14 samples were processed for single cell DNA sequencing
Captured single-cell long-read data of a cohort of CLL patients receiving VEN treatment for resistance study
Single-cell Long read data of a cohort of CLL patients receiving Venetoclax treatment for VEN resistance study.
Raw FASTQ files for 77 RS + DLBCL + CLL samples. RNA-sequencing with single-end 50 nt reads.
Consists of 88 cases
Clinical data for IMpower150 (one patient per line): anonymized_patient_id, train_test_split, ctDNA_status, ARM1, OS_months, OS_event, PFS_months, PFS_event, TTEOS_rebaseline_BL, TTEPFS_rebaseline_BL, TTEOS_rebaseline_C2D1, TTEPFS_rebaseline_C2D1, TTEOS_rebaseline_C3D1, TTEPFS_rebaseline_C3D1, TTEOS_rebaseline_C4D1, TTEPFS_rebaseline_C4D1, TTEOS_rebaseline_C8D1, TTEPFS_rebaseline_C8D1, pdl1_high, number_metastatic_sites, baseline_ECOG, age, sex_female, history_of_tobacco_use, sld_baseline, sld_wk6, sld_percent_change_bl_to_wk6, sld_difference_bl_to_wk6, AGEGRP, tumor_assessment_week_6, tumor_assessment_week_12, tumor_assessment_week_18, tumor_assessment_week_24, PFS_days, days_between_randomization_c3
ZPM WES Pilot consisting of 30 samples paired tumor/normal analyzed with WES at four different laboratories in Germany.
Tissue-specific driver mutations in non-coding genomic regions remain undefined for most cancer types. In this study, we unbiasedly analysed 212 gastric cancer whole genomes to identify recurrently mutated non-coding regions in gastric cancer. Applying comprehensive statistical approa- ches to accurately model background mutational processes, we observe significant enrich- ment of non-coding indels (insertions/deletions) in three gastric lineage-specific genes. We further identify 34 mutation hotspots, of which 11 overlap CTCF binding sites (CBSs).
RNA sequencing data for 170 medulloblastoma tumor samples
We performed single-cell RNA-sequencing of 18,403 cells unbiasedly collected from 7 treatment-naive HGSOC tumours. For each phenotypic cluster of tumour or stromal cells, we identified specific transcriptomic markers. Next, we explored which phenotypic clusters correlate with overall survival based on expression of these transcriptomic markers in 1467 bulk RNA-seq tumours. By evaluating molecular subtype signatures in single cells, we assessed to what extent a phenotypic cluster of tumour or stromal cells contributes to each molecular subtype.