Prognostic biomarkers for pancreatic ductal adenocarcinoma: A contemporary systematic review and modelling study

Table 1 Population, intervention, comparison, outcome, and study design framework for study eligibility

Criteria	Review stage	Inclusion	Exclusion
Study design	Abstract/full article review	Original human studies evaluating the prognostic significance of tumor-derived transcriptomic and/or proteomic biomarkers in PDAC. Eligible designs include prospective or retrospective cohort studies, nested biomarker studies, translational correlative studies embedded within clinical trials, and secondary analyses of publicly available human molecular datasets (e.g., TCGA, ICGC, CPTAC). Eligible only if the study demonstrated an independent prognostic biomarker, i.e. the tumor transcriptomic/proteomic biomarker remained significantly associated with the survival outcome in an adjusted multivariable time-to-event model including clinicopathological covariates	In vitro studies, cell line studies, animal studies, narrative reviews, systematic reviews, meta-analyses, editorials, letters, commentaries, protocols, case reports, case series with insufficient outcome data, and conference abstracts without full-text data
Population	Abstract/full article review	Adults (≥ 18 years) with histologically confirmed PDAC, including resectable, locally advanced unresectable, and metastatic disease, provided that survival or other prognostic outcome data were available	Studies focused exclusively on non-PDAC malignancies, including pancreatic neuroendocrine neoplasms, periampullary cancers, ampullary cancers, cholangiocarcinoma, acinar cell carcinoma, or mixed pancreatic tumor populations where PDAC-specific results cannot be disaggregated
Treatment/intervention	Abstract/full article review	Tumor molecular profiling using transcriptomic or proteomic methods, including RNA sequencing, gene expression microarrays, qPCR-based tumor expression profiling, mass spectrometry-based proteomics, RPPA, or molecular signatures derived from transcriptomic/proteomic datasets	Studies based solely on clinical variables, histopathology without molecular profiling, circulating biomarkers only, imaging biomarkers only, radiomics without molecular tumor data, genomic/DNA-only biomarkers without transcriptomic or proteomic readout, or studies lacking explicit biomarker assessment
Comparator	Abstract/full article review	Comparisons across biomarker-defined strata, such as high vs low expression, biomarker-positive vs biomarker-negative status, molecular subtype classification, or low- vs high-risk prognostic groups derived from transcriptomic/proteomic signatures	Studies with no biomarker-based stratification or no analysable comparison across molecular groups
Outcomes	Abstract/full article review	Primary outcome: OS. Secondary outcomes: PFS, DFS, RFS, CSS, PFI, and other clinically relevant time-to-event prognostic outcomes	Studies not reporting survival, recurrence, or other prognostic time-to-event outcomes; studies reporting only treatment response without survival correlation
Biomarker modality and sample type	Abstract/full article review	Eligible only if the biomarker was a transcriptomic (RNA) or proteomic readout measured in PDAC tumor tissue (resection specimen, biopsy, or FFPE/fresh-frozen archival tissue), including tumor tissue profiled by RNA-seq, microarray, qPCR, NanoString, mass spectrometry, RPPA, or IHC-validated protein expression where the protein readout was the tested prognostic marker. Multimodal studies are eligible if tumor transcriptomic/proteomic results are reported separately and can be disaggregated	Not eligible: (1) Liquid biopsy/circulating analytes as the sole readout (ctDNA, cfDNA, CTCs, circulating or exosomal miRNA/mRNA, plasma or serum proteomics, CA19-9 and other serum markers); (2) Histopathology alone (grade, stage, margin status, lymphovascular or perineural invasion, tumor budding, stroma scoring) without a molecular readout; (3) Genomic/DNA-only markers (KRAS, TP53, SMAD4, or CDKN2A mutations; copy number; methylation; TMB; MSI) with no transcript- or protein-level measurement; (4) Imaging/radiomics markers; and (5) Germline variants. These modalities were recorded at screening but excluded from data extraction unless accompanied by a tumor transcriptomic or proteomic result

PDAC: Pancreatic ductal adenocarcinoma; TCGA: The Cancer Genome Atlas; ICGC: International Cancer Genome Consortium; CPTAC: Clinical Proteomic Tumor Analysis Consortium; RPPA: Reverse-phase protein array; qPCR: Quantitative polymerase chain reaction; OS: Overall survival; PFS: Progression-free survival; RFS: Recurrence-free survival; DFS: Disease-free survival; CSS: Cancer-specific survival; PFI: Progression-free interval; FFPE: Formalin-fixed paraffin-embedded; RNA-seq: RNA sequencing; IHC: Immunohistochemistry; ctDNA: Circulating tumor DNA; cfDNA: Cell-free DNA; miRNA: MicroRNA; mRNA: Messenger RNA; CTC: Circulating tumor cell; CA19-9: Carbohydrate antigen 19-9; MSI: Microsatellite instability; TMB: Tumor mutational burden.

