A global network of biomedical relationships derived from text

This repository contains labeled, weighted networks of chemical-gene, gene-gene, gene-disease, and chemical-disease relationships based on single sentences in PubMed abstracts. All raw dependency paths are provided in addition to the labeled relationships. PART I: Connects dependency paths to labels, or "themes". Each record contains a dependency path followed by its score for each theme, and indicators of whether or not the path is part of the flagship path set for each theme (meaning that it was manually reviewed and determined to reflect that theme). The themes themselves are listed below and are in our paper (reference below). PART II: Connects sentences to dependency paths. It consists of sentences and associated metadata, entity pairs found in the sentences, and dependency paths connecting those entity pairs. Each record contains the following information: PubMed ID Sentence number (0 = title) First entity name, formatted First entity name, location (characters from start of abstract) Second entity name, formatted Second entity name, location First entity name, raw string Second entity name, raw string First entity name, database ID(s) Second entity name, database ID(s) First entity type (Chemical, Gene, Disease) Second entity type (Chemical, Gene, Disease) Dependency path Sentence, tokenized The "with-themes.txt" files only contain dependency paths with corresponding theme assignments from Part I. The plain ".txt" files contain all dependency paths. This release contains the annotated network for the September 15, 2017 version of PubTator . The version discussed in our paper, below, is an older one - from April 30, 2016. If you're interested in that network, it can be found in Version 1 of this repository. We will be releasing updated networks periodically, as the PubTator community continues to release new versions of named entity annotations for Medline each month or so. ------------------------------------------------------------------------------------ REFERENCES Percha B, Altman RBA (2017) A global network of biomedical relationships derived from text. (Submitted to Bioinformatics ; currently in revision.) Percha B, Altman RBA (2015) Learning the structure of biomedical relationships from unstructured text. PLoS Computational Biology, 11(7): e1004216. This project depends on named entity annotations from the PubTator project: https://www.ncbi.nlm.nih.gov/CBBresearch/Lu/Demo/PubTator/ Reference: Wei CH et. al., PubTator: a Web-based text mining tool for assisting Biocuration, Nucleic acids research, 2013, 41 (W1): W518-W522. doi: 10.1093/nar/gkt44 Dependency parsing was provided by the Stanford CoreNLP toolkit: https://stanfordnlp.github.io/CoreNLP/index.html Reference: Manning, Christopher D., Mihai Surdeanu, John Bauer, Jenny Finkel, Steven J. Bethard, and David McClosky. 2014. The Stanford CoreNLP Natural Language Processing Toolkit In Proceedings of the 52nd Annual Meeting of the Association for Computational Linguistics: System Demonstrations, pp. 55-60. ------------------------------------------------------------------------------------ THEMES chemical-gene (A+) agonism, activation (A-) antagonism, blocking (B) binding, ligand (esp. receptors) (E+) increases expression/production (E-) decreases expression/production (E) affects expression/production (neutral) (N) inhibits gene-chemical (O) transport, channels (K) metabolism, pharmacokinetics (Z) enzyme activity chemical-disease (T) treatment/therapy (including investigatory) (C) inhibits cell growth (esp. cancers) (Sa) side effect/adverse event (Pr) prevents, suppresses (Pa) alleviates, reduces (J) role in disease pathogenesis disease-chemical (Mp) biomarkers (of disease progression) gene-disease (U) causal mutations (Ud) mutations affecting disease course (D) drug targets (J) role in pathogenesis (Te) possible therapeutic effect (Y) polymorphisms alter risk (G) promotes progression disease-gene (Md) biomarkers (diagnostic) (X) overexpression in disease (L) improper regulation linked to disease gene-gene (B) binding, ligand (esp. receptors) (W) enhances response (V+) activates, stimulates (E+) increases expression/production (E) affects expression/production (neutral) (I) signaling pathway (H) same protein or complex (Rg) regulation (Q) production by cell population