scholarly journals Effect of Retinoids on Growth Inhibition of Two Canine Melanoma Cell Lines.

2001 ◽  
Vol 63 (1) ◽  
pp. 83-86 ◽  
Author(s):  
Emi OHASHI ◽  
Sung-Hyeok HONG ◽  
Tomoko TAKAHASHI ◽  
Takayuki NAKAGAWA ◽  
Manabu MOCHIZUKI ◽  
...  
Keyword(s):  
Growth Inhibition ◽  
Cell Lines ◽  
Melanoma Cell ◽  
Canine Melanoma ◽  
Melanoma Cell Lines

scholarly journals Unbiased High-Throughput Drug Combination Pilot Screening Identifies Synergistic Drug Combinations Effective against Patient-Derived and Drug-Resistant Melanoma Cell Lines

2020 ◽  
pp. 247255522097091
Author(s):  
David A. Close ◽  
John M. Kirkwood ◽  
Ronald J. Fecek ◽  
Walter J. Storkus ◽  
Paul A. Johnston
Keyword(s):  
Growth Inhibition ◽  
Cell Lines ◽  
Melanoma Cell ◽  
High Throughput ◽  
Drug Combination ◽  
High Throughput Screening ◽  
Dna Methyltransferase ◽  
Cross Resistance ◽  
Braf Mutations ◽  
Melanoma Cell Lines

We describe the development, optimization, and validation of 384-well growth inhibition assays for six patient-derived melanoma cell lines (PDMCLs), three wild type (WT) for BRAF and three with V600E- BRAF mutations. We conducted a pilot drug combination (DC) high-throughput screening (HTS) of 45 pairwise 4×4 DC matrices prepared from 10 drugs in the PDMCL assays: two B-Raf inhibitors (BRAFi), a MEK inhibitor (MEKi), and a methylation agent approved for melanoma; cytotoxic topoisomerase II and DNA methyltransferase chemotherapies; and drugs targeting the base excision DNA repair enzyme APE1 (apurinic/apyrimidinic endonuclease-1/redox effector factor-1), SRC family tyrosine kinases, the heat shock protein 90 (HSP90) molecular chaperone, and histone deacetylases. Pairwise DCs between dasatinib and three drugs approved for melanoma therapy—dabrafenib, vemurafenib, or trametinib—were flagged as synergistic in PDMCLs. Exposure to fixed DC ratios of the SRC inhibitor dasatinib with the BRAFis or MEKis interacted synergistically to increase PDMCL sensitivity to growth inhibition and enhance cytotoxicity independently of PDMCL BRAF status. These DCs synergistically inhibited the growth of mouse melanoma cell lines that either were dabrafenib-sensitive or had acquired resistance to dabrafenib with cross resistance to vemurafenib, trametinib, and dasatinib. Dasatinib DCs with dabrafenib, vemurafenib, or trametinib activated apoptosis and increased cell death in melanoma cells independently of their BRAF status or their drug resistance phenotypes. These preclinical in vitro studies provide a data-driven rationale for the further investigation of DCs between dasatinib and BRAFis or MEKis as candidates for melanoma combination therapies with the potential to improve outcomes and/or prevent or delay the emergence of disease resistance.

scholarly journals Effect of Natural and Synthetic Retinoids on the Proliferation and Differentiation of Three Canine Melanoma Cell Lines

2002 ◽  
Vol 64 (2) ◽  
pp. 169-172 ◽  
Author(s):  
Emi OHASHI ◽  
Kaori INOUE ◽  
Hiroyuki KAGECHIKA ◽  
Sung-Hyeok HONG ◽  
Takayuki NAKAGAWA ◽  
...  
Keyword(s):  
Cell Lines ◽  
Melanoma Cell ◽  
Proliferation And Differentiation ◽  
Canine Melanoma ◽  
Melanoma Cell Lines ◽  
Natural And Synthetic

scholarly journals Biologic activity of the novel orally bioavailable selective inhibitor of nuclear export (SINE) KPT-335 against canine melanoma cell lines

2014 ◽  
Vol 10 (1) ◽  
pp. 160 ◽  
Author(s):  
Megan N Breit ◽  
William C Kisseberth ◽  
Misty D Bear ◽  
Yosef Landesman ◽  
Trinayan Kashyap ◽  
...  
Keyword(s):  
Cell Lines ◽  
Melanoma Cell ◽  
Nuclear Export ◽  
Selective Inhibitor ◽  
The Novel ◽  
Biologic Activity ◽  
Orally Bioavailable ◽  
Canine Melanoma ◽  
Melanoma Cell Lines

scholarly journals 6-Bromoindirubin-3′oxime (BIO) decreases proliferation and migration of canine melanoma cell lines

2015 ◽  
Vol 205 (2) ◽  
pp. 305-312 ◽  
Author(s):  
Esther Chon ◽  
Brandi Flanagan ◽  
Lucas Campos de Sá Rodrigues ◽  
Caroline Piskun ◽  
Timothy J. Stein
Keyword(s):  
Cell Lines ◽  
Melanoma Cell ◽  
And Migration ◽  
Canine Melanoma ◽  
Melanoma Cell Lines ◽  
Proliferation And Migration

Anticancer effects of high-dose ascorbate on canine melanoma cell lines

2018 ◽  
Vol 16 (4) ◽  
pp. 616-621 ◽  
Author(s):  
Hyeri Shin ◽  
Aryung Nam ◽  
Kun-Ho Song ◽  
Kupil Lee ◽  
Robert B. Rebhun ◽  
...  
Keyword(s):  
Cell Lines ◽  
Melanoma Cell ◽  
High Dose ◽  
Anticancer Effects ◽  
Canine Melanoma ◽  
Melanoma Cell Lines

