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2,884 results for “cancer resistance”
Clonal heterogeneity of endocrine therapy resistance in breast cancer
<p>We barcoded endocrine therapy sensitive cell lines (MCF7 and T47D) and rendered them resistant to commonly applied first line endocrine therapeutics (Tamoxifen and estrogen deprivation). Next, we isolated single cell clones of endocrine therapy resistant populations and subjected clonal cell lines to RNA-Seq and Phosphoproteomics profiling.</p>
The spindle assembly checkpoint is a therapeutic vulnerability of CDK4/6 inhibitor-resistant ER+ breast cancer with mitotic aberrations
<p>This study aims to investigate the accumulation of genomic instability and chromosome segregation errors after the acquisition of resistance to CDK4/6i in ER+ breast cancer and to test the efficacy of mitotic kinase inhibitors as a potential treatment for CDK4/6i-resistant breast cancer patients.</p> <p><strong>This repository contains whole-exome and shallow whole-genome sequencing from luminal breast cancer cell lines (T47D, LY2, MDA-MB-361, CAMA1, MCF7, KPL1, ZR751, HCC1428) both at the untreated or Parental state and post resistance to Palbociclib.</strong></p> <p>Palbociclib resistance was developed by continuous dose-escalation of palbociclib up to 0.5-1 μM until cell growth was observed in the presence of the drug (6-8 months for cell lines). During this time, parental cell lines and organoids were cultured in regular media to match the time spent in culture. Once resistance was established, Palbo-R cell lines were cultured in a regular growth medium without palbociclib. Cells were cultured without palbociclib for at least two weeks before evaluating resistance.</p>
FOLFOXIRI resistance induction and characterization in human colorectal cancer cells
<p>Supplementary dataset to "FOLFOXIRI resistance induction and characterization in human colorectal cancer cells"</p>
Valproic Acid Synergizes With Cisplatin and Cetuximab in vitro and in vivo in Head and Neck Cancer by Targeting the Mechanisms of Resistance - Unpublished data
<p>Antitumor effects of valproic acid (VPA) in combination with Cisplatin/Cetuximab doublet in head and neck squamous cell carcinoma (HNSCC) models. We reported unpublished data of the effects of this combination on cell cycle and 3D cell cultures</p>
Data supplement for the paper "An integrated computational strategy to predict personalized cancer drug combinations by reversing drug resistance signatures"
<p>This dataset contains the the following data created for the paper "An integrated computational strategy to predict personalized cancer drug combinations by reversing drug resistance signatures".</p> <p>Data listing:</p> <p>Cell line-specific drug resistance signatures (CDRSR)</p> <p>Patient-specific drug resistance signatures (CTR-DB)</p>
Dataset on prognostic factors in patients with metastatic castration-resistant prostate cancer undergoing radioligand therapy with [177Lu]Lu-PSMA-617
<p>This upload provides Open Data associated with the publication "Prognostic value of the De Ritis ratio for overall survival in patients with metastatic castration-resistant prostate cancer undergoing [<sup>177</sup>Lu]Lu-PSMA-617 radioligand therapy" by Gaal S <em>et al.</em> (2023).</p> <p>The upload contains the anonymized dataset of 91 patients analyzed in this publication with all variables that are required to reproduce the results.</p> <p>However, to fully comply with requirements for data anonymization, the patients' age was categorized into groups spanning 5 years each. A dataset with the age variable in exact years can be obtained from the corresponding author (julian.rogasch@charite.de) upon reasonable request.</p> <p>Besides the dataset, this upload provides a dictionary to explain all variables and their categories.</p>
A Study of Rucaparib Versus Physician's Choice of Therapy in Participants With Metastatic Castration-resistant Prostate Cancer and Homologous Recombination Gene Deficiency
ClinicalTrials.gov study NCT02975934. IPD Sharing: YES. Countries: 12. Publications: 3.
Cabazitaxel Versus the Switch to Alternative AR-targeted Agent (Enzalutamide or Abiraterone) in Metastatic Castration-resistant Prostate Cancer (mCRPC) Patients Previously Treated With Docetaxel and W
ClinicalTrials.gov study NCT02485691. IPD Sharing: YES. Countries: 13. Publications: 5.
