Genetic Risk Factors Associated With Antiemetic Efficacy of Palonosetron, Aprepitant, and Dexamethasone in Japanese Breast Cancer Patients Treated With Anthracycline-based Chemotherapy

Yokoyama, S.; Tamaru, Satoshi; Tamaki, Shinya; Nakanishi, Daisuke; Mori, Akiya; Yamakawa, Tomokazu; Ao, Takaaki; Sakata, Yasuhiko; Mizuno, Toshiro; Iwamoto, Takuya; Watanabe, Kenichi; Simomura, Makoto; Kawakami, Keiki; Konishi, Naomi; Kageyama, Shinichi; Ohtani, Shoichiro; Yamada, Tomomi; S, Ban; Ooi, Kazuya

doi:10.1016/j.clbc.2017.05.013

Cited by 4 publications

(5 citation statements)

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“…ABCG2 overexpression can lead to MDR. Substrates of ABCG2 include anthracyclines, camptothecins and methotrexate (38). Since ABCG2 is an important contributor to MDR, inhibiting ABCG2 activity may help improve the efficacy of chemotherapeutic drugs.…”

Section: Discussionmentioning

confidence: 99%

Reversal Effect of ALK Inhibitor NVP-TAE684 on ABCG2-Overexpressing Cancer Cells

Wang

Cai

et al. 2020

Front. Oncol.

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Failure of cancer chemotherapy is mostly due to multidrug resistance (MDR). Overcoming MDR mediated by overexpression of ATP binding cassette (ABC) transporters in cancer cells remains a big challenge. In this study, we explore whether NVP-TAE684, a novel ALK inhibitor which has the potential to inhibit the function of ABC transport, could reverse ABC transporter-mediated MDR. MTT assay was carried out to determine cell viability and reversal effect of NVP-TAE684 in parental and drug resistant cells. Drug accumulation and efflux assay was performed to examine the effect of NVP-TAE684 on the cellular accumulation and efflux of chemotherapeutic drugs. The ATPase activity of ABCG2 transporter in the presence or absence of NVP-TAE684 was conducted to determine the impact of NVP-TAE684 on ATP hydrolysis. Western blot analysis and immunofluorescence assay were used to investigate protein molecules related to MDR. In addition, the interaction between NVP-TAE684 and ABCG2 transporter was investigated via in silico analysis. MTT assay showed that NVP-TAE684 significantly decreased MDR caused byABCG2-, but not ABCC1-transporter. Drug accumulation and efflux tests indicated that the effect of NVP-TAE684 in decreasing MDR was due to the inhibition of efflux function of ABCG2 transporter. However, NVP-TAE684 did not alter the expression or change the subcellular localization of ABCG2 protein. Furthermore, ATPase activity analysis indicated that NVP-TAE684 could stimulate ABCG2 ATPase activity. Molecular in silico analysis showed that NVP-TAE684 interacts with the substrate binding sites of the ABCG2 transporter. Taken together, our study indicates that NVP-TAE684 could reduce the resistance of MDR cells to chemotherapeutic agents, which provides a promising strategy to overcome MDR.

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Section: Discussionmentioning

confidence: 99%

Reversal Effect of ALK Inhibitor NVP-TAE684 on ABCG2-Overexpressing Cancer Cells

Wang

Cai

et al. 2020

Front. Oncol.

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“… 33 , 37 Yokoyama et al found no correlation between CINV and CYP3A5 rs776746 in a triple antiemetic regimen consisting of palonosetron, aprepitant, and dexamethasone that is used in Japanese patients with breast cancer (Chi-squared test, n = 125, p = 1.00). 29 …”

Section: Methodsmentioning

confidence: 99%

“…45 A multivariate analysis by Yokoyama et al showed a significant correlation between the ABCG2 rs2231142 AA genotype and acute severe nausea (p = 0.049). 29 However, Lamba et al failed to find any correlations among ABCC1 rs246240, rs2238476, and CINV. 4 The ATP7B gene encodes the ATP7B enzyme.…”

Section: Abcc1 Abcg2 and Atp7bmentioning

confidence: 99%

“…20 Data suggest that variants in the HTR3A-D gene may be associated with CINV as well as the therapeutic effect of 5-HT3RA in patients. 16,17,19,[21][22][23][24][25][26][27][28][29] Kaiser et al sequenced and performed a haplotype analysis of the HTR3A gene in 233 patients on highly emetogenic chemotherapy regimens; the results showed that HTR3A CT haplotype carriers (unreported rs IDs) were less likely to develop CINV after prophylactic antiemetic treatment (Chi-squared test, p = 0.01). 21 Certain studies analyzed the relationship between some common HTR3A loci (rs1062613, rs1176722, rs1176719, rs2276303, rs909411, and rs1176713) and CINV; no correlation was discovered.…”

