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Elemento, O.

Publications and source records attributed to Elemento, O..

At least 73 records · Page 4Linked to original sources

A machine learning and network framework to discover new indications for small molecules

Drug repurposing, identifying novel indications for drugs, bypasses common drug development pitfalls to ultimately deliver therapies to patients faster. However, most repurposing discoveries have been led by anecdotal observations (e.g. Viagra) or experimental-based repurposing screens, which are costly, time-consuming, and imprecise. Recently, more systematic computational approaches have been proposed, however these rely on utilizing the information from the diseases a drug is already approved to treat. This inherently limits the algorithms, making them unusable for investigational molecules. Here, we present a computational approach to drug repurposing, CATNIP, that requires only biological and chemical information of a molecule. CATNIP is trained with 2,576 diverse small molecules and uses 16 different drug similarity features, such as structural, target, or pathway based similarity. This model obtains significant predictive power (AUC = 0.841). Using our model, we created a repurposing network to identify broad scale repurposing opportunities between drug types. By exploiting this network, we identified literature-supported repurposing candidates, such as the use of systemic hormonal preparations for the treatment of respiratory illnesses. Furthermore, we demonstrated that we can use our approach to identify novel uses for defined drug classes. We found that adrenergic uptake inhibitors, specifically amitriptyline and trimipramine, could be potential therapies for Parkinsons disease. Additionally, using CATNIP, we predicted the kinase inhibitor, vandetanib, as a possible treatment for Type 2 Diabetes. Overall, this systematic approach to drug repurposing lays the groundwork to streamline future drug development efforts.

pharmacology and toxicology↗

A machine learning approach predicts essential genes and pharmacological targets in cancer

Loss-of-function (LoF) screenings have the potential to reveal novel cancer-specific vulnerabilities, prioritize drug treatments, and inform precision medicine therapeutics. These screenings were traditionally done using shRNAs, but with the recent emergence of CRISPR technology there has been a shift in methodology. However, recent analyses have found large inconsistencies between CRISPR and shRNA essentiality results. Here, we examined the DepMap project, the largest cancer LoF effort undertaken to date, and find a lack of correlation between CRISPR and shRNA LoF results; we further characterized differences between genes found to be essential by either platform. We then introduce ECLIPSE, a machine learning approach, which combines genomic, cell line, and experimental design features to predict essential genes and platform specific essential genes in specific cancer cell lines. We applied ECLIPSE to known drug targets and found that our approach strongly differentiated drugs approved for cancer versus those that have not, and can thus be leveraged to identify potential cancer repurposing opportunities. Overall, ECLIPSE allows for a more comprehensive analysis of gene essentiality and drug development; which neither platform can achieve alone.

cancer biology↗

Single-cell analysis of the muscle stem cell hierarchy identifies heterotypic communication signals involved in skeletal muscle regeneration

Muscle stem cells (MuSCs) are an essential adult stem cell population with the capacity to self-renew and regenerate muscle tissue. Functionally heterogeneous subpopulations of MuSCs have been identified based on their expression of myogenic regulatory factors and surface markers. However, a unified organization of muscle stem and progenitor cells and their subpopulations remains unresolved. Here, we performed temporal analysis of skeletal muscle regeneration using single-cell RNA-sequencing (scRNA-seq) of myotoxin-injured adult mouse hindlimb muscles. We generated over 34,000 single-cell transcriptomes spanning four muscle regeneration time-points and identified 15 distinct cell types, including a heterogeneous population of MuSCs and progenitor cells. Our analysis provides a hierarchical map of myogenic cell populations and identifies stage-specific regulatory programs that govern their contributions to muscle regeneration. In this transcriptomic atlas, we observed cell type-specific regenerative dynamics, exemplified by waves of transient amplification and diversification of multiple immune cell types and, subsequently, myogenic cells. Unbiased trajectory inference organized the myogenic cell populations within the atlas into a continuum, consisting of a hierarchy of quiescent MuSCs, cycling progenitors, committed myoblasts, and terminally differentiated myocytes. This myogenic trajectory matched prior understanding and also revealed that MuSC stages are defined by synchronous changes in regulatory factors, cell cycle-associated, and surface receptor gene expression. Lastly, we analyzed the transcriptomic atlas to identify over 100 candidate heterotypic communication signals between myogenic and non-myogenic cell populations, including many involving the fibroblast growth factor (FGF), Notch, and Syndecan receptor families and their associated ligands. Syndecan receptors were implicated in a large fraction of these cell communication interactions and were observed to exhibit transcriptional heterogeneity within the myogenic continuum. Using multiparameter mass cytometry (CyTOF), we confirmed that cycling MuSCs exhibit diversified Syndecan-1/2 expression, which suggests that dynamic alterations in Syndecan signaling interactions may coordinate stage-specific myogenic cell fate regulation. This scRNA-seq reference atlas provides a resolved hierarchical organization of myogenic subpopulations as a resource to investigate cell-cell interactions that regulate myogenic stem and progenitor cell fates in muscle regeneration.

