monoclonal antibody wst-1 proliferation assay high-dose retinyl acetate atra-induced growth inhibition trastuzumab-resistant bt474 cells er-positive bt474 cells endocrine therapy refractory annexin v-positive cells ifnβ/retinyl palmitate/tamoxifen human breast cancer serum-free rpmi media breast cancer revealed renilla luciferase activities early breast cancer atra/trastuzumab/tamoxifen combinations resulted er-negative skbr3 cells er-negative/skbr3 cells single-agent atra caused

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         description:HER2 and estrogen receptor (ER) are important in breast cancer and are therapeutic targets of trastuzumab (Herceptin) and tamoxifen, respectively. Retinoids inhibit breast cancer growth, and modulate signaling by HER2 and ER. We hypothesized that treatment with retinoids and simultaneous targeting of HER2 and/or ER may have enhanced anti-tumor effects. The effects of retinoids combined with trastuzumab or tamoxifen were examined in two human breast cancer cell lines in culture, BT474 and SKBR3. Assays of proliferation, apoptosis, differentiation, cell cycle distribution, and receptor signaling were performed. In HER2-overexpressing/ER-positive BT474 cells, combining all-trans retinoic acid (atRA) with tamoxifen or trastuzumab synergistically inhibited cell growth, and altered cell differentiation and cell cycle. Only atRA/trastuzumab-containing combinations induced apoptosis. BT474 and HER2-overexpressing/ER-negative SKBR3 cells were treated with a panel of retinoids (atRA, 9-cis-retinoic acid, 13-cis-retinoic acid, or N-(4-hydroxyphenyl) retinamide (fenretinide) (4-HPR)) combined with trastuzumab. In BT474 cells, none of the single agents except 4-HPR induced apoptosis, but again combinations of each retinoid with trastuzumab did induce apoptosis. In contrast, the single retinoid agents did cause apoptosis in SKBR3 cells; this was only modestly enhanced by addition of trastuzumab. The retinoid drug combinations altered signaling by HER2 and ER. Retinoids were inactive in trastuzumab-resistant BT474 cells. Combining retinoids with trastuzumab maximally inhibits cell growth and induces apoptosis in trastuzumab-sensitive cells. Treatment with such combinations may have benefit for breast cancer patients.
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            Trastuzumab
            Retinoid
            Combination Index
            BT474 Cell
            Cancer Research
            Oncology
            Surgical Oncology
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      description:HER2 and estrogen receptor (ER) are important in breast cancer and are therapeutic targets of trastuzumab (Herceptin) and tamoxifen, respectively. Retinoids inhibit breast cancer growth, and modulate signaling by HER2 and ER. We hypothesized that treatment with retinoids and simultaneous targeting of HER2 and/or ER may have enhanced anti-tumor effects. The effects of retinoids combined with trastuzumab or tamoxifen were examined in two human breast cancer cell lines in culture, BT474 and SKBR3. Assays of proliferation, apoptosis, differentiation, cell cycle distribution, and receptor signaling were performed. In HER2-overexpressing/ER-positive BT474 cells, combining all-trans retinoic acid (atRA) with tamoxifen or trastuzumab synergistically inhibited cell growth, and altered cell differentiation and cell cycle. Only atRA/trastuzumab-containing combinations induced apoptosis. BT474 and HER2-overexpressing/ER-negative SKBR3 cells were treated with a panel of retinoids (atRA, 9-cis-retinoic acid, 13-cis-retinoic acid, or N-(4-hydroxyphenyl) retinamide (fenretinide) (4-HPR)) combined with trastuzumab. In BT474 cells, none of the single agents except 4-HPR induced apoptosis, but again combinations of each retinoid with trastuzumab did induce apoptosis. In contrast, the single retinoid agents did cause apoptosis in SKBR3 cells; this was only modestly enhanced by addition of trastuzumab. The retinoid drug combinations altered signaling by HER2 and ER. Retinoids were inactive in trastuzumab-resistant BT474 cells. Combining retinoids with trastuzumab maximally inhibits cell growth and induces apoptosis in trastuzumab-sensitive cells. Treatment with such combinations may have benefit for breast cancer patients.
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         Trastuzumab
         Retinoid
         Combination Index
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         Cancer Research
         Oncology
         Surgical Oncology
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      name:Department of Internal Medicine (Section of Medical Oncology), Yale Cancer Center and Smilow Cancer Hospital at Yale-New-Haven Hospital, Yale University School of Medicine, New Haven, USA
      name:Department of Internal Medicine (Section of Medical Oncology), Yale Cancer Center and Smilow Cancer Hospital at Yale-New-Haven Hospital, Yale University School of Medicine, New Haven, USA
      name:Department of Internal Medicine (Section of Medical Oncology), Yale Cancer Center and Smilow Cancer Hospital at Yale-New-Haven Hospital, Yale University School of Medicine, New Haven, USA

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