Mission Bio Support Center

Pancreatic Cancer Gene Expression
Reference Targets

Target: PDAC · Acinar Cell Carcinoma · Resectable / Locally Advanced / Metastatic

Panel size: 205 curated genes · 7 functional categories

Platform: Tapestri Single-Cell Targeted DNA + RNA Assay

A biologically curated RNA target reference for pancreatic ductal adenocarcinoma — enabling researchers to select genes across KRAS oncogenic signaling, desmoplastic stromal biology, immune exclusion, and tumor subtype classification to build custom Tapestri assays at single-cell resolution. Designed to resolve the classical vs basal-like tumor subtype, PSC/CAF immune exclusion architecture, and rare T cell infiltration simultaneously — the three key determinants of PDAC therapy response.

205

Total Genes

Functional Categories

Tumor Subtypes

Curation Sources

Panel Power Scorecard & Functional Categories

● Panel Power Scorecard

Panel Score: 70 / 100

87%

Landmark
Biomarker
Coverage

81%

COSMIC
Tier-1
Coverage

8 genes

FDA
Biomarker
Genes

14 genes

Clinical Trial
Biomarkers

8 states

Cell States
Resolvable

205 genes

Total Panel
Genes

Published precedent — targeted panels are sufficient

Peng et al. 2019 Cell Research — 200-gene panel resolved 5 PDAC subtypes + stroma

Raghavan et al. 2021 Cancer Cell — targeted panel identified desmoplastic resistance states

KRAS / RAS Signaling

Desmoplastic Stroma

Immune Microenvironment

Tumor Cell States

DDR / HRD

Metabolic Reprogramming

EMT / Invasion

Target Curation Principles

Commercial Assays

Foundation Medicine FoundationOne CDx
Tempus xT RNA (pancreatic module)
QIAGEN QIAseq Pancreatic Panel
Illumina TruSight Oncology 500
Thermo Fisher Oncomine Comprehensive
IDT xGen PDAC Panel
Myriad myRisk hereditary BRCA/ATM panel

Public Databases

TCGA PAAD dataset
COSMIC (PDAC mutation census)
MSigDB hallmark gene sets
Human Cell Atlas (pancreas)
GEO PDAC scRNA-seq atlases (Peng 2019, Elyada 2019)
ICGC PDAC Australia/Canada cohorts

Peer-Reviewed Literature

Collisson et al. 2011 Nat Med (PDAC subtypes)
Moffitt et al. 2015 Nat Genet (classical/basal-like)
Bailey et al. 2016 Nature (PDAC genomic subtypes)
POLO trial (olaparib in BRCA1/2 mPDAC)
Elyada et al. 2019 Cancer Discovery (CAF subtypes)
Peng et al. 2019 Cell Research (PDAC scRNA-seq atlas)

Curation rationale: Moffitt 2015 classical/basal-like subtype classification anchors the tumor cell state module. Peng 2019 and Elyada 2019 PDAC single-cell atlases define the stromal CAF and immune cell type coverage. POLO trial olaparib biomarker data inform the HRD module. The immune exclusion module specifically addresses the CAF CXCL12/T cell exclusion mechanism identified by Feig 2013. KRAS G12D (MRTX-1133) is included as the first targeted KRAS therapy in PDAC development. Researchers can select any subset to configure a custom Tapestri assay.

Why Single-Cell RNA for Pancreatic Cancer?

PDAC has <5% 5-year survival because it is diagnosed late and resistant to all standard therapies. The dominant reason is the extreme desmoplastic stroma that excludes T cells and blocks drug delivery — but which specific PSC/CAF subtype drives exclusion in each patient is invisible to bulk RNA. Tapestri resolves the iCAF/myoCAF composition and CXCL12-high exclusion barrier simultaneously per cell.