cell biology↗

Age, Sex, and Genetics Influence the Abundance of Infiltrating Immune Cells in Human Tissues

Despite infiltrating immune cells playing an essential role in human disease and the patient response to treatment, the central mechanisms influencing variability in infiltration patterns are unclear. Using bulk RNA-seq data from 53 GTEx tissues, we applied cell-type deconvolution algorithms to evaluate the immune landscape across the healthy human body. We first performed a differential expression analysis of inflamed versus non-inflamed samples to identify essential pathways and regulators of infiltration. Next, we found 21 of 73 infiltration-related phenotypes to be associated with either age or sex (FDR < 0.1). Through our genetic analysis, we discovered 13 infiltration-related phenotypes have genome-wide significant associations (iQTLs) (P < 5.0 x 10-8), with a significant enrichment of tissue-specific expression quantitative trait loci in suggested iQTLs (P < 10-5). We highlight an association between neutrophil content in lung tissue and a variant near the CUX1 transcription factor gene (P = 9.7 x 10-11), which has been previously linked to neutrophil infiltration, inflammatory mechanisms, and the regulation of several immune response genes. Together, our results identify key factors influencing inter-individual variability of specific tissue infiltration patterns, which could provide insights on therapeutic targets for shifting infiltration profiles to a more favorable one.

genetics↗

Function and clinical relevance of RHAMM isoforms in pancreatic tumor progression

The receptor for hyaluronic acid-mediated motility (RHAMM) is upregulated in various cancers. We previously screened genes upregulated in human hepatocellular carcinomas for their metastatic function in a mouse model of pancreatic neuroendocrine tumor (PNET) and identified that human RHAMMB promoted liver metastasis. It was unknown whether RHAMMB is upregulated in pancreatic cancer or contributes to its progression. In this study, we found that RHAMM protein was frequently upregulated in human PNETs. We investigated alternative splicing isoforms, RHAMMA and RHAMMB, by RNA-Seq analysis of primary PNETs and liver metastases. RHAMMB, but not RHAMMA, was significantly upregulated in liver metastases. RHAMMB was crucial for in vivo metastatic capacity of mouse and human PNETs. RHAMMA, carrying an extra 15-amino acid-stretch, did not promote metastasis in spontaneous and experimental metastasis mouse models. Moreover, RHAMMB was substantially higher than RHAMMA in pancreatic ductal adenocarcinoma (PDAC). RHAMMB, but not RHAMMA, correlated with both higher EGFR expression and poorer survival of PDAC patients. Knockdown of EGFR abolished RHAMMB-driven PNET metastasis. Altogether, our findings suggest a clinically relevant function of RHAMMB, but not RHAMMA, in promoting PNET metastasis in part through EGFR signaling. RHAMMB can thus serve as a prognostic factor for pancreatic cancer.

cancer biology↗

Multi-task learning predicts drug combination synergy in cells and in the clinic

Combination therapies for various cancers have been shown to increase efficacy, lower toxicity, and circumvent resistance. However, despite the promise of combinatorial therapies, the biological mechanisms behind drug synergy have not been fully characterized, and the systematic testing of all possible synergistic therapies is experimentally infeasible due to the sheer volume of potential combinations. Here we apply a novel big data approach in the evaluation and prediction of drug synergy by using the recently released NCI-ALMANAC. We found that each traditional drug synergy metric (Bliss, Loewe, ZIP, HSA, ALMANAC Score) identified unique synergistic drug pairs with distinct underlying joint mechanisms of action. Leveraging these findings, we developed a suite of context specific drug synergy predictive models for each distinct synergy type and achieved significant predictive performance (AUC = 0.89-0.953). Furthermore, our models accurately identified clinically tested drug pairs and characterized the clinical relevance of each drug synergy metric, with Bliss Independence capturing clinically tested combinations best. Our findings demonstrate that drug synergy can be obtained from numerous unique joint mechanisms of action, captured by different synergy metrics. Additionally, we show that drug synergy, of all kinds, can be predicted with high degrees of accuracy with significant clinical potential. This breakthrough understanding of joint mechanisms of action will allow for the design of rational combinatorial therapeutics on a large scale, across various cancer types.