177Lu-PSMA-617 vs. Androgen Receptor-Directed Therapy in the Treatment of Progressive Metastatic Castrate Resistant Prostate Cancer
ClinicalTrials.gov study NCT04689828. IPD Sharing: YES. Countries: 14. Publications: 2.
Alpelisib Plus Olaparib in Platinum-resistant/Refractory, High-grade Serous Ovarian Cancer, With no Germline BRCA Mutation Detected
ClinicalTrials.gov study NCT04729387. IPD Sharing: YES. Countries: 26. Publications: 1.
A Study of Rucaparib in Patients With Metastatic Castration-resistant Prostate Cancer and Homologous Recombination Gene Deficiency
ClinicalTrials.gov study NCT02952534. IPD Sharing: YES. Countries: 12. Publications: 4.
Study of 177Lu-PSMA-617 In Metastatic Castrate-Resistant Prostate Cancer
ClinicalTrials.gov study NCT03511664. IPD Sharing: YES. Countries: 10. Publications: 12.
Supplementary material: CYB561 supports the neuroendocrine phenotype in castration-resistant prostate cancer
<p>Castration-resistant prostate cancer (CRPC) is associated with resistance to androgen deprivation therapy, and an increase in the population of neuroendocrine (NE) differentiated cells. It is hypothesized that NE differentiated cells secrete neuropeptides that support androgen-independent tumor growth and induce aggressiveness of adjacent proliferating tumor cells through a paracrine mechanism. The cytochrome b561 (<em>CYB561</em>) gene, which codes for a secretory vesicle transmembrane protein, is constitutively expressed in NE cells and highly expressed in CRPC. CYB561 is involved in the α-amidation-dependent activation of neuropeptides and contributes to regulating iron metabolism which is often dysregulated in cancer. These findings led us to hypothesize that CYB561 may be a key player in the NE differentiation process that drives the progression and maintenance of the highly aggressive NE phenotype in CRPC. In our study, we found that <em>CYB561</em> expression is upregulated in metastatic and NE prostate cancer (NEPC) tumors and cell lines compared to normal prostate epithelia and that its expression is independent of androgen regulation. Knockdown of <em>CYB561</em> in androgen-deprived LNCaP cells dampened NE differentiation potential and transdifferentiation-induced increase in iron levels. In NEPC PC-3 cells, depletion of CYB561 reduced the secretion of growth-promoting factors, lowered intracellular ferrous iron concentration, and mitigated the highly aggressive nature of these cells in complementary assays for cancer hallmarks. These findings demonstrate the role of CYB561 in facilitating transdifferentiation and maintenance of NE phenotype in CRPC through its involvement in neuropeptide biosynthesis and iron metabolism pathways.</p>
Sensitization of FOLFOX-resistant colorectal cancer cells via the modulation of a novel pathway involving protein phosphatase 2A
<p>The treatment of colorectal cancer (CRC) with FOLFOX shows some efficacy, but these tumors quickly develop resistance to this treatment. We have observed an increased phosphorylation of AKT1/mTOR/4EBP1 and levels of p21 in FOLFOX-resistant CRC cells. We have identified a small molecule, NSC49L, that stimulates protein phosphatase 2A (PP2A) activity, downregulates the AKT1/mTOR/4EBP1-axis, and inhibits p21 translation. We have provided evidence that NSC49L- and TRAIL-mediated sensitization is synergistically induced in p21-knockdown CRC cells, which is reversed in p21-overexpressing cells. p21 binds with procaspase 3 and prevents activation of caspase 3. We have shown that TRAIL induces apoptosis through the activation of caspase 3 by NSC49L-mediated downregulation of p21 translation, and thereby cleavage of procaspase 3 into caspase 3. NSC49L does not affect global protein synthesis. These studies provide a mechanistic understanding of NSC49L as a PP2A agonist, and how its combination with TRAIL sensitizes FOLFOX-resistant CRC cells.</p>
Acidic Microenvironment Enhances Cisplatin Resistance in Bladder Cancer via Bcl-2 and XIAP
Open the record for dataset details and reuse information.