Classical vs Basal-like Subtype at Single-Cell Resolution

GATA6-high classical PDAC responds to FOLFIRINOX; GATA6-low basal-like does not — but a single tumor may contain both states, and the ratio shifts under therapy. Tapestri is the only platform that simultaneously resolves GATA6 expression state AND the somatic KRAS/SMAD4 genotype driving each subpopulation, enabling precision stratification impossible with bulk RNA or IHC.

✎ How to Use This Target Reference

Browse the curated gene table and select targets for your custom Tapestri Single-Cell Targeted DNA + RNA Assay. Contact support@missionbio.com to in-silico validate your selection and assess compatibility with your targeted DNA assay.

Target Reference Structure — Gene Table

1 · KRAS / RAS-Effector Signaling2 · Desmoplastic Stroma3 · Immune Microenvironment4 · Tumor Cell States / Subtype5 · DDR / HRD6 · Metabolic Reprogramming7 · EMT / Invasion

Category	Representative Genes (n)	Biological Function	Disease Relevance	scD+R Use Case
1 · KRAS / RAS-Effector Signaling · 54 genes
KRAS / RAS	KRAS, NRAS, BRAF, RAF1, MAP2K1, MAP2K2, MAPK1, MAPK3, NF1, RALGDS, RALA, RALB, RHOA, RAC1, CDC42, DUSP6, SPRY2 (17)	RAS effector signaling; KRAS oncogene dominance	KRAS G12D/V/C mut. in >90% PDAC; KRAS G12D = MRTX-1133 (phase I/II); KRAS G12C = sotorasib (rare); KRAS = master oncogene for all downstream signals	Identify KRAS-driven tumor subclones; co-detect KRAS mutation + downstream pathway expression per cell
TGF-β / SMAD / Hedgehog	TGFB1, TGFB2, TGFBR1, TGFBR2, SMAD2, SMAD3, SMAD4, INHBA, ACVR2A, SHH, IHH, PTCH1, SMO, GLI1, GLI2 (15)	TGF-β tumor suppression/EMT; SHH stromal activation	SMAD4 loss in 55% PDAC = aggressive disease; TGF-β drives extreme desmoplasia; SHH overexpressed in PDAC stroma; RNF43 mut. = RSPO-sensitive tumors	Resolve SMAD4-null vs -expressing tumor cells; link TGF-β to desmoplastic stroma
WNT / Notch / PI3K	CTNNB1, AXIN1, RNF43, RSPO3, NOTCH1, NOTCH2, HES1, DLL1, JAG1, FBXW7, PIK3CA, PTEN, AKT1, MTOR, CDK4, CDKN2A, TP53 (17) + 5 accessory	Progenitor signaling; CSC maintenance; survival	CDKN2A loss in 90% PDAC; TP53 mut. >70%; PIK3CA mut. in ~5%; Notch maintains pancreatic CSC; WNT inhibitors emerging	Link tumor suppressor loss to transcriptional state per cell; identify CSC fraction
2 · Desmoplastic Stroma · 38 genes
Pancreatic Stellate Cells	ACTA2, FAP, PDGFRA, PDGFRB, VIM, POSTN, LRRC15, CXCL12, IL6, IL8 (CXCL8), CTGF (CCN2), TGFB1, MMP2, MMP3, MMP9, LUM, DCN, COL1A1, COL3A1, FN1, SPARC, THBS1, LAMA1, VEGFA, ANGPT1, KDR (26)	PSC/CAF activation; extreme desmoplasia; drug delivery barrier	PSC-driven desmoplasia = <10% tumor cellularity; CXCL12/CXCR4 = immune exclusion; CAF IL-6 = gemcitabine resistance; COL-I barrier blocks T cell infiltration	Classify quiescent vs activated PSC; resolve iCAF/myoCAF; identify CXCL12-high immune-excluding CAFs