Neurokinin-1 receptor expression and antagonism by the NK-1R antagonist maropitant in canine melanoma cell lines and primary tumour tissues

2014 ◽  
Vol 14 (2) ◽  
pp. 210-224 ◽  
Author(s):  
J. F. Borrego ◽  
M. K. Huelsmeyer ◽  
M. E. Pinkerton ◽  
J. L. Muszynski ◽  
S. A. K. Miller ◽  
...  
Keyword(s):  
Cell Lines ◽  
Melanoma Cell ◽  
Primary Tumour ◽  
Receptor Expression ◽  
Neurokinin 1 Receptor ◽  
Neurokinin 1 ◽  
Canine Melanoma ◽  
Melanoma Cell Lines

scholarly journals Adamantam Derivatives, Part 111* : Synthesis of Some Aminoadamantanes as Novel Antitumor Agents

2003 ◽  
Vol 71 (3) ◽  
pp. 195-209 ◽  
Author(s):  
M. El-Sherbeny ◽  
K. Youssef ◽  
M. Mahran
Keyword(s):  
Antitumor Activity ◽  
Growth Inhibition ◽  
Cell Lines ◽  
Melanoma Cell ◽  
Broad Spectrum ◽  
Antitumor Agents ◽  
Leukemia Cell ◽  
Biological Data ◽  
Leukemia Cell Lines ◽  
Melanoma Cell Lines

New series of 1-(1-adamantyl)semicarbazide 3a, 1-(1-adamantyl)4(4-subsMuted pheny1)semicarbazides 3b-e, 1-(1-adamantyl)-3-(subsMuted aminosulfonyl)ureas 5a-g, 1-(1-adamantyl)-4-(1-adamantylamino-methylene)-semicarbazide 7, 1-(1-adamantyl)-4-(1-adamantylcarbonylmethyl)semicarbazide 8, 1-(Iadamantyl)-4-acylsemicarbazides Sad and 1-(1-adamantyl)-4-(1-adamantylaminocarbonyl) thiosemicarbazide 10 have been synthesized and tested for their anMumor activity. Among them, compounds 3a, 5a, 9a. and 9d exhibited a broad spectrum antitumor activity with full panel (MG-MID) median growth inhibition (GI50) of 1 0.5, 12.0, 6.8 and 5.5 μM respectively. In addition, compounds 3a, 3c, and 5d proved to be of moderate selectivity toward leukemia cell lines wrth ratios of 3.0, 3.9 and 4.0 respectively. Moreover, compounds 5a and 5g showed moderate selectivrty toward melanoma cell lines with ratios of 3.6 and 4.4 respectively. The detailed synthesis, specroscopic and biological data are reported.

scholarly journals Interleukin-6 undergoes transition from paracrine growth inhibitor to autocrine stimulator during human melanoma progression.

1993 ◽  
Vol 120 (5) ◽  
pp. 1281-1288 ◽  
Author(s):  
C Lu ◽  
R S Kerbel
Keyword(s):  
Growth Inhibition ◽  
Cell Lines ◽  
Melanoma Cell ◽  
Interleukin 6 ◽  
Neutralizing Antibodies ◽  
Growth Inhibitor ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Advanced Stage ◽  
Melanoma Cell Lines

The ability to penetrate the dermal basement membrane and subsequently proliferate in the underlying mesenchyme is one of the key steps in malignant progression of human melanomas. We previously undertook studies aimed at assessing how normal dermal fibroblasts (one of the main cellular components of mesenchyme) may affect the growth of human melanoma cells and facilitate the overgrowth of malignant subpopulations (Cornil, I., D. Theodorescu, S. Man, M. Herlyn, J. Jambrosic, and R. S. Kerbel. 1991. Proc. Natl. Acad. Sci. USA. 88:6028-6032). We found that melanoma cell lines from early-stage (metastatically incompetent) lesions were growth inhibited whereas those from advanced-stage (metastatically competent) lesions were stimulated under the same conditions by co-culture with fibroblasts; conditioned medium from such cells gave the same result. Subsequent studies using biochemical purification and neutralizing antibodies revealed the inhibitory activity to be identical to interleukin-6 (IL-6). We now report that addition of purified recombinant human IL-6 resulted in a growth inhibition in vitro by G1/G0 arrest of early, but not advanced stage melanoma cells. Despite this alteration in response there was no significant difference in melanoma cell lines of varying malignancy in respect to their expression of genes encoding the IL-6 receptor, or gp130, the IL-6 signal transducer. Scatchard analysis also revealed similar [125I]IL-6 binding activities in both IL-6 sensitive and resistant groups. However, studies of IL-6 production indicated that five out eight IL-6 melanoma cell lines known to be resistant to exogenous IL-6-mediated growth inhibition constitutively expressed mRNA for IL-6; they also secreted bioactive IL-6 into culture medium. To assess the possible role of this endogenous IL-6 in melanoma cell growth, antisense oligonucleotides to the IL-6 gene were added to cultures of melanoma cells. This resulted in a significant growth inhibition only in cell lines that produced endogenous IL-6. In contrast, neutralizing antibodies to IL-6 were ineffective in causing such growth inhibition. This indicates that endogenous IL-6 may behave as a growth stimulator by an intracellular ("private") autocrine mechanism. Thus, a single cytokine, IL-6, can switch from behaving as a paracrine growth inhibitor to an autocrine growth stimulator within the same cell lineage during malignant tumor progression. Such a switch may contribute to the growth advantage of metastatically competent melanoma cells at the primary or distant organ sites and thereby facilitate progression of disease.

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