Table 2 Prognostic strength of biomarkers in pancreatic ductal adenocarcinoma (57 biomarker studies; 14 interventional trials are presented separately in Table 3)

Biomarker	Type	Outcome	Multivariable analysis	Independent prognostic association	Validation	Internal descriptive category	Ref.
UFM1	Single protein	OS/PFS	Yes	Yes	Limited	B	Wang et al[14]
9-gene signature	Multi-gene	OS	Yes	Yes	External	A-	Wang et al[15]
3-gene MRS	Multi-gene	OS	Yes	Yes	External	A	Li et al[16]
LMRGS	Multi-gene ML	OS	Yes	Yes	Multi-cohort	A	Ge et al[17]
PCLM-BM signature	Multi-gene	OS	Yes	Yes	External	A-	Zhou et al[18]
MCMBP	Single gene	OS	Yes	Yes	External	A	Zhang et al[19]
APOBEC score	Genomic	OS	Yes	Yes	External	A	Yu et al[20]
JUP	Single gene	OS	Yes	Likely	Limited	B	Yang et al[21]
Manganese metabolism signature	Multi-gene	OS	Yes	Yes	External	A	Xiong et al[22]
ALDH family	Multi-gene	OS	Yes	Likely	Limited	B	Wu et al[23]
EFFscore/P2RY6	Multi-gene	OS	Yes	Yes	External	A	Wang et al[24]
mCAF signature	Multi-gene	OS	Yes	Yes	Multi-cohort	A	Wang et al[25]
18-gene immune signature	Multi-gene	OS	Yes	Yes	External	A	Wang et al[26]
PCD signature	Multi-gene	OS	Yes	Yes	Multi-cohort	A	Wang et al[27]
ICD signature (AJM1)	Multi-gene	OS	Yes	Yes	External	A	Ma et al[28]
MDRG/CITED4	Multi-gene	OS	Yes	Likely	Limited	B	Liu et al[29]
IGFBP signature	Multi-gene	OS	Yes	Yes	External	A	Guan et al[30]
A2ML1 subtype model	Multi-gene	OS	Yes	Yes	Multi-cohort	A	Ge et al[31]
BM-related signature (LAMA3/ITGA3/ITGB6)	Multi-gene	OS	Yes	Yes	External	A	Ge et al[32]
ER stress-related TF signature	Multi-gene	OS	Yes	Yes	External	A	Gao et al[33]
PLAAT2	Single gene	OS	Yes	Yes	External	A	Chen et al[34]
LY6D (stem-like, gastric-like cell-state marker)	Single gene	OS	Yes	Yes	Limited	B	Shi et al[35]
Disulfidptosis-related gene signature; key genes: RPN1, PML; Model genes: NDUFA11, MYH14, TRIP6, ACTN1, ANP32E, PML, CD2AP, RPN1	Multi-gene signature	OS	Yes	Yes	External	A-	Pei et al[36]
Palmitoylation-related gene signature (7 genes: DCBLD2, CXCL5, ASPH, LAMC2, KRT6A, TOP2A, NPNT); Upstream regulators: ZDHHC family (palmitoyl transferases)	Multi-gene signature	OS	Yes	Yes	External	A-	Lu et al[37]
7-gene SASP prognostic signature: ANGPTL4, DKK1, EREG, IGFBP3, IL18, MMP13, PLAU; Plus SASP molecular subtypes	Multi-gene signature	OS	Yes	Yes	Multi-cohort	A	Kuang et al[38]
SEMA3 family genes; 9-gene prognostic signature derived from SEMA3-related DEGs; key driver: SEMA3C	Multi-gene signature	OS	Yes	Yes	External	A-	Jin et al[39]
Six-gene mitophagy-related signature (PAPPA, NBPF12, CXCL11, CKLF-CMTM1, CCDC6, AHNAK)	Multi-gene signature	OS	Yes	Yes	Multi-cohort	A	Cai et al[40]
Six ICD-associated lncRNA prognostic signature: ZEB2-AS1, AC099792.1, LINC01091, LINC02613, AC005304.3, LINC00705	Multi-gene signature	OS	Yes	Yes	External	A-	Zhu et al[41]
11-gene ITH-related prognostic signature	Multi-gene signature	OS	Yes	Yes	Multi-cohort	A	Zhao et al[42]
Ferroptosis-related 3-gene signature (NOTCH2, KRT18, H1-2); key single biomarker: NOTCH2	Multi-gene signature	OS	Yes	Yes	Multi-cohort	A	Zhang et al[43]
16-gene DNA damage and repair-related prognostic risk score model; key experimental gene: LY6D	Multi-gene signature	OS	Yes	Yes	Multi-cohort	A	Zhang et al[44]
STING signalling pathway-derived 6-gene prognostic signature: DTX4, IFI16, MAVS, PRKDC, ZDHHC1, IFIT2	Multi-gene signature	OS	Yes	Yes	External	A	Yu et al[45]