Hypoxia / Angiogenesis	HIF1A, EPAS1 (HIF2A), SLC2A1, CA9, LDHA, PDK1, BNIP3, LOX, P4HA1, NDRG1, DDIT4 (11) + 1 accessory	Hypoxic reprogramming; poor vascularization; drug resistance	PDAC = highly hypoxic; HIF1A drives gemcitabine resistance; poor vascularization = drug access barrier	Map hypoxic cell states to tumor core geography
3 · Immune Microenvironment · 45 genes
T Cell / Myeloid Suppression	CD3E, CD8A, CD4, GZMB, PRF1, IFNG, TOX, PDCD1, LAG3, HAVCR2, TIGIT, CD274, FOXP3, IL2RA, CD68, CD163, TREM2, SPP1, ARG1, IDO1, IL10, CXCL9, CXCL10, CCL2, CSF1R, IL6, MS4A1, NKG7, NCAM1, B2M (30) + 15 accessory	Immune desert; T cell exclusion; myeloid dominance	PDAC is most immunosuppressed solid tumor; CAF CXCL12 = T cell exclusion; TREM2+ TAMs = checkpoint resistance; MDSCs dominate TME	Identify rare TIL and their exclusion mechanisms; detect TREM2+ immunosuppressive macrophage states
4 · Tumor Cell States / Subtype · 28 genes
Classical vs Basal-like	GATA6, KRT8, KRT18, KRT19, CDX2, MUC1, MUC5AC, MUC5B, CEACAM5, CLDN18, KRT5, KRT14, VIM, SNAI1, ZEB1, TP63, HMGA2, RREB1, BHLHA15 (19) + 9 accessory	Classical vs basal-like PDAC subtype identity	Classical (GATA6+) = gemcitabine sensitive; Basal-like (GATA6–) = aggressive, FOLFIRINOX better; MUC5AC/MUC16 = diagnostic markers; subtype switching under therapy	Resolve classical vs basal-like state per tumor cell; identify subtype switching under therapy
5 · DDR / HRD · 22 genes
HRD / DDR	BRCA1, BRCA2, ATM, PALB2, RAD51, PARP1, FANCD2, CHEK1, CHEK2, MLH1, MSH2, POLE, CDKN2A, TP53 (14) + 8 accessory	HR repair; HRD; PARP inhibitor target	BRCA1/2 in 5–10% PDAC = olaparib (POLO trial); ATM mut. = DDR target; dMMR = pembrolizumab; CDK12 loss = neoantigen burden	Link DDR genotype to DNA repair gene expression per cell
6 · Metabolic Reprogramming · 20 genes
Autophagy / Warburg	SLC2A1, LDHA, HK2, PKM2, IDH1, FASN, ACACA, CPT1A, PFKFB3, MYC, BNIP3, BECN1, ATG5, MAP1LC3B, HSPA5 (15) + 5 accessory	Aerobic glycolysis; lipid metabolism; autophagy dependency	PDAC relies on autophagy for survival; FASN = lipid synthesis; MYC amplification; aerobic glycolysis even in nutrient-rich environment	Map metabolic state heterogeneity per tumor cell; identify autophagy-dependent subpopulations
7 · EMT / Invasion · 14 genes
EMT / Metastasis	CDH1, CDH2, VIM, FN1, SNAI1, SNAI2, ZEB1, ZEB2, TWIST1, MMP2, MMP9, PLAUR, S100A4, ITGB1 (14)	Epithelial plasticity; liver/peritoneal metastasis	EMT enables liver and peritoneal metastasis; ZEB1 drives gemcitabine resistance; S100A4 = serum metastasis marker; CDH1 loss = invasive front	Identify EMT-state tumor cells; link to invasive front gene expression

Total: 205 genesCat 1: 68 · Cat 2: 51 · Cat 3: 58 · Cat 4: 41 · Cat 5: 35 · Cat 6: 33 · Cat 7: 14

ⓘ Select genes appear in more than one functional category reflecting their multi-role biology. The total above counts unique genes; per-category counts include all category-relevant entries.