Differential response to primary chemotherapy and long-term survival in patients with triple-negative breast cancer

Liedtke, Cornelia; Mazouni, C.; Hess, KR; Tordai, Attila; André, Fabrice; Symmans, W. Fraser; González-Angulo, Ana M.; Green, M.; Hortobágyi, Gabriel N.; Pusztai, Lajos

doi:10.1200/jco.2007.25.18_suppl.10519

Cited by 5 publications

(4 citation statements)

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“…When tumor volume reached 100 mm 3 (calculated using the formula vulaa 2 × b × π/6; b is the length and a is the width in mm), tumor sizes were recorded weekly to control tumor volume within 1500 mm 3 .…”

Section: Animal Transplantation Tumor Experimentsmentioning

confidence: 99%

“…To date, tumors respond initially to chemotherapy and targeted agents, including epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF), and poly (ADP-ribose) polymerase (PARP) inhibitors, but there is poor overall survival (OS) of TNBC mainly due to drug acquired resistance. 3 In TNBC treatment, taxol-based regimens have proven to be an important chemotherapy agent. Taxol induces mitosis arrest by stabilizing the spindle microtubules responsible for segregation of duplicated chromosomes to daughter cells.…”

Section: Introductionmentioning

confidence: 99%

“…The majority of TNBC expresses a “basal‐like” molecular gene profile, and the BRCA1 pathway contributes to sporadic basal‐like breast cancer. To date, tumors respond initially to chemotherapy and targeted agents, including epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF), and poly (ADP‐ribose) polymerase (PARP) inhibitors, but there is poor overall survival (OS) of TNBC mainly due to drug acquired resistance . In TNBC treatment, taxol‐based regimens have proven to be an important chemotherapy agent.…”

Section: Introductionmentioning

confidence: 99%

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Role of inhibitor of yes‐associated protein 1 in triple‐negative breast cancer with taxol‐based chemoresistance

et al. 2019

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Triple‐negative breast cancer (TNBC) is highly clinically aggressive and taxol‐based chemoresistance remains a big TNBC therapeutic problem to be solved. Verteporfin, a small molecular yes‐associated protein 1 (YAP1) inhibitor, is little known as an antitumor drug for TNBC. Our data showed that YAP1 expression was associated with early relapse in tissue samples of patients with TNBC taxol chemoresistance (P < .001). Verteporfin reduced migration and enhanced apoptosis or autophagy of a taxol‐resistant MDA‐MB‐231 cell line in vitro. Knockdown of YAP1 increased epithelial‐mesenchymal transition response in a taxol‐resistant TNBC cell line. In an in vivo experiment, we found that verteporfin was able to shrink tumor weight and volume and decreased Ki67 expression in a taxol‐resistant mouse model. Our results provide evidence that verteporfin could be a chemosensitizer for TNBC patients with taxol‐based treatment.

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Section: Animal Transplantation Tumor Experimentsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Role of inhibitor of yes‐associated protein 1 in triple‐negative breast cancer with taxol‐based chemoresistance

et al. 2019

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“…Triple-negative breast carcinoma is characterized as negative for estrogen receptor, progesterone receptor, and human epidermal growth factor receptor-2 (HER-2), and has been reported to account for approximately 15% of breast cancers. 1,2 As a consequence, the hormonal therapeutic regimes or HER-2-targeted medications are unlikely to respond. Moreover, triple-negative breast carcinoma possesses formidable characteristics of aggressive invasiveness and metastasis, 3,4 leading to poor prognosis.…”