SERPINE1	Single gene	OS	Yes	Yes	External	A	Wang et al[46]
KRAS protein level, KRAS mRNA expression, KRAS mutation status/subtype	Single gene	OS	Yes	Yes	Limited	B	Stålberg et al[47]
RAD51AP1 (DNA repair-associated protein)	Single gene	OS	Yes	Yes	External	A-	Rezagholizadeh et al[48]
Mitochondrial 12-gene prognostic signature; mechanistic emphasis on CAMK2A and THEM4	Multi-gene signature	OS	Yes	Yes	Multi-cohort	A	Nie et al[49]
Innate immune barrier gene signature (84 genes); key genes: UBASH3B, ITGB6, COL17A1, MMP28, DIAPH3 (focus on UBASH3B)	Multi-gene signature	OS	Yes	Yes	Multi-cohort	A	Luo et al[50]
P4HA1, CCDC148, UCA1, TMPRSS11E + tumour stage	Multi-gene signature	OS	Yes	Yes	Multi-cohort	A	Lin et al[51]
KRAS mutational status as key biomarker; integrated molecular classifier of KRAS wild-type vs KRAS-mutant classical vs KRAS-mutant basal-like; exploratory HRD and other somatic mutations	Multi-gene signature	OS	Yes	Yes	Internal	B+	Lansbergen et al[52]
PAUF (ZG16B-related protein product)	Single gene	OS	Yes	Yes	Limited	B	Kim et al[53]
Six BA-related prognostic genes: SERPINB5, CALU, TFRC, LY6D, SFRP1, GBP2	Multi-gene signature	OS	Yes	Yes	External	A-	Kang et al[54]
TIPARP (PARP7) expression	Single gene	OS	Yes	Yes	Limited	B	Jiang et al[55]
Microenvironmental, stromal, and immune markers, including MFAP4, EGR3, KRT8, monocyte infiltration, CD68+ macrophages, CD3/CD4/CD8 T-cell infiltration	Multi-gene signature	OS	Yes	Yes	Limited	B	Han et al[56]
Hypoxia score; 13-gene signature (including LYZ, PLAU, INSIG2, and KRTCAP2)	Multi-gene signature	OS/PFS	Yes	Yes	External	A	Ge et al[57]
CSCLPI genes (SHCBP1, CEP55, GMNN, CDCA5, FAM111B)	Multi-gene signature	OS	Yes	Yes	Limited	B	Fang et al[58]
23 ISGS-based features in risk score model	Multi-gene signature	OS	Yes	Yes	External	A	Fang et al[59]
Cuproptosis-related lncRNA prognostic model; key lncRNAs: LINC00900 and AC078820.1	Multi-gene signature	OS	Yes	Yes	Partial	B+	Duo et al[60]
ST3GAL2, SLCO1B3, PTGES, PRKACA	Multi-gene signature	OS/PFS	Yes	Yes	External	A-	Deng et al[61]
DCBLD2, OCIAD2, SAMD9	Multi-gene signature	OS	Yes	Yes	External	A	Cui et al[62]
Disulfidptosis-related prognostic signature (8-gene signature: SLC3A2, HMGA1, S100A2, DUSP5, SPRR1B, MET, CREB5, MACROD2)	Multi-gene signature	OS	Yes	Yes	Multi-cohort	A	Cui et al[63]
M2 macrophage-related 6-gene prognostic signature: CCL2, CD9, FBP1, LIMS1, LYZ, TGFBI; M2/TAM biology and TNFRSF12A also highlighted	Multi-gene signature	OS	Yes	Yes	Partial	B+	Chen et al[64]
20-protein diagnostic panel; 4 proteomic prognostic subtypes; 18-protein prognostic risk score (PURB, SDCBP2, CD2BP2, GALM, SERPINA3, OAS3, FAN1, ZPR1, KRT2, NUDT2, SMNDC1, SERPINA4, CUTA, WDR36, POSTN, CLEC11A, PEX14, PI4KA)	Multi-protein signature	OS	Yes	Yes	External	A	Aref et al[65]
Complement pathway genes (C1R, C1S, C3, C4B, C7) in tumour microenvironment	Multi-gene signature	OS	Yes	Yes	Partial	B+	Zhang et al[66]
13-gene autophagy-related signature (EIF4EBP1, HDAC6, GABARAP, CASP4, ATG16 L2, BCL2 L1, BAG3, ATG4B, TNFSF10, PTK6, ITGA3, BIRC5, BAK1)	Multi-gene signature	OS	Yes	Yes	External	A-	Wang et al[67]
Fibroblast-related 14-gene prognostic signature	Multi-gene signature	OS	Yes	Yes	Multi-cohort	A	Wang et al[68]
ANP32E	Single gene	OS	Yes	Yes	External	A-	Liu et al[69]
Cuproptosis-related signature score (MIR3677, AC068620.2, UPK2, LDHAP7, FAM83A)	Multi-gene signature	OS	Yes	Yes	External	A-	Ge et al[70]

