Predictive markers of endocrine response in breast cancer

Mosly, Duniya; Turnbull, Arran; Sims, Andrew H.; Ward, Carol; Langdon, Simon

doi:10.5493/wjem.v8.i1.1

Cited by 21 publications

(15 citation statements)

References 54 publications

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“…The expression of the progesterone receptor (PR) is highly estrogen-dependent and has, therefore, been linked to endocrine therapy sensitivity prediction [41]. We found high expression levels of RB1, BCL11A, and KRT5 in patients diagnosed with PR-negative tumors, which might suggest their participation in endocrine resistance in some luminal cases.…”

Section: Discussionmentioning

confidence: 80%

CTCs Expression Profiling for Advanced Breast Cancer Monitoring

Pereira-Veiga¹,

Martínez‐Fernández

Abuín³

et al. 2019

Cancers

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The study of circulating tumor cells (CTCs) has a huge clinical interest in advance and metastatic breast cancer patients. However, many approaches are biased by the use of epithelial markers, which underestimate non-epithelial CTCs phenotypes. CTCs enumeration provides valuable prognostic information; however, molecular characterization could be the best option to monitor patients throughout the disease since it may provide more relevant clinical information to the physicians. In this work, we aimed at enumerating and performing a molecular characterization of CTCs from a cohort of 20 patients with metastatic breast cancer (MBC), monitoring the disease at different time points of the therapy, and at progression when it occurred. To this end, we used a CTC negative enrichment protocol that allowed us to recover a higher variety of CTCs phenotypes. With this strategy, we were able to obtain gene expression data from CTCs from all the patients. In addition, we found that high expression levels of PALB2 and MYC were associated with a worse outcome. Interestingly, we identified that CTCs with an EpCAMhighVIMlowALDH1A1high signature showed both shorter overall survival (OS) and progression-free survival (PFS), suggesting that CTCs with epithelial-stem features had the most aggressive phenotype.

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Section: Discussionmentioning

confidence: 80%

CTCs Expression Profiling for Advanced Breast Cancer Monitoring

Pereira-Veiga¹,

Martínez‐Fernández

Abuín³

et al. 2019

Cancers

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“…Nevertheless, breast cancer patients may acquire resistance to antiestrogenic drugs complicating treatment. On the other hand, the existence of more complex and undiscovered signaling pathways beyond estrogen receptors appears to control cancer progression (33,34). Thereby, the use of tamoxifen on breast cancer patients with initial GPER-1 positive tumors increased GPER-1 protein expression and markedly reduced survival (20).…”

Section: Discussionmentioning

confidence: 99%

Continuous Exposure of Breast Cancer Cells to Tamoxifen Upregulates GPER-1 and Increases Cell Proliferation

et al. 2020

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GPER-1 is a novel membrane sited G protein-coupled estrogen receptor. Clinical studies have shown that patients suffering an estrogen receptor a (ERa)/GPER-1 positive, breast cancer have a lower survival rate than those who have developed ERa-positive/GPER-1 negative tumors. Moreover, absence of GPER-1 improves the prognosis of patients treated with tamoxifen, the most used selective estrogen receptor modulator to treat ERapositive breast cancer. MCF-7 breast cancer cells were continuously treated with 1,000 nM tamoxifen for 7 days to investigate its effect on GPER-1 protein expression, cell proliferation and intracellular [Ca 2+ ]i mobilization, a key signaling pathway. Breast cancer cells continuously treated with tamoxifen, exhibited a robust [Ca 2+ ]i mobilization after stimulation with 1,000 nM tamoxifen, a response that was blunted by preincubation of cells with G15, a commercial GPER-1 antagonist. Continuously treated cells also displayed a high [Ca 2+ ]i mobilization in response to a commercial GPER-1 agonist (G1) and to estrogen, in a magnitude that doubled the response observed in untreated cells and was almost completely abolished by G15. Proliferation of cells continuously treated with tamoxifen and stimulated with 2,000 nM tamoxifen, was also higher than that observed in untreated cells in a degree that was approximately 90% attributable to GPER-1. Finally, prolonged tamoxifen treatment did not increase ERa expression, but did overexpress the kinin B1 receptor, another GPCR, which we have previously shown is highly expressed in breast tumors and increases proliferation of breast cancer cells. Although we cannot fully extrapolate the results obtained in vitro to the patients, our results shed some light on the occurrence of drug resistance in breast cancer patients who are ERa/GPER-1 positive, have been treated with tamoxifen and display low survival rate. Overexpression of kinin B1 receptor may explain the increased proliferative response observed in breast tumors under continuous treatment with tamoxifen.

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“…The grid was kept in an inverted state and a drop of the prepared formulation was applied to the grid for 10s. were obtained using the DECON program from the PCG software package 5,6 (Anton Paar, Austria).…”

Section: Size and Morphological Analysismentioning

confidence: 99%

Synthesis, Physiochemical and Biological evaluation of Inclusion Complex of Benzyl Isothiocyanate encapsulated in cyclodextrins for triple negative breast cancer

Uppal

Kumar

Kaur

et al. 2021

Preprint

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Benzyl isothiocyanate (BITC), an organic dietary compound, is allied with a major role in the potential chemopreventive effects. BITC has acknowledged rising attention as a therapeutic compound to be used in medicine because of its high potency and characteristic biopharmaceutical properties, like high permeability with marginal aqueous solubility. The highly volatile and hydrophobic nature brought a need to provide a suitable delivery-matrix to BITC to exploit its pharmacological potential to the fullest. It has been successfully incorporated in β-CD and HP-β-CD using acoustic forces and thoroughly characterized using UV-vis spectroscopy, FTIR, DSC, TEM, and SAXS. The complexation helped in masking the acute odour, achieving a controlled release of BITC, and made its use viable by prolonging the retention time and thereby sustaining the biological effects. Different models like Higuchi, first-order kinetic decay, Korsmeyer-Peppas model were applied, suggesting a diffusion-controlled mechanism of release. Also, the bioaccessibility and stability of BITC in an in vitro digestion model was evaluated. The main objective of the present work was to systemically study the credibility of BITC-CD complexes in well-established tumor mimicking 2D cell culture models and produce a conclusive report on its chemotherapeutic activity. The in vitro anti-cancer activity of BITC and the formed sonochemical complexes was confirmed by MTT assay and further evaluated using apoptosis assay and production of ROS like moieties. Cell cycle analysis was done to evaluate the growth inhibitory mechanism of BITC. Strikingly, BITC and its complexes showcased ROS generation and lysosome-mediated cell death. Effect on cell migration was assessed using wound healing assay. The results promptly suggest the functional efficacy of the CDs in releasing BITC and attest the ability of the complexes to provide alternate to otherwise remedially sparse triple-negative breast cancer.

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Predictive markers of endocrine response in breast cancer

Cited by 21 publications

References 54 publications

CTCs Expression Profiling for Advanced Breast Cancer Monitoring

CTCs Expression Profiling for Advanced Breast Cancer Monitoring

Continuous Exposure of Breast Cancer Cells to Tamoxifen Upregulates GPER-1 and Increases Cell Proliferation

Synthesis, Physiochemical and Biological evaluation of Inclusion Complex of Benzyl Isothiocyanate encapsulated in cyclodextrins for triple negative breast cancer

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