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To advance our understanding of the role of breast cancer driver genes' mutational status with pathological complete response (pCR; ypT0\/isypN0) prediction and to identify distinct gene sets for MTIs like eribulin and paclitaxel, we carried out targeted genomic (<jats:italic>n<\/jats:italic>\u2009=\u200950) and whole transcriptomic profiling (<jats:italic>n<\/jats:italic>\u2009=\u200964) of TNBC tumor samples from the Japan Breast Cancer Research Group 22 (JBCRG\u201022) clinical trial. Lower <jats:italic>PIK3CA<\/jats:italic>, <jats:italic>PTEN<\/jats:italic>, and <jats:italic>HRAS<\/jats:italic> mutations were found in homologous recombination deficiency (HRD)\u2010high (HRD score\u2009\u2265\u200942) tumors with higher pCR rates. When HRD\u2010high tumors were stratified by tumor <jats:italic>BRCA<\/jats:italic> mutation status, the pCR rates in <jats:italic>BRCA2<\/jats:italic>\u2010mutated tumors were higher (83% vs. 36%). Transcriptomic profiling of TP53\u2010positive tumors identified downregulation of <jats:italic>FGFR2<\/jats:italic> (false discovery rate <jats:italic>p<\/jats:italic> value\u2009=\u20092.07e\u20107), which was also the only common gene between HRD\u2010high and \u2010low tumors with pCR\/quasi\u2010pCR treated with paclitaxel and eribulin combined with carboplatin, respectively. Differential enrichment analysis of the HRD\u2010high group posttreatment tumors revealed significant correlation (<jats:italic>p<\/jats:italic>\u2009=\u20090.006) of the glycan degradation pathway. <jats:italic>FGFR2<\/jats:italic> expression and the differentially enriched pathways play a role in the response and resistance to MTIs containing carboplatin treatment in TNBC patients.<\/jats:p>","DOI":"10.1111\/cas.16339","type":"journal-article","created":{"date-parts":[[2024,10,8]],"date-time":"2024-10-08T05:39:55Z","timestamp":1728365995000},"page":"3928-3942","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Genomic and transcriptomic profiling of pre\u2010 and postneoadjuvant chemotherapy triple negative breast cancer tumors"],"prefix":"10.1111","volume":"115","author":[{"given":"Tomomi","family":"Nishimura","sequence":"first","affiliation":[{"name":"Department of Next\u2010generation Clinical Genomic Medicine, 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