Cisplatin and its analogues in the treatment of advanced breast cancer: a review

Smith, Ian; Talbot, Denis

doi:10.1038/bjc.1992.169

Cited by 72 publications

(41 citation statements)

References 31 publications

(23 reference statements)

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“…The clinical activity of platinum compounds against unselected breast tumors was showed to be modest many years ago with an ORR of 32-54/. 20,21 Nevertheless, based on the potential molecular similarities shared between BRCA1 tumors and TNBC and preclinical results mentioned previously, 5-7 the role of platinums was reconsidered in TNBC. After the remarkable pCR in neoadjuvant setting was obtained by Silver and colleagues, 8 Sirohi et al 22 demonstrated that platinum-based regimens were associated with higher chemosensitivity in TNBC than in other subtypes both in neoadjuvant and metastatic settings, and even showed an advantage in PFS.…”

Section: Discussionmentioning

confidence: 99%

A phase II study of capecitabine plus cisplatin in metastatic triple-negative breast cancer patients pretreated with anthracyclines and taxanes

Zhang

et al. 2015

Cancer Biology & Therapy

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Background: Cisplatin is an effective agent for triple-negative breast cancer (TNBC) and synergistic activity between cisplatin and capecitabine has been demonstrated by in vitro and in vivo studies. This study was designed as a prospective clinical trial to evaluate the efficacy and safety of capecitabine plus cisplatin (XP) regimen in metastatic TNBC patients pretreated with anthracyclines and taxanes. Patients and Methods: Thirty-three patients with metastatic TNBC who had anthracyclines and taxanes as prior therapy were treated with capecitabine 2000 mg/m 2 orally on day 1 through 14 plus cisplatin 75mg/m 2 intravenously on day 1 of a 21-day cycle, followed by capecitabine maintenance medications after a maximum of 6 cycles. The primary end point was objective response rate (ORR) and the secondary end points included progression-free survival (PFS), overall survival (OS) and toxicity profiles. Results: A total of 162 cycles was given. ORR was 63.6%. Median PFS was 8.2 (95%CI: 4.8-11.6) months in the entire population and 10.8 (95%CI: 6.5-15.1) months in responding patients. Median OS was 17.8 (95%CI: 14.4-21.2) months in all enrolled patients and 25.8 (95%CI: 14.6-37.0) months in responding patients. Most adverse events were mild and manageable, with neutropenia and nausea/vomiting as the most common toxicities. Grade 3/4 toxicities included leukopenia (10, 30.3%), neutropenia (10, 30.3%), anemia (2, 6.1%), thrombocytopenia (1, 3.0%), nausea/vomiting (3, 9.1%), hand-foot syndrome (HFS; 1, 3.0%), and sensory neuropathy (1, 3.0%). Conclusions: Capecitabine plus cisplatin demonstrated an excellent activity and an acceptable safety profile in metastatic TNBC patients pretreated with anthracyclines and taxanes.

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Section: Discussionmentioning

confidence: 99%

A phase II study of capecitabine plus cisplatin in metastatic triple-negative breast cancer patients pretreated with anthracyclines and taxanes

Zhang

et al. 2015

Cancer Biology & Therapy

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“…Since its fi rst approval in 1978 by US Food and Drug Administration, it has been widely used for various types of cancer such as lung, ovarian, lymphomas, breast and bladder cancers (Smith and Talbot, 1992;von der Maase et al, 2000;Crino et al, 2001;Muggia, 2009). The mechanism of anticancer effect is cytotoxicity due to DNA cross-linking, oxidative damages and apoptosis (Gong et al, 1999;Pruefer et al, 2008).…”

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Identification of Urinary Biomarkers Related to Cisplatin-Induced Acute Renal Toxicity Using NMR-Based Metabolomics

