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Chuang, J. H.

Publications and source records attributed to Chuang, J. H..

3 recordsLinked to original sources

Bioinformatics workflows for genomic analysis of tumors from Patient Derived Xenografts (PDX): challenges and guidelines

Bioinformatics workflows for analyzing genomic data obtained from xenografted tumor (e.g., human tumors engrafted in a mouse host) must address several challenges, including separating mouse and human sequence reads and accurate identification of somatic mutations and copy number aberrations when paired normal DNA from the patient is not available. We report here data analysis workflows that address these challenges and result in reliable identification of somatic mutations, copy number alterations, and transcriptomic profiles of tumors from patient derived xenograft models. We validated our analytical approaches using simulated data and by assessing concordance of the genomic properties of xenograft tumors with data from primary human tumors in The Cancer Genome Atlas (TCGA). The commands and parameters for the workflows are available at https://github.com/TheJacksonLaboratory/PDX-Analysis-Workflows.

bioinformatics

Evolution of an intratumoral ecology susceptible to successive treatment in breast cancer xenografts

The processes by which tumors evolve are essential to the efficacy of treatment, but quantitative understanding of intratumoral dynamics has been limited. Although intratumoral heterogeneity is common, quantification of evolution is difficult from clinical samples because treatment replicates cannot be performed and because matched serial samples are infrequently available. To circumvent these problems we derived and assayed large sets of human triple-negative breast cancer xenografts and cell cultures from two patients, including 86 xenografts from cyclophosphamide, doxorubicin, cisplatin, docetaxel, or vehicle treatment cohorts as well as 45 related cell cultures. We assayed these samples via exome-seq and/or high-resolution droplet digital PCR, allowing us to distinguish complex therapy-induced selection and drift processes among endogenous cancer subclones with cellularity uncertainty <3%. For one patient, we discovered two predominant subclones that were granularly intermixed in all 48 co-derived xenograft samples. These two subclones exhibited differential chemotherapy sensitivity -- when xenografts were treated with cisplatin for 3 weeks, the post-treatment volume change was proportional to the post-treatment ratio of subclones on a xenograft-to-xenograft basis. A subsequent cohort in which xenografts were treated with cisplatin, allowed a drug holiday, then treated a second time continued to exhibit this proportionality. In contrast, xenografts from other treatment cohorts, spatially dissected xenograft fragments, and cell cultures evolved unsystematically but with substantial population bottlenecks. These results show that ecologies susceptible to successive retreatment can arise spontaneously in breast cancer in spite of a background of irregular subclonal bottlenecks, and our work provides to our knowledge the first quantification of the population genetics of such a system. Intriguingly, in such an ecology the ratio of common subclones is predictive of the state of treatment susceptibility, suggesting that this ratio can be measured to optimize dynamic treatment protocols in patients.\n\nAUTHOR SUMMARYAn overarching challenge of cancer is that patients develop resistance to treatment -- an essentially evolutionary process. However, there is currently very little understanding of how tumor evolution can be exploited to improve treatment. One reason for this is that usually only 1-2 samples can be obtained per patient, so cancer evolutionary processes are still poorly understood. To solve this problem, we created many dozens of copies of the tumors from two breast cancer patients using xenografting and cell culture methods. We then compared the evolution in these tumor copies in response to different treatments, including four of the most common breast cancer chemotherapies. These studies present the most exhaustive comparisons of treatment-induced evolution that have yet been performed for individual cancer patients. Unexpectedly, high-resolution sequencing of these samples revealed a special dynamically treatable ecology in one tumor, in which tumor growth during platinum therapy was determined by the ecological balance of two tumor cell populations. Our work shows that ecologies that can be targeted by dynamic treatment strategies arise spontaneously in breast cancers. Population heterogeneity is common within cancers, and our work suggests how tracking of intratumoral evolution can be used to optimize treatment.

cancer biology

SARNAclust: Semi-Automatic Detection Of RNA Protein Binding Motifs From Immunoprecipitation Data

RNA-protein binding is critical to gene regulation, controlling fundamental processes including splicing, translation, localization and stability, and aberrant RNA-protein interactions are known to play a role in a wide variety of diseases. However, molecular understanding of RNA-protein interactions remains limited, and in particular identification of the RNA motifs that bind proteins has long been a difficult problem. To address this challenge, we have developed a novel semi-automatic algorithm, SARNAclust, to computationally identify combined structure/sequence motifs from immunoprecipitation data. SARNAclust is, to our knowledge, the first unsupervised method that can identify RNA motifs at full structural resolution while also being able to simultaneously deconvolve multiple motifs. SARNAclust makes use of a graph kernel to evaluate similarity between sequence/structure objects, and provides the ability to isolate the impact of specific features through the bulge graph formalism. SARNAclust includes a key method for predicting RNA secondary structure at CLIP peaks, RNApeakFold, which we have verified to be effective on synthetic motif data. We applied SARNAclust to 30 ENCODE eCLIP datasets, identifying known motifs and novel predictions. Notably, we predicted a new motif for the protein ILF3 similar to that for the splicing factor hnRNPC, providing evidence for interaction between these two proteins. To validate our predictions, we performed a directed RNA bind-n-seq assay for two proteins: ILF3 and SLBP, in each case revealing the effectiveness of SARNAclust in predicting RNA sequence and structure elements important to protein binding. Availability: https://github.com/idotu/SARNAclust

bioinformatics