Section: Cinv and Drug-receptor Pathway-related Gene Polymorphisms Serotonin Pathwaymentioning

confidence: 99%

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An Update in Our Understanding of the Relationships Between Gene Polymorphisms and Chemotherapy-Induced Nausea and Vomiting

Jin¹,

Li²,

Jiang³

et al. 2021

IJGM

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The occurrence and severity of chemotherapy-induced nausea and vomiting (CINV) are influenced by many factors; this includes therapeutic factors, such as the dose, administration mode, and chemotherapeutic agent emetogenicity, as well as patient-related risk factors, such as the gender, age, alcohol consumption history, and anxiety level. However, these factors cannot fully explain the individual CINV differences. In recent years, the correlation between gene polymorphism and CINV has been a hot research topic; the present paper reviews current research on CINV-related gene polymorphisms, and the results indicate that the use of gene polymorphism for the optimization of CINV efficacy is of important clinical significance.

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“…In clinical practice, patients with the same tumor stage, pathological type, and treatment regimen experience varying degrees of adverse reactions after treatment with anthracycline- and paclitaxel-based chemotherapy. It may be related to the patient’s clinical characteristics, environmental factors, and genetic factors [ 14 , 15 ]. Some studies showed that the metabolism of cytotoxic chemotherapy drugs in vivo is affected by glutathione S-transferases (GSTs) [ 16 , 17 ].…”

Section: Introductionmentioning

confidence: 99%

GSTP1 c.313A > G mutation is an independent risk factor for neutropenia hematotoxicity induced by anthracycline-/paclitaxel-based chemotherapy in breast cancer patients

Zeng

Liu

et al. 2022

World J Surg Onc

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Background The link between glutathione S-transferase P1 (GSTP1) c.313A > G polymorphism and chemotherapy-related adverse events remains controversial. The goal of this study was to assess how this variant affected the toxicity of anthracycline-/paclitaxel-based chemotherapy in patients with breast cancer. Methods This study retrospectively investigated pharmacogenetic associations of GSTP1 c.313A > G with chemotherapy-related adverse events in 142 breast cancer patients who received anthracycline and/or paclitaxel chemotherapy. Results There were 61 (43.0%), 81 (57.0%), 43 (30.3%), and 99 (69.7%) patients in the T0-T2, T3-T4, N0-N1, and N2-N3 stages, respectively. There were 108 (76.1%) patients in clinical stages I–III and 34 (23.9%) patients in clinical stage IV. The numbers of patients with luminal A, luminal B, HER2 + , and triple-negative breast cancer (TNBC) were 10 (7.0%), 77 (54.2%), 33 (23.2%), and 22 (15.5%), respectively. The numbers of patients who carried GSTP1 c.313A > G A/A, A/G, and G/G genotypes were 94 (66.2%), 45 (31.7%), and 3 (2.1%), respectively. There were no statistically significant differences in the proportion of certain toxicities in patients with A/G, G/G, and A/G + G/G genotypes, except for neutropenia, in which the proportion of patients with A/G + G/G (χ2 = 6.586, P = 0.035) genotypes was significantly higher than that with the AA genotype. The logistic regression analysis indicated that GSTP1 c.313A > G mutation (A/G + G/G vs. A/A genotype) (adjusted OR 4.273, 95% CI 1.141–16.000, P = 0.031) was an independent variable associated with neutropenia. Conclusions The findings of this study indicate that the GSTP1 c.313A > G mutation is an independent risk factor for neutropenia hematotoxicity in breast cancer patients induced by anthracycline-/paclitaxel-based chemotherapy.

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Genetic Risk Factors Associated With Antiemetic Efficacy of Palonosetron, Aprepitant, and Dexamethasone in Japanese Breast Cancer Patients Treated With Anthracycline-based Chemotherapy

Cited by 4 publications

References 47 publications

Reversal Effect of ALK Inhibitor NVP-TAE684 on ABCG2-Overexpressing Cancer Cells

Reversal Effect of ALK Inhibitor NVP-TAE684 on ABCG2-Overexpressing Cancer Cells

An Update in Our Understanding of the Relationships Between Gene Polymorphisms and Chemotherapy-Induced Nausea and Vomiting

GSTP1 c.313A > G mutation is an independent risk factor for neutropenia hematotoxicity induced by anthracycline-/paclitaxel-based chemotherapy in breast cancer patients

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