Browse
Submit Data
Databases
API
Help

Dataset Information

6 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The Cancer Drug Fraction of Metabolism Database.

ABSTRACT: This study aims to create a database for quantifying the fraction of metabolism of cytochrome P450 isozymes for cancer drugs approved by the US Food and Drug Administration. A reproducible data collection protocol was developed to extract essential information, including both substrate-depletion and metabolite-formation data from publicly available in vitro selective cytochrome P450 enzyme inhibition studies. We estimated the fraction of metabolism from the curated data. To demonstrate the utility of this database, we conducted an in vitro drug interaction prediction for the 42 cancer drugs. In the drug-drug interaction prediction, we identified 31 drug pairs with at least one cancer drug in each pair that had predicted area under concentration ratios > 2. We further found clinical drug interaction pieces of evidence in the literature to support 20 of these 31 drug-drug interaction pairs.

SUBMITTER: Hua L

PROVIDER: S-EPMC6656935 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Similar Datasets

DDIEM: drug database for inborn errors of metabolism.

Project description:BackgroundInborn errors of metabolism (IEM) represent a subclass of rare inherited diseases caused by a wide range of defects in metabolic enzymes or their regulation. Of over a thousand characterized IEMs, only about half are understood at the molecular level, and overall the development of treatment and management strategies has proved challenging. An overview of the changing landscape of therapeutic approaches is helpful in assessing strategic patterns in the approach to therapy, but the information is scattered throughout the literature and public data resources.ResultsWe gathered data on therapeutic strategies for 300 diseases into the Drug Database for Inborn Errors of Metabolism (DDIEM). Therapeutic approaches, including both successful and ineffective treatments, were manually classified by their mechanisms of action using a new ontology.ConclusionsWe present a manually curated, ontologically formalized knowledgebase of drugs, therapeutic procedures, and mitigated phenotypes. DDIEM is freely available through a web interface and for download at http://ddiem.phenomebrowser.net.

| S-EPMC7291537 | biostudies-literature

CancerDR: cancer drug resistance database.

Project description:Cancer therapies are limited by the development of drug resistance, and mutations in drug targets is one of the main reasons for developing acquired resistance. The adequate knowledge of these mutations in drug targets would help to design effective personalized therapies. Keeping this in mind, we have developed a database "CancerDR", which provides information of 148 anti-cancer drugs, and their pharmacological profiling across 952 cancer cell lines. CancerDR provides comprehensive information about each drug target that includes; (i) sequence of natural variants, (ii) mutations, (iii) tertiary structure, and (iv) alignment profile of mutants/variants. A number of web-based tools have been integrated in CancerDR. This database will be very useful for identification of genetic alterations in genes encoding drug targets, and in turn the residues responsible for drug resistance. CancerDR allows user to identify promiscuous drug molecules that can kill wide range of cancer cells. CancerDR is freely accessible at http://crdd.osdd.net/raghava/cancerdr/

| S-EPMC3595698 | biostudies-literature

Anticancer drug clustering in lung cancer based on gene expression profiles and sensitivity database

Project description:Anticancer drug clustering in lung cancer based on gene expression profiles. We performed gene expression analysis in lung cancer cell lines. (used: Affymetrix GeneChip Human Genome U133 Array Set HG-U133A). We also examines the sensitivity of these cell lines to commonly used anti-cancer agents (docetaxel, paclitaxel, gemcitabine, vinorelbine, 5-FU, SN38, cisplatin, and carboplatin) via MTT assay. We related the cytoxic activity of each of these agents to corresponding expression pattern in each of the cell lines using modified NCI program. Keywords: cytotoxicity, lung cancer, anticancer drugs

2006-02-10 | GSE4127 | GEO

Sphingolipid metabolism and drug resistance in ovarian cancer.

Project description:Despite progress in understanding molecular aberrations that contribute to the development and progression of ovarian cancer, virtually all patients succumb to drug resistant disease at relapse. Emerging data implicate bioactive sphingolipids and regulation of sphingolipid metabolism as components of response to chemotherapy or development of resistance. Increases in cytosolic ceramide induce apoptosis in response to therapy with multiple classes of chemotherapeutic agents. Aberrations in sphingolipid metabolism that accelerate the catabolism of ceramide or that prevent the production and accumulation of ceramide contribute to resistance to standard of care platinum- and taxane-based agents. The aim of this review is to highlight current literature and research investigating the influence of the sphingolipids and enzymes that comprise the sphingosine-1-phosphate pathway on the progression of ovarian cancer. The focus of the review is on the utility of sphingolipid-centric therapeutics as a mechanism to circumvent drug resistance in this tumor type.

| S-EPMC6936734 | biostudies-literature

Human microbiome signatures of differential colorectal cancer drug metabolism.

