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Cisplatin

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Cisplatin is a metal-based chemotherapy drug used in the treatment of various types of cancer. It functions as a platinum-based compound that interferes with DNA replication, ultimately leading to cell death. The core function of Cisplatin is to inhibit the growth and proliferation of cancer cells.

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Lab products found in correlation

Bleomedac, by Medac (1 mentions) Nupage 4 12 bis tris, by Thermo Fisher Scientific (1 mentions) Pemetrexed disodium heptahydrate, by Eli Lilly (1 mentions) Chaps, by Thermo Fisher Scientific (1 mentions) Xbai, by Thermo Fisher Scientific (1 mentions) Celltiter glo luminescent cell viability assay, by Promega (1 mentions) Matrigel, by BD (1 mentions) Trametinib, by Selleck Chemicals (1 mentions) Carboplatin, by Medac (1 mentions) Temozolomide, by Merck Group (1 mentions) 5 fluorouracil, by R&D Systems (1 mentions) Vemurafenib, by LC Laboratories (1 mentions) Paclitaxel, by Merck Group (1 mentions) 5 fluorouracil, by Merck Group (1 mentions) Doxorubicin, by Medac (1 mentions) Nivolumab, by InvivoGen (1 mentions) Nivolumab, by Bristol-Myers Squibb (1 mentions)

5 protocols using cisplatin

1

Electrochemotherapy for Cutaneous Melanoma

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Patients were treated according to the Standard Operating Procedure (SOP) for electrochemotherapy.16 Briefly, electrochemotherapy of cutaneous melanoma nodules was performed using either intravenous bleomycin (Bleomedac, Medac, Wedel, Germany) in a dose of 15,000 IU/m2 (link) or intratumoral Cisplatin (Cisplatin, Medac) injection in a concentration of 2 mg/ml and dose is applied according to ESOPE protocol.16 Standard pulse parameters for electrochemotherapy (voltage to distance ratio 1300 V/cm, 8 pulses, 100 μs, 5000 Hz) were used.16 Electric pulses were generated by Cliniporator pulse generator (IGEA, s.r.l., Carpi, Italy) and delivered by parallel stainless steel plate electrodes with 6 or 8 mm distance in between. Electric pulses were applied to the tumors nodules in a way so as to cover the whole tumor area, including the safety margin.
Hribernik A., Cemazar M., Sersa G., Bosnjak M, & Snoj M. (2016). Effectiveness of electrochemotherapy after IFN-α adjuvant therapy of melanoma patients. Radiology and Oncology, 50(1), 21-27.
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2

Evaluation of IGF-I/IGF-II Signaling Inhibitors

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Chemicals and materials were obtained from the following sources: CHAPS (Affymetrix, Santa Clara, CA, USA); Cisplatin (Medac GmbH, Hamburg, Germany); Linsitinib (OSI-906) (Selleckchem, Houston, TX, USA), Matrigel (BD Bioscience, Sparks Glencoe, MD, USA); Ham’s F12 Nutrient Mix (F-12 HAM), Roswell Park Memorial Institute (RPMI) 1640 medium, Improved Minimum Essential Medium (IMEM), NuPage 4–12% Bis-Tris, iBlot Gel Transfer Stacks Nitrocellulose, puromycin (Invitrogen, Carlsbad, CA, USA); plasmids Lv-105-IGF-I, Lv105-IGF-II, Lv-105-IGF-IR (GeneCopoeia, Rockville, MD, USA); recombinant human IGF-I, IGF-II (R&D Systems, Minneapolis, MN, USA); Complete® Protease Inhibitor Cocktail, PhosSTOP® Phosphatase Inhibitor Cocktail, recombinant human insulin (Roche, Indianapolis, IN, USA); Xba-I, Spe-I, Pierce Protein Assay, Spectra Multicolor Broad Range Protein Ladder (Thermo Scientific, Glen Burnie, MD, USA); CellTiter-Glo Luminescent Cell Viability Assay (Promega, Madison, WI, USA); pemetrexed disodium heptahydrate (Eli Lilly, Indianapolis, IN, USA).
Forest A., Amatulli M., Ludwig D.L., Damoci C.B., Wang Y., Burns C.A., Donoho G.P., Zanella N., Fiebig H.H., Prewett M.C., Surguladze D., DeLigio J.T., Houghton P.J., Smith M.A, & Novosiadly R. (2015). Intrinsic Resistance to Cixutumumab is Conferred by Distinct Isoforms of the Insulin Receptor. Molecular cancer research : MCR, 13(12), 1615-1626.
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3