The categories below were developed by the authors for this review. Categories were defined as follows: A+: Multivariable significance with robust external validation across multiple independent cohorts and prospective validation; no included study met these criteria, and the category was therefore unawarded. A: Multivariable significance with external validation in more than 1 independent cohort, or in a single independent cohort with no recorded limitations. A-: Multivariable significance with external validation in a single independent cohort where limitations were recorded (e.g., dataset overlap, limited cohort diversity, or methodological concerns). B+: Moderate evidence; multivariable significance with internal validation or partial external validation. B: Multivariable significance without adequate validation. Studies without a statistically significant multivariable result are shown as not applicable because every category presupposes a significant result. MRS: Mitochondrial unfolded protein response-related gene risk score; LMRGS: Lactate metabolism-related gene signature; PCLM-BM: Pancreatic cancer liver metastasis and basement membrane; EFFscore: Efferocytosis-related score; mCAF: Myofibroblastic cancer-associated fibroblast; PCD: Programmed cell death; ICD: Immunogenic cell death; MDRG: Metastatic dissemination-related gene; BM: Basement membrane; TF: Transcription factor; ER: Endoplasmic reticulum; zDHHC: Zinc finger DHHC-type palmitoyl transferase; SASP: Senescence-associated secretory phenotype; DEGs: Differentially expressed genes; lncRNA: Long noncoding RNA; mRNA: Messenger RNA; ITH: Intratumoral heterogeneity; HRD: Homologous recombination deficiency; BA: Brown adipocyte; CD: Cluster of differentiation; ISGS: Immunologic signature gene sets; TAM: Tumor-associated macrophage; OS: Overall survival; PFS: Progression-free survival.

Table 3 Characteristics and reported outcomes of interventional trials included for clinical context in pancreatic ductal adenocarcinoma

