Find research datasets worth reusing

opencc-by-4.0Sep 2024View details →

Supplemental Materials - Performance Figures for "A Model for Predicting the (re)-occurrence of a ≥40% eGFR Decline in a large Population-based cohort of Persons with or At-Risk of Chronic Kidney Disease " paper

The zip file contains performance metrics figures for each dynamic Bayesian Network (DBN) model, stratified by comorbidities, race, CKD stages, and ethnicity. Contains: <ul> <li>Stratified: Bootstrapping of 1000 iterations and 1000 samples with stratified proportions (as in the original population of the test set) of rapid eGFR decliners and non-decliners.</li> </ul>   Second zip contains DBN structures as matrices for 2 periods study entry to entry period and entry period to year 1 for all sites in 2 excel files.

opencc-by-4.0Sep 2022View details →

Data for: Identification of activating mutations in the transmembrane and extracellular domains of EGFR

The epidermal growth factor receptor (EGFR) is frequently mutated in human cancer, most notably non-small-cell lung cancer and glioblastoma. While many frequently occurring EGFR mutations are known to confer constitutive EGFR activation, the situation is less clear for rarely detected variants. In fact, more than 1000 distinct EGFR mutations are listed in the Catalogue of Somatic Mutations in Cancer (COSMIC), but for most of them, the functional consequence is unknown. To identify additional, previously unknown activating mutations in EGFR, we screened a randomly mutated EGFR library for constitutive EGFR phosphorylation using a recently developed high-throughput approach termed PhosphoFlowSeq. Enrichment of the well-known activating mutations S768I, T790M, and L858R validated the experimental approach. Importantly, we also identified the activating mutations S442I and L658Q located in the extracellular and transmembrane domains of EGFR, respectively. To the best of our knowledge, neither S442I nor L658Q has been associated with an activating phenotype before. However, both have been detected in cancer samples. Interestingly, molecular dynamics (MD) simulations suggest that the L658Q mutation located in the hydrophobic transmembrane region forms intermolecular hydrogen bonds, thereby promoting EGFR dimerization and activation. Based on these findings, we screened the COSMIC database for additional hydrophilic mutations in the EGFR transmembrane region and indeed detected moderate constitutive activation of EGFR-G652R. Together, this study demonstrates that unbiased screening for activating mutations in EGFR not only yields well-established substitutions located in the kinase domain but also activating mutations in other regions of EGFR, including the extracellular and transmembrane domains.   A. Wagner, E. Galicia-Andrés, M. Teufl, L. Gold, C. Obinger, P. Sykacek, C. Oostenbrink and M.W. Traxlmayr Identification of activating mutations in the transmembrane and extracellular domains of EGFR Biochemistry 61 (2022) 2049 – 2062 doi: <a href="https://doi.org/10.1021/acs.biochem.2c00384" target="_blank" rel="noopener">10.1021/acs.biochem.2c00384</a>

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LPCAT1 promotes cSCC development via EGFR

Cutaneous squamous cell carcinoma (cSCC) is the second most common form of skin cancer. LPCAT1, a lysophosphatidylcholine acyltransferase, takes a center stage in membrane lipid remodeling. LPCAT1 is elevated in several cancers and contributes to cancer development. However, its role and molecular mechanisms in cSCC remain to be elucidated. In this study, we found that LPCAT1 was upregulated in cSCC tissues and in cell lines. In vitro, loss-of-function and gain-of-function experiments demonstrated that LPCAT1 facilitated cSCC cell proliferation, protected cells against apoptosis, accelerated epithelial‒mesenchymal transition, and enhanced cell metastasis. Mechanistically, LPCAT1 regulated EGFR signaling. The oncogenic effect of LPCAT1 was mediated by EGFR/protein kinase B and EGFR/p38MAPK pathways in cSCC. Using the xenograft mouse model, we consolidated the results mentioned earlier. In conclusion, LPCAT1 contributed to cSCC progression through EGFR-mediated protein kinase B and p38MAPK signaling pathways. LPCAT1 may serve as a target for therapeutic intervention in cSCC. And the datasets related to this study are available in this repository.

opencc-zeroJun 2022View details →

opencc-by-4.0Jun 2022View details →

Data of FigS1, "The Potential Tumor-Suppressor DHRS7 Inversely Correlates with EGFR Expression in Prostate Cancer Cells and Tumor Samples"

Data of FigS1, “The Potential Tumor-Suppressor DHRS7 Inversely Correlates with EGFR Expression in Prostate Cancer Cells and Tumor Samples” The Dataset (original publication: doi: 10.3390/cancers14133074) contains the original figure as PNG-format (10.3390-cancers14133074_FigS1.PNG). The Corresponding raw data and subsequent data analysis obtained for TCGA analysis contains three files in csv-format (31003A-179400_10.3390-cancers14133074_SSDHRS7_23_2-1-3 .csv), three files in sps-format (31003A-179400_10.3390-cancers14133074_SSDHRS7_23_2-1-3 .sps), all further related information provided as one meta-data-file in pdf-format (31003A-179400_10.3390-cancers14133074_SSDHRS7_23_2_M1.pdf)  and one in txt-format (31003A-179400_10.3390-cancers14133074_SSDHRS7_23_2_M.txt).

