Anthracycline could be essential for triple-negative breast cancer: A randomised phase II study by the Kanagawa Breast Oncology Group (KBOG) 1101

Narui, Kazutaka; Ishikawa, Takashi; Shimizu, Daisuke; Yamada, Akihiro; Tanabe, Mikiko; Sasaki, Takeshi; Oba, Mari S.; Morita, Satoshi; Nawata, Shuichi; Kida, Kumiko; Mogaki, Masatoshi; Doi, Takako; Tsugawa, Koichiro; Ogata, Haruki; Ota, T.; Kosaka, Yoshimasa; Sengoku, Norihiko; Kuranami, Masaru; Niikura, Naoki; Saito, Yuki; Suzuki, Yasuhiro; Suto, Akihiko; Arioka, Hitoshi; Chishima, Takashi; Ichikawa, Yasushi; Endo, Itaru; Tokuda, Yutaka

doi:10.1016/j.breast.2019.06.003

Cited by 13 publications

(7 citation statements)

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“…The copyright holder for this preprint this version posted May 21, 2021. ; https://doi.org/10.1101/2021.05.20.445072 doi: bioRxiv preprint 36% for breast and almost 100% for brain cancer) and make tumors refractory to future treatments 21 . The risk of anthracycline related cardiomyopathy increases with a higher cumulative anthracycline dose 22 . About 3% of the dose persist even after the completion of therapy leading to heart failure and death for a dose 400 mg/m 2 , 7% for a dose of 550 mg/m 2 , and 18% for a dose of 700 mg/m 2 .…”

Section: Introductionmentioning

confidence: 99%

Rational Drug Design of Targeted and Enzyme Cleavable Vitamin E Analogs as Neoadjuvant to Chemotherapy: In Vitro and In Vivo Evaluation on Reduction of Cardiotoxicity of Doxorubicin.

Rs¹,

Cseh²,

Luchman³

et al. 2021

Preprint

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Traditional drug design focus on specific target (s) expressed by cancer cells. However, cancer cells outsmart the interventions by activating survival pathways and/or downregulating cell death pathways. As the research in molecular biology of cancer grows exponentially, new methods of drug designs are needed to target multiple pathways/targets which are involved in survival of cancer cells. Vitamin E analogues including a-tocopheryl succinate (TOS) is a well-known anti-tumoregenic agent which is well studied both in vitro and in vivo tumor models. However, lack of targeting cancer cells and unexpected toxicity along with the poor water solubility of TOS compelled a rational drug design using both targeting and cleavable technologies incorporated in the new drug design. A plethora of Vitamin E derivatives (AMP-001, 002 and 003) were synthesized, characterized and studied for the improved efficacy and lowered toxicity in various cancer cells in vitro. Preliminary studies revealed AAAPT leading candidates reduced the invasive potential of brain tumor stem cells, synergized with different drugs and different treatments. AAAPT leading drug AMP-001 enhanced the therapeutic index of front-line drug Doxorubicin in triple negative breast cancer (TNBC) tumor rat model preserving the ventricular function when used as a neoadjuvant to Doxorubicin. These results may pave the way for reducing the cardiotoxicity of chemotherapy in clinical settings.

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Section: Introductionmentioning

confidence: 99%

Rational Drug Design of Targeted and Enzyme Cleavable Vitamin E Analogs as Neoadjuvant to Chemotherapy: In Vitro and In Vivo Evaluation on Reduction of Cardiotoxicity of Doxorubicin.

Rs¹,

Cseh²,

Luchman³

et al. 2021

Preprint

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“…Indeed, many BC treatment options yield significant cardiotoxicity: anthracyclines and radiation therapy have long been linked to a dose-related development of myocardial fibrosis, whereas trastuzumab and immune checkpoint inhibitors have been associated to stochastic cardiotoxic effects [ 4 ]. Nonetheless, anthracyclines still represent a cornerstone of BC treatment, especially in patients with advanced disease or triple negative neoplasms [ 5 ]. In addition to the well-known toxic effects on cardiomyocytes, anthracyclines are metabolised by adipose tissue and may produce shifts in adipocytes activity in different adipose tissues [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