NCT	Study design	n	Intervention	Stage	Primary outcome	Result	Secondary outcomes	Key finding	Ref.
NCT01726582	Single-arm	130	Personalised perioperative treatment (chemo/CRT/surgery)	Resectable/borderline resectable	Completion of surgery (feasibility)	108/130 (83.1%)	OS: 45 months vs 11 months; PFS: 36/130 (27.7%); Biomarker: 93/130 (71.5%); CR: 0/107; Near CR: 17/107; PR: 44/107; Poor: 42/107	The study demonstrated a high rate of completion of surgery (83.1%)	Tsai et al[71]
NCT00536874	Single-arm	35	Gem + oxaliplatin (neoadjuvant)	Resectable	18-month OS rate	63% (95%CI: 45-76)	OS: 39.6 months; PR: 4/35; SD: 28/35; PD: 3/35; CEA Δ: -5.1%; CA19-9 Δ: -25.6%	The 18-month OS rate was 63% (95%CI: 45%-76%)	O’Reilly et al[72]
NCT01926197	Randomised	13/12	mFOLFIRINOX vs mFOLFIRINOX + SBRT	Locally advanced (unresectable)	PFS (median)	6.5 months vs 8.4 months	Local PFS: 6.5 vs 8.4; PFS 1 year: 5/13 vs 2/12; MFS: 12.9 vs 10.8; OS: 12.9 vs 13.4; GI toxicity events: 16 vs 19	Median PFS was numerically higher in the SBRT arm (8.4 months vs 6.5 months)	Vitzthum[73]
NCT00810719	Single-arm	30	Gem + erlotinib	Advanced/metastatic	PFS (median)	2.07 months (1.87-5.50)	ORR: 11%; OS: 5.67 months (2.83-11.87)	The observed median PFS of 2.07 months indicated limited disease control	Semrad et al[74]
NCT00769483	Phase I/II, non-randomised, multi-arm	Approximately 15/arm	MK-0646 + Gem ± erlotinib	Stage IV (metastatic)	MTD + PFS (time to progression/death)	MTD: 10 mg/kg (Gem), 5 mg/kg (Gem + erlotinib); PFS: Approximately 1.8-2.0 months	OS: 5.7-10.4 months; ORR: Approximately 13%-17%; Toxicity: High	The study achieved its dose-escalation objective (MTD), but showed limited efficacy with median PFS of approximately 2 months	Abdel-Wahab et al[75]
NCT00365144	Single-arm	36	Bevacizumab + erlotinib	Metastatic, Gem-refractory	OS rate (6 months) + safety	8/36 (22.2%)	ORR: 1/36 (2.8%); TTP: 40 days (35-41); CA19-9 decline ≥ 25%: 4/26 (15.4%)	Low 6-month OS rate (22.2%)	Ko et al[76]
NCT00550836	Randomised	46/46	Gem + erlotinib vs + panitumumab	Metastatic	OS (median; arm A vs arm B)	4.2 months vs 8.3 months; P = 0.36	ORR: 8.7% vs 6.5%; PFS: 2.0 months vs 3.6 months, P = 0.419; TTF: 2.0 months vs 3.8 months, P = 0.36; G3+ AE: 41/46 vs 41/46; G4+ AE: 15/46 vs 14/46	Primary endpoint was not met	Halfdanarson et al[77]
NCT03941093	Randomised, double-blind	143/141	Pamrevlumab + G/nab-P or FOLFIRINOX vs placebo + G/nab-P or FOLFIRINOX	Locally advanced, unresectable	OS	17.25 months vs 17.94 months; HR 1.08 (0.83-1.41); P = 0.5487	EFS: 5.72 months vs 5.78 months; PFS: 9.36 months vs 9.40 months; ORR: 43/143 (30.1%) vs 64/141 (45.4%)	Primary endpoint not met	Picozzi et al[78]
NCT00408564	Single-arm	38-39	Gem + oxaliplatin + cetuximab, reassessment, surgery or RT/capecitabine	Locally advanced, unresectable, nonmetastatic	6-month PFS rate	82% (70%-95%)	G3-4 AE: 9/39 (23.1%); OS rate: 49% (36%-68%); ORR: 5/38 (13.2%)	High 6-month PFS rate	Medical University of South Carolina[79]
NCT00521404	Single-arm	61	CS-1008 (anti-DR5) + Gem	Unresectable/metastatic (chemo-naive)	16-week PFS rate	52.5% (39.3%-64.1%)	PFS: 3 months 59%, 6 months 34.4%; OS: 6 months 55.7%, 12 months 24.6%; ORR: 5/61 (8.2%); SD: 28/61 (45.9%)	Modest activity	Sankyo[80]
NCT00417976	Single-arm	39-40	Bevacizumab + Gem + infusional 5-FU	Stage III-IV	6-month PFS rate	49%	ORR: 12/40 (30%); SD: 18/40 (45%); PD: 10/40 (25%)	Moderate activity	Bekaii-Saab[81]
NCT00499486	Single-arm	31	Sirolimus monotherapy	Advanced PDAC, post-Gem (refractory)	6-month OS rate	26%	CR + PR: 0%. SD: 4 patients (approximately 13%). ORR = 0%	mTOR inhibition alone is insufficient in PDAC	Garrido-Laguna et al[82]
NCT01560949	Single-arm	33	mFOLFIRINOX, Gem-based CRT, surgery	Borderline resectable/high-risk resectable	Resectability rate	15/33 (45.5%)	R0: 10/15 (66.7%); DFS: 11.1 months (5.8-NA); OS: 24.0 months (16.2-29.6); SMAD4+ pre: 4/15 (26.7%); SMAD4+ post: 4/15 (26.7%); Local recurrence: 0/15; Distant recurrence: 10/15 (66.7%)	Moderate conversion to surgery; distant failure predominates	M.D. Anderson Cancer Center[83]
NCT01146054	Single-arm	49	SBRT + Gem	Locally advanced, unresectable, nonmetastatic	Late GI toxicity ≥ grade 2 at 1 year	5/49 (10.2%)	Acute GI toxicity: 14/49 (28.6%); PFS: 7.8 months (5.8-10.2); OS: 13.9 months (10.2-16.7); FFLP: 0.78 (0.60-0.89)	Low late GI toxicity; local control > systemic control	Koong[84]