He¹,

Yang²,

Choi³

et al. 2011

Biomolecules and Therapeutics

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Cisplatin is the founding member of the platin-group drugs that has platinum metal and ammonium group. Since its fi rst approval in 1978 by US Food and Drug Administration, it has been widely used for various types of cancer such as lung, ovarian, lymphomas, breast and bladder cancers (Smith and Talbot, 1992;von der Maase et al., 2000;Crino et al., 2001;Muggia, 2009). The mechanism of anticancer effect is cytotoxicity due to DNA cross-linking, oxidative damages and apoptosis (Gong et al., 1999;Pruefer et al., 2008). Due to these cytotoxic effect, cisplatin kills not only cancer cells but also normal cells, resulting in undesirable effects in various tissues including kidney, nerves, ear and gastroenteric ones (Loehrer and Einhorn, 1984). Among these, the nephrotoxicity is most common and can be a cause for the cessation of the drug therapy (Arany and Safi rstein, 2003;Yao et al., 2007). Typically, BloodCisplatin is widely used for various types of cancers. However, its side effects, most notably, renal toxicity often limit its clinical utility. Although previous metabolomic studies reported possible toxicity markers, they used small number of animals and statistical approaches that may not perform best in the presence of intra-group variation. Here, we identifi ed urinary biomarkers associated with renal toxicity induced by cisplatin using NMR-based metabolomics combined with Orthogonal Projections to Latent Structures-Discriminant Analysis (OPLS-DA). Male Sprague-Dawley rats (n=22) were treated with cisplatin (10 mg/kg single dose), and the urines obtained before and after treatment were analyzed by NMR. Multivariable analysis of NMR data presented clear separation between non-treated and treated groups. The OPLS-DA statistical results revealed that 1,3-dimethylurate, taurine, glucose, glycine and branched-chain amino acid (isoleucine, leucine and valine) were signifi cantly elevated in the treated group and that phenylacetylglycine and sarcosine levels were decreased in the treated group. To test the robustness of the approach, we built a prediction model for the toxicity and were able to predict all the unknown samples (n=14) correctly. We believe the proposed NMR-based metabolomics with OPLS-DA approach and the resulting urine markers can be used to augment the currently available blood markers. AbstractUrea Nitrogen (BUN), and blood creatinine are checked to monitor the expression of renal toxicity. In addition, hydration and diuretic measures are taken to minimize possible kidney damages. Still, BUN and creatinine are measured from blood and are late stage kidney functional markers (Hewitt et al.,

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“…A number of previous studies (Kolaric and Roth, 1983;Sledge et al, 1988;Smith and Talbot, 1992) have demonstrated the efficacy of cisplatin-based chemotherapy regimens both in previously untreated patients with metasatic breast cancer, and following anthracycline failure (Vassilomanolakis et al, 2000;Mustacchi et al, 2002). However, the widespread use of platinum-based treatments has been undermined by the alleged lower tolerability of these regimens and the requirement for prolonged infusion protocols.…”

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confidence: 99%

Mitomycin C, vinblastine and cisplatin (MVP): an active and well-tolerated salvage regimen for advanced breast cancer

et al. 2005

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This phase II study assessed the clinical efficacy and tolerability of a combination of mitomycin C, vinblastine and cisplatin in patients with metastatic breast cancer (MBC) previously treated with chemotherapy. A total of 87 patients with MBC, most of whom had been exposed to anthracyclines (92%) and/or taxanes (29%) in the adjuvant and/or metastatic setting, were treated with mitomycin C (8 mg m À2 day 1 cycles 1, 2, 4 and 6), vinblastine (6 mg m À2 day 1) and cisplatin (50 mg m À2 day 1) repeated each 21 days for a maximum of six cycles. The overall response rate (ORR) was 32% (95% CI: 22 -42%) with 31% partial response (PR) and one complete response (CR). Stable disease (SD) rate was 21% (95% CI: 12 -29%). There was no statistically significant difference in the ORR when MVP was given as the first-line treatment for MBC vs second or subsequent line (38 vs 30%, P ¼ 0.6), or between patients with an early (o6 months) vs late (46 months) relapse post-anthracyclines (30 vs 52%, P ¼ 0.3). Toxicity profile was mild. This platinum-based chemotherapy is an effective, well-tolerated and low-cost regimen for patients with MBC, including those pretreated with anthracyclines.

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Cisplatin and its analogues in the treatment of advanced breast cancer: a review

Cited by 72 publications

References 31 publications

A phase II study of capecitabine plus cisplatin in metastatic triple-negative breast cancer patients pretreated with anthracyclines and taxanes

A phase II study of capecitabine plus cisplatin in metastatic triple-negative breast cancer patients pretreated with anthracyclines and taxanes

Identification of Urinary Biomarkers Related to Cisplatin-Induced Acute Renal Toxicity Using NMR-Based Metabolomics

Mitomycin C, vinblastine and cisplatin (MVP): an active and well-tolerated salvage regimen for advanced breast cancer

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