Project description:It is well appreciated that microbial metabolism of drugs can influence treatment efficacy. Microbial β-glucuronidases in the gut can reactivate the excreted, inactive metabolite of irinotecan, a first-line chemotherapeutic for metastatic colorectal cancer. Reactivation causes adverse drug responses, including severe diarrhea. However, a direct connection between irinotecan metabolism and the composition of an individual's gut microbiota has not previously been made. Here, we report quantitative evidence of inter-individual variability in microbiome metabolism of the inactive metabolite of irinotecan to its active form. We identify a high turnover microbiota metabotype with potentially elevated risk for irinotecan-dependent adverse drug responses. We link the high turnover metabotype to unreported microbial β-glucuronidases; inhibiting these enzymes may decrease irinotecan-dependent adverse drug responses in targeted subsets of patients. In total, this study reveals metagenomic mining of the microbiome, combined with metabolomics, as a non-invasive approach to develop biomarkers for colorectal cancer treatment outcomes.

| S-EPMC5665930 | biostudies-literature

The Role of Sphingolipids Metabolism in Cancer Drug Resistance.

Project description:Drug resistance continues to be one of the major challenges to cure cancer. As research in this field evolves, it has been proposed that numerous bioactive molecules might be involved in the resistance of cancer cells to certain chemotherapeutics. One well-known group of lipids that play a major role in drug resistance are the sphingolipids. Sphingolipids are essential components of the lipid raft domains of the plasma membrane and this structural function is important for apoptosis and/or cell proliferation. Dysregulation of sphingolipids, including ceramide, sphingomyelin or sphingosine 1-phosphate, has been linked to drug resistance in different types of cancer, including breast, melanoma or colon cancer. Sphingolipid metabolism is complex, involving several lipid catabolism with the participation of key enzymes such as glucosylceramide synthase (GCS) and sphingosine kinase 1 (SPHK1). With an overview of the latest available data on this topic and its implications in cancer therapy, this review focuses on the main enzymes implicated in sphingolipids metabolism and their intermediate metabolites involved in cancer drug resistance.

| S-EPMC8733468 | biostudies-literature

HNCDB: An Integrated Gene and Drug Database for Head and Neck Cancer.

Project description:Head and neck cancer (HNC) is the sixth most common cancer worldwide. Over the last decade, an enormous amount of well-annotated gene and drug data has accumulated for HNC. However, a comprehensive repository is not yet available. Here, we constructed the Head and Neck Cancer Database (HNCDB: http://hncdb.cancerbio.info) using text mining followed by manual curation of the literature to collect reliable information on the HNC-related genes and drugs. The high-throughput gene expression data for HNC were also integrated into HNCDB. HNCDB includes the following three separate but closely related components: "HNC GENE," "Connectivity Map," and "ANALYSIS." The "HNC GENE" component contains comprehensive information for the 1,173 HNC-related genes manually curated from 2,564 publications. The "Connectivity Map" includes information on the potential connections between the 176 drugs manually curated from 2,032 publications and the 1,173 HNC-related genes. The "ANALYSIS" component allows users to conduct correlation, differential expression, and survival analyses in the 2,403 samples from 78 HNC gene expression datasets. Taken together, we believe that HNCDB will be of significant benefit for the HNC community and promote further advances for precision medicine research on HNC.

| S-EPMC6527845 | biostudies-literature

Tuberculosis drug resistance mutation database.

Project description: Not available

| S-EPMC2637921 | biostudies-literature

Perturbations of cancer cell metabolism by the antidiabetic drug canagliflozin.

Project description:Notwithstanding that high rates of glucose uptake and glycolysis are common in neoplasia, pharmacological efforts to inhibit glucose utilization for cancer treatment have not been successful. Recent evidence suggests that in addition to classical glucose transporters, sodium-glucose transporters (SGLTs) are expressed by cancers. We therefore investigated the possibility that SGLT inhibitors, which are used in treatment of type 2 diabetes, may exert antineoplastic activity by limiting glucose uptake. We show that the SGLT2 inhibitor canagliflozin inhibits proliferation of breast cancer cells. Surprisingly, the antiproliferative effects of canagliflozin are not affected by glucose availability nor by the level of expression of SGLT2. Canagliflozin reduces oxygen consumption and glutamine metabolism through the citric acid cycle. The antiproliferative effects of canagliflozin are linked to inhibition of glutamine metabolism that fuels respiration, which represents a previously unanticipated mechanism of its potential antineoplastic action.

| S-EPMC8027095 | biostudies-literature

Lipid metabolism analysis in esophageal cancer and associated drug discovery.

Project description:Esophageal cancer is an upper gastrointestinal malignancy with a bleak prognosis. It is still being explored in depth due to its complex molecular mechanisms of occurrence and development. Lipids play a crucial role in cells by participating in energy supply, biofilm formation, and signal transduction processes, and lipid metabolic reprogramming also constitutes a significant characteristic of malignant tumors. More and more studies have found esophageal cancer has obvious lipid metabolism abnormalities throughout its beginning, progress, and treatment resistance. The inhibition of tumor growth and the enhancement of antitumor therapy efficacy can be achieved through the regulation of lipid metabolism. Therefore, we reviewed and analyzed the research results and latest findings for lipid metabolism and associated analysis techniques in esophageal cancer, and comprehensively proved the value of lipid metabolic reprogramming in the evolution and treatment resistance of esophageal cancer, as well as its significance in exploring potential therapeutic targets and biomarkers.

| S-EPMC10859535 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data