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Karuturi, R. K. M.

Publications and source records attributed to Karuturi, R. K. M..

7 recordsLinked to original sources

Collaborative partnership model to transform bioinformatics core into a highly effective research partner and multiply the impact

Many bioinformatics cores face a multitude of challenges. We recognized that the primary source of these challenges was the service-centric approach. So, we initiated the transformation of our bioinformatics core, Computational Sciences (CS), at the Jackson Laboratory (Jax) to be a science-centric collaborative research partner for our faculty and project stakeholders. We call our model as collaborative partnership model. With the effective replacement of the service model with the collaborative partnership model, CS now acts as both an effective collaborator and a co-driver of scientific research and innovation at Jax. In this paper, we describe the principles and practices we adopted to realize this transformation and present the resulting growth in the impact of CS in the research enterprise at Jax.

scientific communication and education↗

NetAct: a computational platform to construct core transcription factor regulatory networks using gene activity

A major question in systems biology is how to identify the core gene regulatory circuit that governs the decision-making of a biological process. Here, we develop a computational platform, named NetAct, for constructing core transcription-factor regulatory networks using both transcriptomics data and literature-based transcription factor-target databases. NetAct robustly infers regulators activity using target expression, constructs networks based on transcriptional activity, and integrates mathematical modeling for validation. Our in-silico benchmark test shows that NetAct outperforms existing algorithms in inferring transcriptional activity and gene networks. We illustrate the application of NetAct to model networks driving TGF-{beta} induced epithelial-mesenchymal transition and macrophage polarization.

systems biology↗

A Genomically and Clinically Annotated Patient Derived Xenograft (PDX) Resource for Preclinical Research in Non-Small Cell Lung Cancer

Patient-derived xenograft models (PDXs) are an effective preclinical in vivo platform for testing the efficacy of novel drug and drug combinations for cancer therapeutics. Here we describe a repository of 79 genomically and clinically annotated lung cancer PDXs available from The Jackson Laboratory that have been extensively characterized for histopathological features, mutational profiles, gene expression, and copy number aberrations. Most of the PDXs are models of non-small cell lung cancer (NSCLC), including 37 lung adenocarcinoma (LUAD) and 33 lung squamous cell carcinoma (LUSC) models. Other lung cancer models in the repository include four small cell carcinomas, two large cell neuroendocrine carcinomas, two adenosquamous carcinomas, and one pleomorphic carcinoma. Models with both de novo and acquired resistance to targeted therapies with tyrosine kinase inhibitors are available in the collection. The genomic profiles of the LUAD and LUSC PDX models are consistent with those observed in patient tumors of the same tumor type from The Cancer Genome Atlas (TCGA) and to previously characterized gene expression-based molecular subtypes. Clinically relevant mutations identified in the original patient tumors were confirmed in engrafted tumors. Treatment studies performed for a subset of the models recapitulated the responses expected based on the observed genomic profiles. SignificanceThe collection of lung cancer Patient Derived Xenograft (PDX) models maintained at The Jackson Laboratory retain both the histologic features and treatment-relevant genomic alterations observed in the originating patient tumors and show expected responses to treatment with standard-of-care agents. The models serve as a valuable preclinical platform for translational cancer research. Information and data for the models are freely available from the Mouse Models of Human Cancer database (MMHCdb, http://tumor.informatics.jax.org/mtbwi/pdxSearch.do).

cancer biology↗

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↗

Pan-cancer machine learning predictors of tissue of origin and molecular subtype

BackgroundIt is estimated by the American Cancer Society that approximately 5% of all metastatic tumors have no defined primary site (tissue) of origin and are classified as cancers of unknown primary (CUPs). The current standard of care for CUP patients depends on immunohistochemistry (IHC) based approaches to identify the primary site. The addition of post-mortem evaluation to IHC based tests helps to reveal the identity of the primary site for only 25% of the CUPs, emphasizing the acute need for better methods of determination of the site of origin. CUP patients are therefore given generic chemotherapeutic agents resulting in poor prognosis. When the tissue of origin is known, patients can be given site specific therapy with significant improvement in clinical outcome. Similarly, identifying the primary site of origin of metastatic cancer is of great importance for designing treatment.\n\nIdentification of the primary site of origin is an import first step but may not be sufficient information for optimal treatment of the patient. Recent studies, primarily from The Cancer Genome Atlas (TCGA) project, and others, have revealed molecular subtypes in several cancer types with distinct clinical outcome. The molecular subtype captures the fundamental mechanisms driving the cancer and provides information that is essential for the optimal treatment of a cancer. Thus, along with primary site of origin, molecular subtype of a tumor is emerging as a criterion for personalized medicine and patient entry into clinical trials.\n\nHowever, there is no comprehensive toolset available for precise identification of tissue of origin or molecular subtype for precision medicine and translational research.\n\nMethods and FindingsWe posited that metastatic tumors will harbor the gene expression profiles of the primary site of origin of the cancer. Therefore, we decided to learn the molecular characteristics of the primary tumors using the large number of cancer genome profiles available from the TCGA project. Our predictors were trained for 33 cancer types and for the 11 cancers where there are established molecular subtypes. We estimated the accuracy of several machine learning models using cross-validation methods. The extensive testing using independent test sets revealed that the predictors had a median sensitivity and specificity of 97.2% and 99.9% respectively without losing classification of any tumor. Subtype classifiers achieved median sensitivity of 87.7% and specificity of 94.5% via cross validation and presented median sensitivity of 79.6% and specificity of 94.6% in two external datasets of 1,999 total samples. Importantly, these external data shows that our classifiers can robustly predict the primary site of origin from external microarray data, metastatic cancer data, and patient-derived xenograft (PDX) data.\n\nConclusionWe have demonstrated the utility of gene expression profiles to solve the important clinical challenge of identifying the primary site of origin and the molecular subtype of cancers based on machine learning algorithms. We show, for the first time to our knowledge, that our pan-cancer classifiers can predict multiple cancers primary site of origin from metastatic samples. The predictors will be made available as open source software, freely available for academic non-commercial use.

cancer biology↗

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↗

MultiDCoX: Multi-factor Analysis of Differential Co-expression

BackgroundDifferential co-expression signifies change in degree of co-expression of a set of genes among different biological conditions. It has been used to identify differential co-expression networks or interactomes. Many algorithms have been developed for single-factor differential co-expression analysis and applied in a variety of studies. However, in many studies, the samples are characterized by multiple factors such as genetic markers, clinical variables and treatments. No algorithm or methodology is available for multi-factor analysis of differential co-expression.\n\nResultsWe developed a novel formulation and a computationally efficient greedy search algorithm called MultiDCoX to perform multi-factor differential co-expression analysis of transcriptomic data. Simulated data analysis demonstrates that the algorithm can effectively elicit differentially co-expressed (DCX) gene sets and quantify the influence of each factor on co-expression. MultiDCoX analysis of a breast cancer dataset identified interesting biologically meaningful differentially coexpressed (DCX) gene sets along with genetic and clinical factors that influenced the respective differential co-expression.\n\nConclusionsMultiDCoX is a space and time efficient procedure to identify differentially co-expressed gene sets and successfully identify influence of individual factors on differential co-expression.\n\nSoftwareR function will be available upon request.

bioinformatics↗