cancer biology↗

Tumor mutational landscape is a record of the pre-malignant state

Chromatin structure has a major influence on the cell-specific density of somatic mutations along the cancer genome. Here, we present a pan-cancer study in which we searched for the putative cancer cell-of-origin of 2,550 whole genomes, representing 32 cancer types by matching their mutational landscape to the regional patterns of chromatin modifications ascertained in 104 normal tissue types. We found that, in almost all cancer types, the cell-of-origin can be predicted solely from their DNA sequences. Our analysis validated the hypothesis that high-grade serous ovarian cancer originates in the fallopian tube and identified distinct origins of breast cancer subtypes. We also demonstrated that the technique is equally capable of identifying the cell-of-origin for a series of 2,044 metastatic samples from 22 of the tumor types available as primaries. Moreover, cancer drivers, whether inherited or acquired, reside in active chromatin regions in the respective cell-of-origin. Taken together, our findings highlight that many somatic mutations accumulate while the chromatin structure of the cell-of-origin is maintained and that this historical record, captured in the DNA, can be used to identify the often elusive cancer cell-of-origin.

genomics↗

Dynamic transcriptome profiles within spermatogonial and spermatocyte populations during postnatal testis maturation revealed by single-cell sequencing

Spermatogenesis is the process by which male gametes are formed from a self-renewing population of spermatogonial stem cells (SSCs) residing in the testis. SSCs represent less than 1% of the total testicular cell population, but must achieve a stable balance between self-renewal and differentiation. Once differentiation has occurred, the newly formed and highly proliferative spermatogonia must then enter the meiotic program in which DNA content is doubled, then halved twice to create haploid gametes. While much is known about the critical cellular processes that take place during the specialized cell division that is meiosis, much less is known about how the spermatocytes in the \"first-wave\" compare to those that contribute to long-term, \"steady-state\" spermatogenesis. Given the strictly-defined developmental process of spermatogenesis, this study was aimed at exploring the transcriptional profiles of developmental cell stages over the age of the animal. Using a combination of comprehensive germ cell sampling with high-resolution, single-cell-mRNA-sequencing, we have generated a reference dataset of germ cell gene expression. We show that discrete developmental stages possess significant differences in the transcriptional profiles from neonates compared to juveniles and adults. Importantly, these gene expression dynamics are also reflected at the protein level in their respective cell types. We also show differential utilization of many biological pathways with age in both spermatogonia and spermatocytes, demonstrating significantly different underlying gene regulatory programs in these cell types over the course of testis development and spermatogenic waves. This dataset represents the first unbiased sampling of spermatogonia and spermatocytes in the developing testis over developmental age, at high-resolution, single-cell depth. Not only does this analysis reveal previously unknown transcriptional dynamics of a highly transitional cell population, it has also begun to reveal critical differences in biological pathway utilization in developing spermatogonia and spermatocytes, including response to DNA damage and double-strand breaks.\n\nAuthor SummarySpermatogenesis is the process by which male gametes - mature spermatozoa - are produced in the testis. This process requires exquisite control over many developmental transitions, including the self-renewal of the germline stem cell population, commitment to meiosis, and ultimately, spermiogenesis. While much is known about molecular mechanisms regulating single transitions at single time points in the mouse, much less is understood about how the spermatogenic progenitor cells, spermatogonia, or the meiotic cells, spermatocytes, of the testis change over developmental age.\n\nOur single-cell-mRNA-sequencing analysis is the first to profile both spermatogonia and spermatocytes from neonatal mice through adulthood, revealing novel gene expression dynamics and differential utilization of biological pathways. These discoveries help us to understand how the spermatogenic progenitors of this population modulate their activity to adapt to a changing testicular environment. Furthermore, they also begin to explain previously-observed differences - and deficiencies - in spermatocytes that are derived from the first \"wave\" of spermatogenesis. Overall, this dataset is the first of its kind to comprehensively profile gene expression dynamics in male germ cell populations over time, enriching our understanding of the complex and highly-orchestrated process of spermatogenesis.