Drug Cytotoxicity Evaluation Protocol

Cited 1 time
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4-Methylumbelliferyl heptanoate (MUH) assays were performed as previously described22 (link). The cells were treated with cisplatin (Hexal, up to 20 µM), carboplatin (Medac, up to 250 µM), vemurafenib (LC Laboratories, up to 20 µM), trametinib (Selleck Chemicals, up to 250 nM), 5-fluorouracil (R&D Systems, up to 25 µM), paclitaxel (Merck, up to 500 nM) or temozolomide (TMZ; Merck, up to 50 µM) for 72 h.
Makino E., Gutmann V., Kosnopfel C., Niessner H., Forschner A., Garbe C., Sinnberg T, & Schittek B. (2018). Melanoma cells resistant towards MAPK inhibitors exhibit reduced TAp73 expression mediating enhanced sensitivity to platinum-based drugs. Cell Death & Disease, 9(9), 930.
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4

Rb-targeting shRNA Production Protocol

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Erufosine was kindly provided by Prof. Eibl, MPI-Goettingen, Germany [30] (link) and a solution in 0.9% NaCl was used for all experiments. The cytostatics 5-fluorouracil (Sigma), cytosine arabinoside (Ara C, cytarabine, Sigma), doxorubicin (clinical grade) and cisplatin (Medac) were used as reference drugs. For generating a 21 bp long short hairpin RNA, a target site within the Rb-mRNA was selected in silico[31] (link) and the sequence was created with the HiPerformence Design Algorithm of Qiagen (Fig. 1a). Since there were reports, that shRNAs with a longer target site lead to more pronounced knockdown efficiency [32] (link), a 27 nucleotides long shRNA (shRNA Rb-27, Fig. 1a) was constructed in addition [33] (link). A non-specific21 bp long shRNA was used as a nonsense control (NSO, Fig. 1a). The plasmid pSUPER was kindly provided by Reuven Agami. The self-inactivating vector pLL 3.7 puro-eGFP originated from the laboratory of Luk van Parijs.
Zaharieva M.M., Kirilov M., Chai M., Berger S.M., Konstantinov S, & Berger M.R. (2014). Reduced Expression of the Retinoblastoma Protein Shows That the Related Signaling Pathway Is Essential for Mediating the Antineoplastic Activity of Erufosine. PLoS ONE, 9(7), e100950.
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5

Dose-dependent Drug Sensitivity of Tumor Slices

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Twenty four hours after tumor resection, the cultured slices were treated with different drugs. First, slice cultures of six specimens were treated with cisplatin (1, 10 µM) or paclitaxel (1, 10, and 100 nM) (medac GmbH, Germany) for 72 h to investigate dose-response and individual susceptibility. Ten micromolar of cisplatin and 100 nM of paclitaxel were selected for further studies. Tumor specimen from 12 patients were treated with 3 µg/ml of Nivolumab (opdivo; Bristol Myers-Squibb, USA), the same concentration currently used in murine as well as clinical settings. Drug containing medium was prepared at the day of treatment and changed every other day. Control conditions were cultivated as indicated above without cytotoxic supplement and when possible with IgG4 (cat.No. bgal-mab114, invivogen, France) as an isotype control to Nivolumab.
Junk D., Krämer S., Broschewitz J., Laura H., Massa C., Moulla Y., Hoang N.A., Monecke A., Eichfeld U., Bechmann I., Lordick F., Seliger B, & Kallendrusch S. (2021). Human tissue cultures of lung cancer predict patient susceptibility to immune-checkpoint inhibition. Cell Death Discovery, 7, 264.
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