Shyam M. Kavuri

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UNLABELLED Data from 8 breast cancer genome-sequencing projects identified 25 patients with HER2 somatic mutations in cancers lacking HER2 gene amplification. To determine the phenotype of these mutations, we functionally characterized 13 HER2 mutations using in vitro kinase assays, protein structure analysis, cell culture, and xenograft experiments. Seven(More)
Recent advances in mass spectrometry (MS) have enabled extensive analysis of cancer proteomes. Here, we employed quantitative proteomics to profile protein expression across 24 breast cancer patient-derived xenograft (PDX) models. Integrated proteogenomic analysis shows positive correlation between expression measurements from transcriptomic and proteomic(More)
UNLABELLED The Cancer Genome Atlas project identified HER2 somatic mutations and gene amplification in 7% of patients with colorectal cancer. Introduction of the HER2 mutations S310F, L755S, V777L, V842I, and L866M into colon epithelial cells increased signaling pathways and anchorage-independent cell growth, indicating that they are activating mutations.(More)
Smoking is a major risk factor for the development of bladder cancer; however, the functional consequences of the carcinogens in tobacco smoke and bladder cancer-associated metabolic alterations remain poorly defined. We assessed the metabolic profiles in bladder cancer smokers and non-smokers and identified the key alterations in their metabolism. LC/MS(More)
Kuan-lin Huang, Shunqiang Li, Philipp Mertins, Song Cao, Harsha P. Gunawardena, Kelly V. Ruggles, D.R. Mani, Karl R. Clauser, Maki Tanioka, Jerry Usary, Shyam M. Kavuri, Ling Xie, Christopher Yoon, Jana W. Qiao, John Wrobel, Matthew A. Wyczalkowski, Petra Erdmann-Gilmore, Jacqueline E. Snider, Jeremy Hoog, Purba Singh, Beifang Niu, Zhanfang Guo, Sam(More)
Significant endocrine therapy-resistant tumor proliferation is present in ≥20% of estrogen receptor-positive (ER+) primary breast cancers and is associated with disease recurrence and death. Here, we uncover a link between intrinsic endocrine therapy resistance and dysregulation of the MutL mismatch repair (MMR) complex (MLH1/3, PMS1/2), and demonstrate a(More)
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