genomics↗

Robust Automated Assessment of Human Blastocyst Quality using Deep Learning

Morphology assessment has become the standard method for evaluation of embryo quality and selecting human blastocysts for transfer in in vitro fertilization (IVF). This process is highly subjective for some embryos and thus prone to human bias. As a result, morphological assessment results may vary extensively between embryologists and in some cases may fail to accurately predict embryo implantation and live birth potential. Here we postulated that an artificial intelligence (AI) approach trained on thousands of embryos can reliably predict embryo quality without human intervention.\n\nTo test this hypothesis, we implemented an AI approach based on deep neural networks (DNNs). Our approach called STORK accurately predicts the morphological quality of blastocysts based on raw digital images of embryos with 98% accuracy. These results indicate that a DNN can automatically and accurately grade embryos based on raw images. Using clinical data for 2,182 embryos, we then created a decision tree that integrates clinical parameters such as embryo quality and patient age to identify scenarios associated with increased or decreased pregnancy chance. This IVF data-driven analysis shows that the chance of pregnancy varies from 13.8% to 66.3%.\n\nIn conclusion, our AI-driven approach provides a novel way to assess embryo quality and uncovers new, potentially personalized strategies to select embryos with an improved likelihood of pregnancy outcome.

bioinformatics↗

A harmonized meta-knowledgebase of clinical interpretations of cancer genomic variants

Precision oncology relies on the accurate discovery and interpretation of genomic variants to enable individualized diagnosis, prognosis, and therapy selection. We found that knowledgebases containing clinical interpretations of somatic cancer variants are highly disparate in interpretation content, structure, and supporting primary literature, impeding consensus when evaluating variants and their relevance in a clinical setting. With the cooperation of experts of the Global Alliance for Genomics and Health (GA4GH) and six prominent cancer variant knowledgebases, we developed a framework for aggregating and harmonizing variant interpretations to produce a meta-knowledgebase of 12,856 aggregate interpretations covering 3,437 unique variants in 415 genes, 357 diseases, and 791 drugs. We demonstrated large gains in overlap between resources across variants, diseases, and drugs as a result of this harmonization. We subsequently demonstrated improved matching between a patient cohort and harmonized interpretations of potential clinical significance, observing an increase from an average of 33% per individual knowledgebase to 56% in aggregate. Our analyses illuminate the need for open, interoperable sharing of variant interpretation data. We also provide an open and freely available web interface (search.cancervariants.org) for exploring the harmonized interpretations from these six knowledgebases.

bioinformatics↗

Epigenetic analysis identifies factors driving racial disparity in prostate cancer

Prostate cancer (PCa) is the second most leading cause of death in men worldwide. African American men (AA) represent more aggressive form of PCa as compared to Caucasian (CA) counterparts. Evidence suggests that genetic and other biological factors could account for the observed racial disparity. We analyzed the cancer genome atlas (TCGA) dataset (2015) for existing epigenetic variation in AA and CA prostate cancer patients, and carried out Reduced Representation Bisulphite Sequencing (RRBS) analysis to identify global methylation changes in AA and CA prostate cancer patients. The TCGA dataset analysis revealed that the epigenetic heterogeneity could be categorized into 4 classes, where AA associated primarily to methylation cluster 1 (p value 0.048), and CA associated to methylation cluster 3 (p value 0.000146). We identified enrichment of Wnt signaling genes in both AA and CA, however they were differentially activated in terms of canonical and non-canonical Wnt signaling pathway activation. This was further validated using the GenomeDx expression data. Our RRBS data also suggested distinct methylation patterns in AA compared to CA, and in part validated our TCGA findings. Survival analysis using the RRBS data suggested hypomethylated genes to be significantly associated with recurrence of prostate cancer in CA (p=6.07x10-6) as well as in AA (p=0.0077). Overall, the observed racial disparity in the molecular mechanism involved in the pathogenesis of prostate cancer suggests diverse heterogeneity that potentially could affect survival and should be considered during prognosis and treatment.

cancer biology↗

Predicting peptide presentation by major histocompatibility complex class I using one million peptides

Improved computational tools are needed to prioritize putative neoantigens within immunotherapy pipelines for cancer treatment. Herein, we assemble a database of over one million human peptides presented by major histocompatibility complex class I (MHC-I), the largest known database of its type. We use these data to train a random forest classifier (ForestMHC) to predict likelihood of MHC-I presentation. The information content of features mirrors the canonical importance of positions two and nine in determining likelihood of binding. Our random forest-based method outperforms NetMHC and NetMHCpan on test sets, and it outperforms both these methods and MixMHCpred on new mass spectrometry data from an ovarian carcinoma sample. Furthermore, the random forest scores correlate monotonically with peptide binding affinities, when known. Finally, we examine the effect size of gene expression on peptide presentation and find a moderately strong relationship. The ForestMHC method is a promising modality to prioritize neoantigens for experimental testing in immunotherapy.