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Data from: Structural variation and its potential impact on genome instability: novel discoveries in the EGFR landscape by long-read sequencing

Studies of structural variation (SV) have been challenging due to technological contraints. With the advent of third generation (long-read) sequencing technology, exploration of longer stretches of DNA not easily examined previously has been made possible. In the present study, we utilized third generation (long-read) sequencing techniques to examime SV in the EGFR landscape of four haplotypes derived from two human samples. We analyzed the EGFR gene and its landscape (+/- 500,000 base pairs) using this sequencing approach and were able to identify regions of non-coding DNA which had relatively high similarity to the most common activating EGFR mutation in non-small cell lung cancer. We discovered that reverse complements to the exon 19 deletion mutation which had at least 60% homology to the EGFR exon 19 canonical deletion and were within ± 421,000 bp of the deletion varied across the five haploid genomes examined (4 patient landscapes and hg38). Although the sample size is limited in this study, the estimated variation observed in genomic stability between the five EGFR haplotypes examined is novel and encourages further work to examine structural variation in larger cohorts.

opencc-zeroAug 2021View details →

opencc-by-4.0Feb 2023View details →

Single-cell heterogeneity of EGFR and CKD4 co-amplification is linked to immune infiltration in glioblastoma

This upload contains RDS objects of preprocessed publicly available scRNAseq data, required to run scRNAseq analyses in the manuscript "Single cell heterogeneity of EGFR and CDK4 co-amplification is linked to immune infiltration in glioblastoma". The corresponding GitHub repo <a href="https://github.com/Michorlab/GBM_OR_immune">https://github.com/Michorlab/GBM_OR_immune</a> contains code to analyze the data here, as well as plots and tables generated on the basis of this data.

Phase I EGFR BATs in Newly Diagnosed Glioblastoma

ClinicalTrials.gov study NCT03344250. IPD Sharing: NO. Countries: 1. Publications: 3.

A Study to Investigate the Efficacy and Safety of Dato-DXd With or Without Osimertinib Compared With Platinum Based Doublet Chemotherapy in Participants With EGFR-Mutated Locally Advanced or Metastati

ClinicalTrials.gov study NCT06417814. IPD Sharing: YES. Countries: 27. Publications: 1.

To Evaluate the Efficacy/Safety of Osimertinib Prior to CRT and Maintenance of it With Stage III, Unresectable NSCLC With EGFR Mutations

ClinicalTrials.gov study NCT06194448. IPD Sharing: YES. Countries: 9. Publications: 1.

Frequency of EGFR Mutations in Latinos/Hispanics With Non-Small Cell Lung Cancer

ClinicalTrials.gov study NCT01255150. IPD Sharing: Not stated. Countries: 5. Publications: 3.

A Study of BL-B01D1 and Almonertinib in Patients With Resectable EGFR+ Stage II-IIIB NSCLC

ClinicalTrials.gov study NCT06951464. IPD Sharing: YES. Countries: 1. Publications: 1.

In Vivo EGFR Molecular Classification and Treatment Response

ClinicalTrials.gov study NCT02717221. IPD Sharing: UNDECIDED. Countries: 1. Publications: 9.

Aprepitant vs. Desloratadine in EGFR-TKIs Related Pruritus Treatment

ClinicalTrials.gov study NCT02646020. IPD Sharing: NO. Countries: 1. Publications: 24.

Anti-EGFR Immunoliposomes in Solid Tumors

ClinicalTrials.gov study NCT01702129. IPD Sharing: Not stated. Countries: 1. Publications: 3.

A Study to Evaluate the Safety and Efficacy of A2B395, an Allogeneic Logic-gated CAR T, in Participants With Solid Tumors That Express EGFR and Have Lost HLA-A*02 Expression

ClinicalTrials.gov study NCT06682793. IPD Sharing: YES. Countries: 1. Publications: 5.

Effects of a Visual Interactive LINE Chatbot on Self-Management of EGFR-TKI Related Side Effects in Patients With Lung Cancer

ClinicalTrials.gov study NCT07310589. IPD Sharing: YES. Countries: 0. Publications: 4.

A Study of Tarceva vs. Avastin+Tarceva for Advanced NSCLC With EGFR m(+)

ClinicalTrials.gov study NCT03126799. IPD Sharing: NO. Countries: 1. Publications: 1.

Comparison of Biomarker Modulation by Inhibition of EGFR and/or SRC Family

ClinicalTrials.gov study NCT00779389. IPD Sharing: Not stated. Countries: 1. Publications: 3.

Almonertinib as First-line Treatment in Patients With EGFR Mutations Positive in Advanced NSCLC With Brain Metastases

ClinicalTrials.gov study NCT04808752. IPD Sharing: NO. Countries: 1. Publications: 1.

Pemetrexed Plus Tarceva as Salvage Treatment in EGFR Overexpressed Metastatic Colorectal Cancer Patients Who Were Failed After Standard Chemotherapy

ClinicalTrials.gov study NCT03086538. IPD Sharing: Not stated. Countries: 1. Publications: 1.