<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE314nnn/GSE314073/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE314073</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Transcriptomic profiling of KRAS mutants in a panel of isogenic human pancreatic ductal adenocarcinoma (PDAC) cell lines</name><description>KRAS is mutated more than 90% of pancreatic ductal adenocarcinomas (PDAC), where hotspot alterations in codons 12, 13, and 61 drive tumor initiation and progression. Although distinct biochemical properties have been reported for individual KRAS mutants, a comprehensive characterization of allele-specific differences in PDAC cells remains unresolved. Here, we systematically interrogated the molecular consequences of seven common KRAS mutant variants by reconstituting 4 isogenic, KRAS-deficient PDAC cell lines and performing bulk RNA-sequencing. We found that baseline cellular state, rather than allele identity, was the predominant driver of molecular variation across all samples. Pathway analyses highlighted that KRAS mutants upregulated inflammatory and immune-related pathways, including TNFα signaling via NFκB, IL2-STAT5 signaling, and epithelial–mesenchymal transition, while downregulating interferon responses and hypoxia-associated. Importantly, no robust allele-specific molecular programs were identified across all samples. Our study establishes a comprehensive resource for investigating mutant KRAS transcriptome in PDAC and demonstrates that cellular context exerts a stronger influence than allele identity in shaping molecular profiles.</description><dates><publication>2026/09/10</publication></dates><accession>GSE314073</accession><cross_references><GSM>GSM9381146</GSM><GSM>GSM9381168</GSM><GSM>GSM9381167</GSM><GSM>GSM9381145</GSM><GSM>GSM9381144</GSM><GSM>GSM9381166</GSM><GSM>GSM9381143</GSM><GSM>GSM9381165</GSM><GSM>GSM9381164</GSM><GSM>GSM9381142</GSM><GSM>GSM9381141</GSM><GSM>GSM9381163</GSM><GSM>GSM9381162</GSM><GSM>GSM9381140</GSM><GSM>GSM9381161</GSM><GSM>GSM9381160</GSM><GSM>GSM9381139</GSM><GSM>GSM9381138</GSM><GSM>GSM9381137</GSM><GSM>GSM9381159</GSM><GSM>GSM9381158</GSM><GSM>GSM9381157</GSM><GSM>GSM9381156</GSM><GSM>GSM9381155</GSM><GSM>GSM9381176</GSM><GSM>GSM9381154</GSM><GSM>GSM9381153</GSM><GSM>GSM9381175</GSM><GSM>GSM9381152</GSM><GSM>GSM9381174</GSM><GSM>GSM9381173</GSM><GSM>GSM9381151</GSM><GSM>GSM9381150</GSM><GSM>GSM9381172</GSM><GSM>GSM9381171</GSM><GSM>GSM9381170</GSM><GSM>GSM9381149</GSM><GSM>GSM9381148</GSM><GSM>GSM9381147</GSM><GSM>GSM9381169</GSM><GPL>34284</GPL><GSE>314073</GSE><taxon>Homo sapiens</taxon><PMID>[42720273]</PMID></cross_references></HashMap>