NA: Not available; NCT: National clinical trial; CRT: Chemoradiotherapy; Gem: Gemcitabine; SBRT: Stereotactic body radiotherapy; FOLFIRINOX: Fluorouracil, leucovorin, irinotecan, and oxaliplatin; 5-FU: 5-Fluorouracil; DR5: Death receptor 5; RT: Radiotherapy; PDAC: Pancreatic ductal adenocarcinoma; MTD: Maximum tolerated dose; GI: Gastrointestinal; OS: Overall survival; PFS: Progression-free survival; CI: Confidence interval; HR: Hazard ratio; CR: Complete response; CEA: Carcinoembryonic antigen; PR: Partial response; SD: Stable disease; PD: Progressive disease; MFS: Metastasis-free survival; CA19-9: Carbohydrate antigen 19-9; TTP: Time to progression; ORR: Objective response rate; EFS: Event-free survival; TTF: Time to treatment failure; AE: Adverse event; FFLP: Freedom from local progression; R0: Microscopically margin-negative resection; DFS: Disease-free survival; mTOR: Mammalian target of rapamycin.

Table 4 Comparison of prognostic performance between the initial biologically derived signature and the least absolute shrinkage and selection operator-derived 5-gene signature in The Cancer Genome Atlas pancreatic adenocarcinoma cohort

Prognostic model	Cox model	Hazard ratio	P value	Harrell’s C-index	95%CI
Initial biologically derived signature	Univariable	1.13	0.239	0.522	0.472-0.579
	Multivariable	1.08	0.480	0.563	0.498-0.626
LASSO-derived 5-gene signature	Univariable	6.41	< 0.001	0.587	0.526-0.634
	Multivariable	6.13	< 0.001	0.599	0.534-0.653

CI: Confidence interval; LASSO: Least absolute shrinkage and selection operator.

Table 5 Calibration, overall prediction accuracy and baseline survival for the initial biologically derived signature and the least absolute shrinkage and selection operator-derived 5-gene signature in The Cancer Genome Atlas pancreatic adenocarcinoma derivation cohort and the Gene Expression Omnibus dataset GSE71729 validation cohort

Cohort	Model	Calibration slope	Brier score at 1/2/3 year	Integrated Brier score, 0-3 years	Baseline survival at 1/2/3 years (%)
TCGA-PAAD derivation cohort (n = 177, 93 events)	LASSO-derived 5-gene signature, univariable	1.861	0.183/0.203/0.171	0.168	76.9/42.0/35.4
	LASSO-derived 5-gene signature, multivariable	1.817		0.163
	Initial biologically derived signature, univariable	0.124	0.185/0.240/0.225	0.186	75.5/40.5/35.2
	Initial biologically derived signature, multivariable			0.173
GSE71729 validation cohort (n = 125, 84 events)	LASSO-derived 5-gene signature, univariable	0.154	0.234/0.213/0.163	0.189	64.0/33.3/22.2
	LASSO-derived 5-gene signature, subtype-adjusted	0.223		0.177

GSE71729: Gene Expression Omnibus dataset GSE71729; LASSO: Least absolute shrinkage and selection operator; TCGA-PAAD: The Cancer Genome Atlas Pancreatic Adenocarcinoma.