Potential role of epicardial adipose tissue as a biomarker of anthracycline cardiotoxicity

et al. 2021

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Background We investigated the radiodensity of epicardial (EAT), subcutaneous (SAT), and visceral adipose tissue (VAT) before and after treatment with anthracyclines in a population of breast cancer (BC) patients, and in controls not treated with anthracyclines, to detect a potential role of EAT density as a biomarker of changes related to chemotherapy cardiotoxicity. Methods We reviewed BC patients treated with anthracyclines who underwent CT before (CT-t0) and after (CT-t1) chemotherapy, and age- and sex-matched controls who underwent two CT examinations at comparable intervals. On non-contrast scans, EAT was segmented contouring the pericardium and thresholding between -190 and -30 Hounsfield units (HU), and SAT and VAT were segmented with two 15-mm diameter regions of interest thresholded between -195 and -45 HU. Results Thirty-two female patients and 32 controls were included. There were no differences in age (p = 0.439) and follow-up duration (p = 0.162) between patients and controls. Between CT-t0 and CT-t1, EAT density decreased in BC patients (-66 HU, interquartile range [IQR] -71 to -63 HU, to -71 HU, IQR -75 to -66 HU, p = 0.003), while it did not vary in controls (p = 0.955). SAT density increased from CT-t0 to CT-t1 in BC patients (-107 HU, IQR -111 to -105 HU, to -105 HU, IQR -110 to -100 HU, p = 0.014), whereas it did not change in controls (p = 0.477). VAT density did not vary in either BC patients (p = 0.911) or controls (p = 0.627). Conclusions EAT density appears to be influenced by anthracycline treatment for BC, well known for its cardiotoxicity, shifting towards lower values indicative of a less active metabolism.

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“…At present, the treatment methods of BC mainly include surgical treatment, radiotherapy and chemotherapy, endocrine therapy, etc. However, with the deepening of the understanding of the mechanism of BC occurrence and development and the advancement of molecular biology technology, the application of BC targeted therapy has become more and more extensive [ 3 , 4 ].…”

Section: Introductionmentioning

confidence: 99%

Effect of microrna-138 on epithelial-Mesenchymal transition and invasion of breast cancer cells by targeting semaphorin 4C

Liu

2021

Bioengineered

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In view of the role of miR-138 in cancer cells, we predicted the target of miR-138 and its targeting to SEMA4C by bioinformatics software and luciferase experiment. The expression levels of miR-138 in human normal breast epithelial cells and two kinds of BC cells were compared, and the transfection cells were selected. MiR-138 mimetic negative control (miR-NC), miR-138 mimic and miR-138 inhibitor were designed for cell transfection. The results showed that the expression level of miR-138 in MCF-7 cells was the lowest. The up regulation of miR-138 would lead to the high expression of E-cad and the low expression of N-cad, vim and SEMA4C, and the vitality and invasion of BC cells would decrease. The down regulation of miR-138 would lead to the low expression of E-cad and the high expression of N-cad, vim and SEMA4C, and the vitality and invasion of BC cells would increase. miR-138 targeted regulation of SEMA4C can promote the expression of N-cad, inhibit the expression of E-cad, vim and SEMA4C, reverse the EMT of BC cells, and inhibit the activity and invasion of BC cells. MiR-138 has clinical potential as a tumor marker of BC.

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Anthracycline could be essential for triple-negative breast cancer: A randomised phase II study by the Kanagawa Breast Oncology Group (KBOG) 1101

Cited by 13 publications

References 35 publications

Rational Drug Design of Targeted and Enzyme Cleavable Vitamin E Analogs as Neoadjuvant to Chemotherapy: In Vitro and In Vivo Evaluation on Reduction of Cardiotoxicity of Doxorubicin.

Rational Drug Design of Targeted and Enzyme Cleavable Vitamin E Analogs as Neoadjuvant to Chemotherapy: In Vitro and In Vivo Evaluation on Reduction of Cardiotoxicity of Doxorubicin.

Potential role of epicardial adipose tissue as a biomarker of anthracycline cardiotoxicity

Effect of microrna-138 on epithelial-Mesenchymal transition and invasion of breast cancer cells by targeting semaphorin 4C

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