<HashMap><database>biostudies-other</database><scores/><additional><omics_type>Unknown</omics_type><volume>11</volume><submitter>Lucian Smith</submitter><journal>PloS one</journal><pagination>e0152104</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/MODEL1609190000</full_dataset_link><repository>biostudies-other</repository><additional_accession>27015094</additional_accession><pubmed_authors>administrator</pubmed_authors><pubmed_authors>Lucian Smith</pubmed_authors><pubmed_authors>Francesco Pappalardo</pubmed_authors></additional><is_claimable>false</is_claimable><name>Pappalardo2016 - PI3K/AKT and MAPK Signaling Pathways in Melanoma Cancer</name><description>&lt;notes xmlns="http://www.sbml.org/sbml/level2/version4">      &lt;body xmlns="http://www.w3.org/1999/xhtml">        &lt;div class="dc:title">Pappalardo2016 - PI3K/AKT and MAPK SignalingPathways in Melanoma Cancer&lt;/div>        &lt;div class="dc:bibliographicCitation">          &lt;p>This model is described in the article:&lt;/p>          &lt;div class="bibo:title">            &lt;a href="http://identifiers.org/pubmed/27015094" title="Access to this publication">Computational Modeling of    PI3K/AKT and MAPK Signaling Pathways in Melanoma Cancer.&lt;/a>          &lt;/div>          &lt;div class="bibo:authorList">Pappalardo F, Russo G, Candido S,  Pennisi M, Cavalieri S, Motta S, McCubrey JA, Nicoletti F, Libra  M.&lt;/div>          &lt;div class="bibo:Journal">PLoS ONE 2016; 11(3): e0152104&lt;/div>          &lt;p>Abstract:&lt;/p>          &lt;div class="bibo:abstract">            &lt;p>Malignant melanoma is an aggressive tumor of the skin and    seems to be resistant to current therapeutic approaches.    Melanocytic transformation is thought to occur by sequential    accumulation of genetic and molecular alterations able to    activate the Ras/Raf/MEK/ERK (MAPK) and/or the PI3K/AKT (AKT)    signalling pathways. Specifically, mutations of B-RAF activate    MAPK pathway resulting in cell cycle progression and apoptosis    prevention. According to these findings, MAPK and AKT pathways    may represent promising therapeutic targets for an otherwise    devastating disease.Here we show a computational model able to    simulate the main biochemical and metabolic interactions in the    PI3K/AKT and MAPK pathways potentially involved in melanoma    development. Overall, this computational approach may    accelerate the drug discovery process and encourages the    identification of novel pathway activators with consequent    development of novel antioncogenic compounds to overcome tumor    cell resistance to conventional therapeutic agents. The source    code of the various versions of the model are available as S1    Archive.&lt;/p>          &lt;/div>        &lt;/div>        &lt;div class="dc:publisher">          &lt;p>This model is hosted on   &lt;a href="http://www.ebi.ac.uk/biomodels/">BioModels Database&lt;/a>  and identified by:   &lt;a href="http://identifiers.org/biomodels.db/MODEL1609190000">MODEL1609190000&lt;/a>.&lt;/p>          &lt;p>To cite BioModels Database, please use:   &lt;a href="http://identifiers.org/pubmed/20587024" title="Latest BioModels Database publication">BioModels Database:  An enhanced, curated and annotated resource for published  quantitative kinetic models&lt;/a>.&lt;/p>        &lt;/div>        &lt;div class="dc:license">          &lt;p>To the extent possible under law, all copyright and related or  neighbouring rights to this encoded model have been dedicated to  the public domain worldwide. Please refer to   &lt;a href="http://creativecommons.org/publicdomain/zero/1.0/" title="Access to: CC0 1.0 Universal (CC0 1.0), Public Domain Dedication">CC0  Public Domain Dedication&lt;/a> for more information.&lt;/p>        &lt;/div>      &lt;/body>    &lt;/notes></description><dates><release>2016-09-19T00:00:00Z</release><modification>2025-07-15T09:56:28.657Z</modification><creation>2025-03-29T18:23:09.396Z</creation></dates><accession>MODEL1609190000</accession><cross_references><biomodels___db>BIOMD0000000666</biomodels___db><reactome>R-HSA-2219528</reactome><reactome>R-HSA-5683057</reactome><pr>PR:000005201</pr><pr>PR:000029187</pr><pr>PR:000029189</pr><kegg___compound>C05981</kegg___compound><chebi>CHEBI:75045</chebi><mamo>MAMO_0000046</mamo><go>GO:0031932</go><go>GO:1990565</go><go>GO:0030971</go><go>GO:0031931</go><kegg___pathway>map04151</kegg___pathway><kegg___pathway>map04010</kegg___pathway><efo>0007815</efo><ec-code>3.1.3.16</ec-code><ec-code>2.7.1.137</ec-code><ec-code>2.7.11.2</ec-code><ec-code>2.7.11.1</ec-code><ec-code>2.7.10.1</ec-code><ec-code>2.7.12.2</ec-code><pubmed>27015094</pubmed><ncit>C17660</ncit><ncit>C40430</ncit><ncit>C20424</ncit><kegg___orthology>K17700</kegg___orthology><kegg___orthology>K12077</kegg___orthology><kegg___orthology>K00914</kegg___orthology><kegg___orthology>K10167</kegg___orthology><kegg___orthology>K01090</kegg___orthology><kegg___orthology>K16339</kegg___orthology><kegg___orthology>K01110</kegg___orthology><kegg___orthology>K07829</kegg___orthology><kegg___orthology>K03099</kegg___orthology><kegg___orthology>K06277</kegg___orthology><kegg___orthology>K16340</kegg___orthology><kegg___orthology>K05111</kegg___orthology><kegg___orthology>K04352</kegg___orthology><kegg___orthology>K04353</kegg___orthology><kegg___orthology>K04365</kegg___orthology><kegg___orthology>K16172</kegg___orthology><kegg___orthology>K04366</kegg___orthology><kegg___orthology>K04368</kegg___orthology><kegg___orthology>K04688</kegg___orthology><kegg___drug>D10064</kegg___drug><bto>BTO:0000848</bto><uniprot>Q15118</uniprot><uniprot>P04049</uniprot><uniprot>P56279</uniprot><uniprot>P28482</uniprot><uniprot>Q13905</uniprot><uniprot>P10301</uniprot><uniprot>Q02750</uniprot><uniprot>P35568</uniprot><uniprot>P42345</uniprot><uniprot>P15056</uniprot><uniprot>P67775</uniprot><uniprot>P20936</uniprot><uniprot>P60484</uniprot><uniprot>Q07889</uniprot><uniprot>P62834</uniprot><uniprot>P47736</uniprot><uniprot>P23443</uniprot><uniprot>Q5T1C6</uniprot></cross_references></HashMap>