A Single Institution Experience of Incorporation of Cisplatin into Adjuvant Chemotherapy for Patients With Triple-Negative Breast Cancer of Unknown<i>BRCA</i>Mutation Status

Su, Yu‐Jang; Hung, Chen-Yu; Lam, Hung-Bun; Chang, Yuan‐Ching; Yang, Po‐Sheng

doi:10.1177/1179554918794672

Cited by 11 publications

(9 citation statements)

References 32 publications

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“…91 An increased tumor pathological complete response (pCR) was shown in 53.2% of the patients with stage II-III triple-negative breast cancer (TNBC) treated with carboplatin against 36.9% without carboplatin. 92 In the BrighTNess trial, the pCR rate in TNBC increased from 31% without carboplatin to 58% with carboplatin. 92 In gastric cancer, a high amount of TAMs before treatment correlated with prolonged survival in patients who received 5-fluorouracil (FU)-based postoperative chemotherapy.…”

Section: Real-time Pcrmentioning

confidence: 99%

“…92 In the BrighTNess trial, the pCR rate in TNBC increased from 31% without carboplatin to 58% with carboplatin. 92 In gastric cancer, a high amount of TAMs before treatment correlated with prolonged survival in patients who received 5-fluorouracil (FU)-based postoperative chemotherapy. 76 In patients with stage III colorectal cancer treated with 5-FU adjuvant therapy, the high macrophage density before the treatment significantly correlated with a better improved prognosis.…”

Section: Real-time Pcrmentioning

confidence: 99%

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Interaction of tumor-associated macrophages and cancer chemotherapy

et al. 2019

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It has been recently recognized that the tumor microenvironment (TME) is an essential factor that defines the efficiency of chemotherapy. The local TME, consisting of immune cells with diverse phenotypes and functions, can strongly modulate the response to chemotherapy. Tumor-associated macrophages (TAMs) that display pronounced heterogeneity and phenotypic plasticity are the major innate immune component in the microenvironment of solid tumors. In our review, we elucidate the complex role of TAMs in the progression of different types of solid tumors, summarize the current knowledge about the effects of different anticancer chemotherapeutic agents on monocytes/macrophages, and describe the mechanisms of chemotherapy resistance mediated by TAMs.

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Section: Real-time Pcrmentioning

confidence: 99%

Section: Real-time Pcrmentioning

confidence: 99%

Interaction of tumor-associated macrophages and cancer chemotherapy

et al. 2019

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“…As a traditional chemotherapeutic drug, Cisplatin (DDP) has remarkable anti-tumor effect and wide antitumor spectrum, and is widely used in the treatment of various solid tumors (16). The main target site of Cisplatin is DNA.…”

Section: Discussionmentioning

confidence: 99%

Liposomal clodronate combined with Cisplatin or Sorafenib inhibits hepatocellular carcinoma cell proliferation, migration and invasion by suppressing FOXQ1 expression

Zhou

Chen

et al. 2020

Cell Mol Biol (Noisy-le-grand)

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The purpose of this study was to investigate the effect of liposomal clodronate combined with Cisplatin or Sorafenib on the FOXQ1 expression and biological function of hepatocellular carcinoma cell lines. The expression of FOXQ1 was determined in normal hepatic cell line and hepatocellular carcinoma cell lines using quantitative real-time polymerase chain reaction (qRT-PCR). HepG2 and MHCC97H cells were administered low, medium and high concentrations of cisplatin (3, 5 and 7 μg/ml) or Sorafenib (2, 7 and 20 μg/ml) in combination with liposomal clodronate (LC, 20μg/ml), and the expression of FOXQ1 in each group was determined. Cell migration, MTT and transwell assays were used to determine the effects of the treatments on biological functions of HepG2 and MHCC97H cells. qRT-PCR showed that the expression of FOXQ1 mRNA was higher in the four hepatocellular carcinoma cell lines than in normal cells, and the expression of FOXQ1 mRNA in HepG2 and MHCC97H cells were more dominant. All the tested doses of Cisplatin, but only high dose Sorafenib down-regulated the expression of FOXQ1. However, Sorafenib at low and medium concentrations had no significant effect on the expression of FOXQ1. When Cisplatin or Sorafenib was administered in combination with LC, the expression level of FOXQ1 was significantly reduced. Cell migration, MTT and transwell assays showed that proliferation, migration and invasion were inhibited when each drug was administered alone, but was stronger when the drugs were combined with liposomal clodronate.Liposomal clodronate combined with Cisplatin or Sorafenib down-regulates the expression of FOXQ1 in HepG2 and MHCC97H hepatoma cells, and inhibits their proliferation, migration and invasion.

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“…Clinical trials showed mixed results for the treatment of TNBC with cisplatin with convoluted mechanisms [3][4][5][6][7]. To identify potential targets associated with the cisplatin resistance (cisplatin sensitive and resistant) due to unavailable datasets for TNBC, we adopted an ovarian cancer bioinformatics model.…”

Section: Upregulated Gene Expressions Of Egfr and Hypoxia Associate Wmentioning

confidence: 99%

“…Recent clinical trials have showed efficacy of cisplatin in combinational chemotherapy in comparison to conventional chemotherapeutic approaches for the treatment of TNBC [3][4][5]. However, others have demonstrated lackluster outcomes, and underlying mechanisms remain convoluted [6,7].…”

Section: Introductionmentioning

confidence: 99%

Targeting Hypoxia Sensitizes TNBC to Cisplatin and Promotes Inhibition of Both Bulk and Cancer Stem Cells

Sulaiman

McGarry

Chambers

et al. 2020

IJMS

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Development of targeted therapies for triple-negative breast cancer (TNBC) is an unmet medical need. Cisplatin has demonstrated its promising potential for the treatment of TNBC in clinical trials; however, cisplatin treatment is associated with hypoxia that, in turn, promotes cancer stem cell (CSC) enrichment and drug resistance. Therapeutic approaches to attenuate this may lead to increased cisplatin efficacy in the clinic for the treatment of TNBC. In this report we analyzed clinical datasets of TNBC and found that TNBC patients possessed higher levels of EGFR and hypoxia gene expression. A similar expression pattern was also observed in cisplatin-resistant ovarian cancer cells. We, thus, developed a new therapeutic approach to inhibit EGFR and hypoxia by combination treatment with metformin and gefitinib that sensitized TNBC cells to cisplatin and led to the inhibition of both CD44+/CD24− and ALDH+ CSCs. We demonstrated a similar inhibition efficacy on organotypic cultures of TNBC patient samples ex vivo. Since these drugs have already been used frequently in the clinic; this study illustrates a novel, clinically translatable therapeutic approach to treat patients with TNBC.

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A Single Institution Experience of Incorporation of Cisplatin into Adjuvant Chemotherapy for Patients With Triple-Negative Breast Cancer of UnknownBRCAMutation Status

Cited by 11 publications

References 32 publications

Interaction of tumor-associated macrophages and cancer chemotherapy

Interaction of tumor-associated macrophages and cancer chemotherapy

Liposomal clodronate combined with Cisplatin or Sorafenib inhibits hepatocellular carcinoma cell proliferation, migration and invasion by suppressing FOXQ1 expression

Targeting Hypoxia Sensitizes TNBC to Cisplatin and Promotes Inhibition of Both Bulk and Cancer Stem Cells

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