Efficacy and safety of first-line treatment for metastatic triple-negative breast cancer: A network meta-analysis

Shi, Mengsha; Li, Zhoujuan; Shen, Guoshuang; Wang, Tianzhuo; Li, Jinming; Wang, Miaozhou; Liu, Zhen; Zhao, Fuhua; Ren, Dengfeng; Zhao, Jiuda

doi:10.1016/j.cpt.2023.06.002

Cited by 9 publications

(2 citation statements)

References 62 publications

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“…These regimens are weakly recommended as first-line treatment in breast cancer clinical practice guidelines. An overseas study showed that cisplatin combined with nab-paclitaxel or paclitaxel is the preferred first-line treatment for mTNBC [ 16 ]. This difference between Japan and other countries in the commonly used regimen is most likely due to the difference in the treatments covered by insurance.…”

Section: Discussionmentioning

confidence: 99%

Treatment patterns and clinical outcomes in patients with metastatic triple-negative breast cancer: a large-scale data analysis using the Japanese claims database

Kimura,

Takami,

Piao

et al. 2024

Breast Cancer Res Treat

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Purpose This study evaluated treatment patterns and clinical outcomes among patients with metastatic triple-negative breast cancer (mTNBC) in real-world clinical settings in Japan. Methods The treatment patterns, time to next treatment or death (TTNTD), time to treatment discontinuation, adverse events of interest, and medical costs of treating patients with mTNBC in first-, second-, and third-line settings were investigated using data of patients meeting the inclusion criteria between January 2017 and March 2022 in a Japanese medical claims database. The treatment regimens for mTNBC were defined according to the Japanese Breast Cancer Society Clinical Practice Guidelines. Results In this study, 2236 patients with mTNBC (median age 66.0 years; 99.8% female) were included in the first-line cohort. Of these, 46.6% and 20.8% were included in the second- and third-line cohorts, respectively. The two most frequently used treatments were capecitabine (19.1%) and S-1 (tegafur–gimeracil–oteracil) (14.5%) in the first-line cohort, eribulin (18.3%) and bevacizumab/paclitaxel (14.4%) in the second-line cohort, and eribulin (19.4%) and bevacizumab/paclitaxel (17.5%) in the third-line cohort. The TTNTD shortened as the line of therapy progressed (median 8.0, 6.5, and 5.2 months for the first-, second-, and third-line treatments, respectively). Nausea/vomiting and neutropenia/leukopenia occurred in 62.8% and 18.3% of all patients, respectively. The medical total costs per day were 6.7, 10.2, and 12.9 thousand yen during the first-/second-/third-line treatments, respectively. Conclusion This study provides insight into current treatment patterns for mTNBC in Japan. The cost–benefit balance worsens with later-line treatment and a high unmet need for mTNBC drug treatment remains.

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Section: Discussionmentioning

confidence: 99%

Treatment patterns and clinical outcomes in patients with metastatic triple-negative breast cancer: a large-scale data analysis using the Japanese claims database

Kimura,

Takami,

Piao

et al. 2024

Breast Cancer Res Treat

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“…Breast cancer is among the most common human malignancies. Current chemotherapy regimens for breast cancer are based on combinations of anthracyclines (such as doxorubicin, epirubicin, and daunomycin) and/or taxanes (such as taxol/paclitaxel (PTX) and 2 of 18 docetaxel) [1]. Unfortunately, classical effective therapeutic strategies often lead to the acquisition of drug resistance in human tumours [2], which is one of the main reasons for relapse and metastasis.…”

Section: Introductionmentioning

confidence: 99%

Imbalance between Actin Isoforms Contributes to Tumour Progression in Taxol-Resistant Triple-Negative Breast Cancer Cells

Dugina,

Vasileva,

Khromova

et al. 2024

IJMS

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The widespread occurrence of breast cancer and its propensity to develop drug resistance highlight the need for a comprehensive understanding of the molecular mechanisms involved. This study investigates the intricate pathways associated with secondary resistance to taxol in triple-negative breast cancer (TNBC) cells, with a particular focus on the changes observed in the cytoplasmic actin isoforms. By studying a taxol-resistant TNBC cell line, we revealed a shift between actin isoforms towards γ-actin predominance, accompanied by increased motility and invasive properties. This was associated with altered tubulin isotype expression and reorganisation of the microtubule system. In addition, we have shown that taxol-resistant TNBC cells underwent epithelial-to-mesenchymal transition (EMT), as evidenced by Twist1-mediated downregulation of E-cadherin expression and increased nuclear translocation of β-catenin. The RNA profiling analysis revealed that taxol-resistant cells exhibited significantly increased positive regulation of cell migration, hormone response, cell–substrate adhesion, and actin filament-based processes compared with naïve TNBC cells. Notably, taxol-resistant cells exhibited a reduced proliferation rate, which was associated with an increased invasiveness in vitro and in vivo, revealing a complex interplay between proliferative and metastatic potential. This study suggests that prolonged exposure to taxol and acquisition of taxol resistance may lead to pro-metastatic changes in the TNBC cell line.

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The N6-methyladenosine writer METTL3 promotes breast cancer progression through YTHDF2-dependent posttranscriptional silencing of GSDMD

Shuai,

Ma,

et al. 2024

Apoptosis

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Efficacy and safety of first-line treatment for metastatic triple-negative breast cancer: A network meta-analysis

Cited by 9 publications

References 62 publications

Treatment patterns and clinical outcomes in patients with metastatic triple-negative breast cancer: a large-scale data analysis using the Japanese claims database

Treatment patterns and clinical outcomes in patients with metastatic triple-negative breast cancer: a large-scale data analysis using the Japanese claims database

Imbalance between Actin Isoforms Contributes to Tumour Progression in Taxol-Resistant Triple-Negative Breast Cancer Cells

The N6-methyladenosine writer METTL3 promotes breast cancer progression through YTHDF2-dependent posttranscriptional silencing of GSDMD

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