Data from: Aberrant FGFR signaling mediates resistance to CDK4/6 inhibitors in ER+ breast cancer
Using an ORF kinome screen in MCF-7 cells treated with the CDK4/6 inhibitor ribociclib plus fulvestrant, we identified FGFR1 as a mechanism of drug resistance. FGFR1-amplified/ER+ breast cancer cells and MCF-7 cells transduced with FGFR1 were resistant to fulvestrant ± ribociclib or palbociclib. This resistance was abrogated by treatment with the FGFR tyrosine kinase inhibitor (TKI) lucitanib. Addition of the FGFR TKI erdafitinib to palbociclib/fulvestrant induced complete responses of FGFR1-amplified/ER+ patient-derived-xenografts. Next generation sequencing of circulating tumor DNA (ctDNA) in 34 patients after progression on CDK4/6 inhibitors identified FGFR1/2 amplification or activating mutations in 14/34 (41%) post-progression specimens. Finally, ctDNA from patients enrolled in MONALEESA-2, the registration trial of ribociclib, showed that patients with FGFR1 amplification exhibited a shorter progression-free survival compared to patients with wild type FGFR1. Thus, we propose breast cancers with FGFR pathway alterations should be considered for trials using combinations of ER, CDK4/6 and FGFR antagonists.
BLM overexpression as a predictive biomarker for CHK1 inhibitor response in PARP inhibitor–resistant BRCA-mutant ovarian cancer
<p>PARP inhibitors (PARPis) have changed the treatment paradigm in BRCA-mutant high-grade serous ovarian carcinoma (HGSC). However, most patients eventually develop resistance to PARPis, highlighting an unmet need for novel therapeutic strategies. Using high-throughput drug screens, we identified ATR/CHK1 pathway inhibitors as cytotoxic, and further validated monotherapy activity of the CHK1 inhibitor (CHK1i), prexasertib, in PARPi-resistant BRCA-mutant HGSC cells and animal models. As a proof-of-concept trial, we conducted a phase II study of prexasertib in BRCA-mutant HGSC patients. The treatment was well-tolerated but yielded an objective response rate of 6% (1/17; 1 PR) in patients with prior PARPi treatment. Exploratory biomarker analyses revealed that replication stress and fork stabilization were associated with clinical benefit to CHK1i. In particular, overexpression of BLM, and CCNE1 overexpression or copy number gain/amplification were seen in patients deriving durable benefit from CHK1i. Our findings suggest replication fork–related biomarkers should be further evaluated for CHK1i sensitivity in HGSC.</p>
Search strategies for 177 lu-PSMA in the treatment of metastatic castrate-resistant prostate cancer
<p>The dataset includes the complete, reproducible search strategies for all literature databases searched during this project. The search strategies were designed to answer the following research questions:</p> <p><strong>RQ1.</strong> Does the use of radioligand therapy using <sup>177</sup>Lu-PSMA lead to improved overall survival and progression-free survival, compared with other available treatment(s) in patients with metastatic, castrate-resistant prostate cancer?</p> <p><strong>RQ2.</strong> Does the use of radioligand therapy using <sup>177</sup>Lu-PSMA lead to improved quality of life or symptom control, compared with other available treatment(s), in patients with metastatic, castrate-resistant prostate cancer?</p> <p><strong>RQ3. </strong> What is the risk of adverse events and toxicity associated with radioligand therapy using <sup>177</sup>Lu-PSMA, compared with other available treatment in patients with metastatic, castrate-resistant prostate cancer?</p>
High CD8 + / FOXP3+ Ratio is Significantly Associated with Primary Endocrine Therapy Resistance Occurrence in Locally Advanced Luminal B Her-2 Negative Breast Cancer Patients
<p>High CD8 + / FOXP3+ Ratio is Significantly Associated with Primary Endocrine Therapy Resistance Occurrence in Locally Advanced Luminal B Her-2 Negative Breast Cancer Patients</p>
Supplemental Data for "Unraveling Vulnerabilities in Endocrine Therapy-Resistant HER2+/ER+ Breast Cancer"
<p>Supplemental data files for Bahnassy et al, "Unraveling Vulnerabilities in Endocrine Therapy-Resistant HER2+/ER+ Breast Cancer"</p>
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.