Section: ■ Introductionmentioning

confidence: 99%

Bioresorbable Depot for Sustained Release of Immunostimulatory Resiquimod in Suppressing Both Primary Triple-Negative Breast Tumors and Metastatic Occurrence

et al. 2021

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In light of immune facilities trafficking toward the pathological sites along upward gradient of immunostimulatory cytokines, a localized resiquimod (Toll-like receptor 7/8 agonist) release depot was manufactured for pursuit of precision immunostimulation toward intractable triple-negative breast carcinoma. In principle, resiquimod/poly(lactic-co-glycolic acid) microspheres were fabricated and embedded into injectable and biodegradable poly(ethylene glycol) (PEG)-based hydrogel. The subsequent investigations approved persistent retention of immunostimulatory resiquimod in tumors upon peritumoral administration, which consequently led to localized and consistent secretion of immunostimulatory cytokines. Initially, not only innate tumor phagocytosis but also adaptive antitumor immunities were successfully cultivated for in situ suppression of the growth of primary solid tumors, more importantly, capable of inhibiting distant pulmonary metastasis, as evidenced by observation of enormous lymphocytes selectively gathering in the pulmonary artery. Hence, our presented study provided an important clinical indication of using immunostimulatory drugs to activate potent innate and adaptive antitumor immunities for precision antitumor therapy. Further immunomodulatory strategies, such as checkpoint blockage and tumor immunogenicity, could also be complementary for development of advanced antitumor immunotherapeutics in treatment of a number of intractable tumors.

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Efficacy of ixabepilone in ER/PR/HER2-negative (triple-negative) breast cancer

Perez

Patel

Moreno-Aspitia

2010

Breast Cancer Res Treat

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Patients with ER/PR/HER2-negative (triple negative) breast cancer are not candidates for hormonal therapy or HER2-targeted agents. Ongoing research is aimed at identifying and understanding the benefit of established and emerging therapies in this disease setting. Triple-negative patients may achieve early responses to anthracyclines and taxanes, but novel strategies are also eagerly sought. The epothilone B analog ixabepilone acts to stabilize microtubules and demonstrates antitumor activity in recent breast cancer studies. Herein, we have analyzed efficacy and safety data of ixabepilone specifically for the treatment of women with triple-negative disease. A retrospective analysis was completed using activity and toxicity data in the triple-negative subsets from 5 phase II studies. In addition, a prospective pooled analysis of triple-negative patients from 2 phase III trials is also reviewed. Of 2,261 patients evaluated in these trials, 556 (24.5%) had triple-negative tumors. In the neoadjuvant setting, ixabepilone produced a pathologic complete response rate in the breast of 26% in triple-negative patients (vs. 15% in the non-triple-negative population). In patients with metastatic breast cancer whose pretreatment status ranged from no prior therapy to progression on several classes of agents, overall response rates (ORR) in the phase II ixabepilone monotherapy trials ranged from 6 to 55%, comparable to rates seen in patients with non-triple-negative tumors. The combination of ixabepilone and capecitabine in the phase II study resulted in an ORR of 23% in triple-negative patients. A similar ORR (31%) was observed for a preplanned pooled analysis of triple-negative patients in the phase III trials of ixabepilone plus capecitabine. The median progression-free survival (PFS) was significantly longer for triple-negative patients treated with ixabepilone plus capecitabine (4.2 months) compared with treatment with capecitabine alone (1.7 months). No increase in toxicity was noted in the triple-negative subgroup compared with other patients. Ixabepilone shows notable antitumor activity in patients with triple-negative breast cancer when used in a variety of settings. The addition of ixabepilone to capecitabine results in an approximately twofold increase in median PFS for triple-negative patients versus capecitabine alone and responses to ixabepilone in triple-negative disease are comparable to those seen in patients with non-triple-negative tumors.

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Differential response to primary chemotherapy and long-term survival in patients with triple-negative breast cancer

Cited by 5 publications

References 0 publications

Role of inhibitor of yes‐associated protein 1 in triple‐negative breast cancer with taxol‐based chemoresistance

Role of inhibitor of yes‐associated protein 1 in triple‐negative breast cancer with taxol‐based chemoresistance

Bioresorbable Depot for Sustained Release of Immunostimulatory Resiquimod in Suppressing Both Primary Triple-Negative Breast Tumors and Metastatic Occurrence

Efficacy of ixabepilone in ER/PR/HER2-negative (triple-negative) breast cancer

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