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Wm1366

Manufactured by American Type Culture Collection
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Sourced in United States

The WM1366 is a laboratory instrument designed for high-throughput cell culture. It provides reliable and consistent cell growth conditions through precise temperature, humidity, and atmospheric control. The core function of the WM1366 is to provide a controlled environment for the cultivation and maintenance of cell lines.

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Lab products found in correlation

Trametinib, by Selleck Chemicals (3 mentions) Vemurafenib, by Selleck Chemicals (2 mentions) Sbcl2, by American Type Culture Collection (2 mentions) Human melanocyte growth supplement, by Thermo Fisher Scientific (1 mentions) Medium 254, by Thermo Fisher Scientific (1 mentions) Colo679, by American Type Culture Collection (1 mentions) Scov 3, by American Type Culture Collection (1 mentions) Binimetinib, by Selleck Chemicals (1 mentions) Dabrafenib, by Selleck Chemicals (1 mentions) Cobimetinib, by Selleck Chemicals (1 mentions) Encorafenib, by Selleck Chemicals (1 mentions) Wm793, by American Type Culture Collection (1 mentions) Interferon γ infγ, by Merck Group (1 mentions)

5 protocols using wm1366

1

Culturing Diverse Melanoma Cell Lines

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Melanoma cell lines SK-Mel-19, −28, −29, −94, −103, −147, −173, G-361 were obtained from Memorial Sloan Kettering Cancer Center and cultured in Dulbecco’s modified Eagle’s medium supplemented with 10% fetal bovine serum, 2mM glutamine, and 1% penicillin-streptomycin antibiotics. Populations of normal human melanocytes (NHM) were purchased from Invitrogen and maintained in Medium 254 (Invitrogen) supplemented with human melanocyte growth supplement (Invitrogen). Colo679, UACC-257, WM1366, SCOV3 and HeLa were purchased from ATCC. HMLE and HMLER cells were a gift from Dr. Robert A Weinberg (Whitehead Institute). Melan-a mouse melanocytes were grown at 37°C (10% CO2) in RPMI media containing 12-O-Tetradecanoylphorbol-13-acetate (TPA).
Bagati A., Moparthy S., Bianchi-Smiraglia A., Kolesnikova K., Lipchick B.C., Kolesnikova M., Fink E.E., Jowdy P., Polechetti A., Mahpour A., Ross J., Wawrzyniak J.A., Yun D.H., Paragh G., Kozlova N.I., Berman A.E., Wang J., Liu S., Nemeth M.J, & Nikiforov M.A. (2017). Melanoma Suppressor Functions of the Carcinoma Oncogene FOXQ1. Cell reports, 20(12), 2820-2832.
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2

Evaluating Metastatic Melanoma Cell Lines

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Melanoma cell lines Malme3M (lung metastasis, BRAFmut), WM3734 (brain metastasis, BRAFmut), and WM1366 (primary melanoma, vertical growth phase, NRASmut) were purchased from ATCC (Manassas, VI, USA) and Rockland Immunochemicals, Inc. (Pottstown, PA, USA) and were subject to regular tests for excluding Mycoplasma contamination. Malme3M was cultured in RPMI + 20% fetal bovine serum (FBS), WM3734 and WM1366 were cultured in RPMI + 10% FBS. Encorafenib, binimetinib, vemurafenib, cobimetinib, dabrafenib, and trametinib were purchased from Selleckchem and dissolved in dimethylsulfoxide (DMSO).
Schulz A., Raetz J., Karitzky P.C., Dinter L., Tietze J.K., Kolbe I., Käubler T., Renner B., Beissert S., Meier F, & Westphal D. (2022). Head-to-Head Comparison of BRAF/MEK Inhibitor Combinations Proposes Superiority of Encorafenib Plus Trametinib in Melanoma. Cancers, 14(19), 4930.
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3

Melanoma Cell Lines and Samples

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The human melanoma cell lines WM793, WM983A, WM35, WM1366, and the murine cell line B16F10 were purchased from ATCC (Manassass, VA). Mel-624 and Mel-888 were kindly provided by Dr. Shari Pilon-Thomas, and SkMel21 by Dr. Keiran Smalley at H. Lee Moffitt Cancer Center (Tampa, FL). Human cell lines were authenticated using STR profiling within six months prior to manuscript submission. Melanoma patient samples were obtained from surgical biopsies (clinical trial MCC15375; IRB approved protocol #106509; H. Lee Moffitt Cancer Center, Tampa, FL) and provided by Dr. Amod Sarnaik. All cells were cultured in RPMI 1640, supplemented with 10% fetal bovine serum, non-essential amino acids, penicillin, streptavidin, amphotericin B and Mycozap.
Woods D.M., Sodré A.L., Villagra A., Sarnaik A., Sotomayor E.M, & Weber J. (2015). HDAC Inhibition Upregulates PD-1 Ligands in Melanoma and Augments Immunotherapy with PD-1 Blockade. Cancer immunology research, 3(12), 1375-1385.
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4

Characterization of Melanoma Cell Lines

Cited 1 time
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Trametinib was purchased from Selleck Chemicals (Houston, TX) and the pan-RAF inhibitor (Amgen Compd A - hereafter PRi) [26 (link)] was obtained from Amgen (Thousand Oaks, CA) under a materials transfer agreement (MTA). Human melanoma cell lines (M series) were established from patient’s biopsies under UCLA IRB approval # 11–003254. WM1366, SKMEL173 and SBCL2 cell lines were obtained from the American Type Culture Collection (ATCC, Rockville, MD). Cells were maintained and tested for mycoplasma as described before [17 (link)]. Presence of mutations in the genes of interest was checked by OncoMap 3 or Iontrone, and was confirmed by PCR and Sanger sequencing.
Atefi M., Titz B., Avramis E., Ng C., Wong D.J., Lassen A., Cerniglia M., Escuin-Ordinas H., Foulad D., Comin-Anduix B., Graeber T.G, & Ribas A. (2015). Combination of pan-RAF and MEK inhibitors in NRAS mutant melanoma. Molecular Cancer, 14(1), 27.
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5

Melanoma Acquired Resistance Protocol

Cited 1 time
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Vemurafenib and trametinib were purchased from Selleck chemicals (Houston, TX) and the pan-PI3K inhibitor (PI3Ki) GSK2126458 was obtained from GlaxoSmithKline (GSK, PA) under a material transfer agreement. Interferon γ (INFγ) was obtained from Sigma Aldrich (St Louis, MO). Human melanoma cell lines (M series) were established from patient's biopsies under UCLA IRB 11-003254 as previously described (16 (link)). WM1366 and SBCL2 were obtained from the American Type Culture Collection (ATCC, Rockville, MD). Growing media, maintenance and mycoplasma testing of the cell lines were as described before (16 (link)). BRAF mutant cell lines with the in vitro acquired Vemurafenib resistance are indicated by the AR suffixes. Except M249AR4 that contains a secondary NRAS mutation, the rest of acquired resistant cell lines were maintained in the growing media containing 1µM of Vemurafenib.
Atefi M., Avramis E., Lassen A., Wong D., Robert L., Foulad D., Cerniglia M., Titz B., Chodon T., Graeber T.G., Comin-Anduix B, & Ribas A. (2014). Effects of MAPK and PI3K Pathways on PD-L1 Expression in Melanoma. Clinical cancer research : an official journal of the American Association for Cancer Research, 20(13), 3446-3457.
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