bioinformatics↗

A Machine Learning Approach Predicts Tissue-Specific Drug Adverse Events

One of the main causes for failure in the drug development pipeline or withdrawal post approval is the unexpected occurrence of severe drug adverse events. Even though such events should be detected by in vitro, in vivo, and human trials, they continue to unexpectedly arise at different stages of drug development causing costly clinical trial failures and market withdrawal. Inspired by the \"moneyball\" approach used in baseball to integrate diverse features to predict player success, we hypothesized that a similar approach could leverage existing adverse event and tissue-specific toxicity data to learn how to predict adverse events. We introduce MAESTER, a data-driven machine learning approach that integrates information on a compounds structure, targets, and phenotypic effects with tissue-wide genomic profiling and our toxic target database to predict the probability of a compound presenting with different types of tissue-specific adverse events. When tested on 6 different types of adverse events MAESTER maintains a high accuracy, sensitivity, and specificity across both the training data and new test sets. Additionally, MAESTER scores could flag a number of drugs that were approved, but later withdrawn due to unknown adverse events - highlighting its potential to identify events missed by traditional methods. MAESTER can also be used to identify toxic targets for each tissue type. Overall MAESTER provides a broadly applicable framework to identify toxic targets and predict specific adverse events and can accelerate the drug development pipeline and drive the design of new safer compounds.

pharmacology and toxicology↗

Generation of pulmonary neuro-endocrine cells and tumors resembling small cell lung cancers from human embryonic stem cells

SUMMARYBy blocking an important signaling pathway (called NOTCH) and interfering with expression of two tumor suppressor genes in cells derived from human embryonic stem cells, the authors have developed a model for studying highly lethal small cell lung cancers.\n\nABSTRACTCell culture models based on directed differentiation of human embryonic stem cells (hESCs) may reveal why certain constellations of genetic changes drive carcinogenesis in specialized human cell lineages. Here we demonstrate that up to 10 percent of lung progenitor cells derived from hESCs can be induced to form pulmonary neuroendocrine cells (PNECs), the putative normal precursors to small cell lung cancers (SCLCs), by inhibition of NOTCH signaling. By using small inhibitory RNAs in these cultures to reduce levels of retinoblastoma (RB) protein, the product of a gene commonly mutated in SCLCs, we can significantly expand the number of PNECs. Similarly reducing levels of TP53 protein, the product of another tumor suppressor gene commonly mutated in SCLCs, or expressing mutant KRAS or EGFR genes, did not induce or expand PNECs, consistent with lineage-specific sensitivity to loss of RB function. Tumors resembling early stage SCLC grew in immunodeficient mice after subcutaneous injection of PNEC-containing cultures in which expression of both RB and TP53 was blocked. Single-cell RNA profiles of PNECs are heterogeneous; when RB levels are reduced, the profiles show similarities to RNA profiles from early stage SCLC; when both RB and TP53 levels are reduced, the transcriptome is enriched with cell cycle-specific RNAs. Taken together, these findings suggest that genetic manipulation of hESC-derived pulmonary cells will enable studies of the initiation, progression, and treatment of this recalcitrant cancer.

cancer biology↗

Accelerated lipid catabolism and autophagy are cancer survival mechanisms under inhibited glutaminolysis

Suppressing glutaminolysis does not always induce cancer cell death in glutamine-dependent tumors because cells may switch to alternative energy sources. To reveal compensatory metabolic pathways, we investigated the metabolome-wide cellular response to inhibited glutaminolysis. We conducted metabolic profiling in the triple-negative breast cancer cell line MB-MDA-231, treated with different dosages of glutaminase inhibitor C.968 at multiple time points. We found that multiple molecules involved in lipid catabolism responded directly to glutamate deficiency as a presumed compensation for energy deficit. Accelerated lipid catabolism, together with oxidative stress induced by glutaminolysis inhibition, triggered autophagy. We therefore simultaneously inhibited glutaminolysis and autophagy, which induced cancer cell death. Our study emphasizes the potential of non-targeted metabolomics to characterize and identify metabolic escape mechanisms contributing to cancer cell survival under treatment. Our findings add to the increasing evidence that combined inhibition of glutaminolysis and autophagy may be effective in glutamine-addicted cancers.

