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Project ID: MCC-001
Sample ID: MCC-001-01-1A
Submitted by: NCBI (GEO)
Country: USA
BioProject PRJNA483959
Sample name NA
SRA accession: SRP155988
SRS accession: SRS3693909
SRX accession: SRX4579480
SRR accession: SRR7722938
GEO accession: GSE117988
Cancer type: Merkel Cell Carcinoma
Cancer type abbreviation: MCC
Primary site: Skin
Tissue: Skin
Tumor grade: NA
Tumor status: Metastatic
Donor age: 59
Donor gender: Male
Treatment: Cellular immunotherapy targeting MCPyV (autologous endogenous T cell therapy) followed by checkpoint inhibitors (anti-PD1 and anti-CTLA4)
Other metadata: The patient had a 22 month clinical response followed by late/acquired resistance.
Project title: scRNAseq reveals mechanisms of Merkel cell carcinoma acquired immunotherapy resistance [1]
Project abstract: Serial blood draws from a single patient and serial tumor biopsies from the same patient with metastatic Merkel cell polyomavirus Merkel cell carcinoma, who was treated with cellular immunotherapy targeting MCPyV (autologous endogenous T cell therapy) followed by checkpoint inhibitors (anti-PD1 and anti-CTLA4). The patient had a 22 month clinical response followed by late/acquired resistance. We performed scRNAseq using the 10X Genomics 3'' Chromium expression assay to determine potential mechanisms contributing to immunotherapy response and late resistance Overall design: Serial blood draws from four time points, serial tumor biopsies from two time points - single cell digests were viably preserved, comparisons were performed on a within tissue basis, discovery patient for associated manuscript.
Construction protocol: PBMC were isolated with standard FICOLL, tumor tissues were digested in RPMI with DNAse, Collagenase, and hyaluronidase, strained and frozen. All samples were thawed on same day and immediately processed 10X Genomics Gene Expression 3' Chromium V 2.0 per manufacturer's instructions.
Protocol: 10X Genomics
Instrument: Illumina HiSeq 2500
Strategy: RNA-Seq
Layout: PAIRED
Publications: K.G. Paulson et al., Acquired cancer resistance to combination immunotherapy from transcriptional loss of class I HLA. Nature Communications, 2018, 9(1): 3868