cancer biology↗

Breast Cancer Histopathological Image Classification: A Deep Learning Approach

Breast cancer remains the most common type of cancer and the leading cause of cancer-induced mortality among women with 2.4 million new cases diagnosed and 523,000 deaths per year. Historically, a diagnosis has been initially performed using clinical screening followed by histopathological analysis. Automated classification of cancers using histopathological images is a chciteallenging task of accurate detection of tumor sub-types. This process could be facilitated by machine learning approaches, which may be more reliable and economical compared to conventional methods.\n\nTo prove this principle, we applied fine-tuned pre-trained deep neural networks. To test the approach we first classify different cancer types using 6, 402 tissue micro-arrays (TMAs) training samples. Our framework accurately detected on average 99.8% of the four cancer types including breast, bladder, lung and lymphoma using the ResNet V1 50 pre-trained model. Then, for classification of breast cancer sub-types this approach was applied to 7,909 images from the BreakHis database. In the next step, ResNet V1 152 classified benign and malignant breast cancers with an accuracy of 98.7%. In addition, ResNet V1 50 and ResNet V1 152 categorized either benign- (adenosis, fibroadenoma, phyllodes tumor, and tubular adenoma) or malignant- (ductal carcinoma, lobular carcinoma, mucinous carcinoma, and papillary carcinoma) sub-types with 94.8% and 96.4% accuracy, respectively. The confusion matrices revealed high sensitivity values of 1, 0.995 and 0.993 for cancer types, as well as malignant- and benign sub-types respectively. The areas under the curve (AUC) scores were 0.996,0.973 and 0.996 for cancer types, malignant and benign sub-types, respectively. Overall, our results show negligible false negative (on average 3.7 samples) and false positive (on average 2 samples) results among different models. Availability: Source codes, guidelines and data sets are temporarily available on google drive upon request before moving to a permanent GitHub repository.

bioinformatics↗

Challenges in Using ctDNA to Achieve Early Detection of Cancer

Early detection of cancer is a significant unmet clinical need. Improved technical ability to detect circulating tumor-derived DNA (ctDNA) in the cell-free DNA (cfDNA) component of blood plasma via next-generation sequencing and established correlations between ctDNA load and tumor burden in cancer patients have spurred excitement about the possibilities of detecting cancer early by performing ctDNA mutation detection.\n\nWe reanalyze published data on the expected ctDNA allele fraction in early-stage cancer and the population statistics of cfDNA concentration to show that under conservative technical assumptions, high-sensitivity cancer detection by ctDNA mutation detection will require either more blood volume (150-300mL) than practical for a routine screen or variant filtering that may be impossible given our knowledge of cancer evolution, and will likely remain out of economic reach for routine population screening without multiple-order-of-magnitude decreases in sequencing cost. Instead, new approaches that integrate ctDNA mutations with multiple other blood-based analytes (such as exosomes, circulating tumor cells, ctDNA epigenetics, metabolites) as well as integration of these signals over time for each individual may be needed.

cancer biology↗

Deep Convolutional Neural Networks Enable Discrimination of Heterogeneous Digital Pathology Images

Pathological evaluation of tumor tissue is pivotal for diagnosis in cancer patients and automated image analysis approaches have great potential to increase precision of diagnosis and help reduce human error.\n\nIn this study, we utilize various computational methods based on convolutional neural networks (CNN) and build a stand-alone pipeline to effectively classify different histopathology images across different types of cancer. In particular, we demonstrate the utility of our pipeline to discriminate between two subtypes of lung cancer, four biomarkers of bladder cancer, and five biomarkers of breast cancer. In addition, we apply our pipeline to discriminate among four immunohistochemistry (IHC) staining scores of bladder and breast cancers.\n\nOur classification pipeline utilizes a basic architecture of CNN, Googles Inceptions within three training strategies, and an ensemble of two state-of-the-art algorithms, Inception and ResNet. These strategies include training the last layer of Googles Inceptions, training the network from scratch, and fine-tunning the parameters for our data using two pre-trained version of Googles Inception architectures, Inception-V1 and Inception-V3.\n\nWe demonstrate the power of deep learning approaches for identifying cancer subtypes, and the robustness of Googles Inceptions even in presence of extensive tumor heterogeneity. Our pipeline on average achieved accuracies of 100%, 92%, 95%, and 69% for discrimination of various cancer types, subtypes, biomarkers, and scores, respectively. Our pipeline and related documentation is freely available at https://github.com/ih-lab/CNN_Smoothie.

bioinformatics↗