PanCuRx Translational Research Initiative

The goal of the PanCuRx TRI is to seek solutions to the high fatality rate of pancreatic adenocarcinoma (PDAC), the most common type of pancreatic cancer, by generating new knowledge about the genetics and biology of the disease, mechanisms of how tumours grow and tailored treatment options. PDAC is the fourth leading cause of cancer death in Canada and is expected to become the second-leading cause of cancer death within the next decade. The current five-year survival rate of eight per cent is the lowest of all epithelial cancers. There are major clinical challenges to treating the disease, including the fact that PDAC spreads to other parts of the body early so surgical removal of the tumour benefits few patients, that PDAC has proven relatively resistant to systemic therapies such as chemotherapy and that there has been limited benefit from the use of newer molecular targeted agents. The PanCuRx team has created the world’s first resource of tumour-purified PDAC whole genomes; more than 500 PDAC samples, with combined clinical annotation, have been successfully sequenced and analyzed at the Ontario Institute for Cancer research in Toronto. The resulting clinical genomic resource created from this data has led to multiple new findings that have established a framework to better understand PDAC biology and lays the foundation for new genomic approaches to better understanding the disease. The team also launched a clinical trial called COMPASS (Comprehensive Molecular Characterization of Advanced Ductal Pancreas Adenocarcinoma for Better Treatment Selection: A Prospective Study), which is recruiting patients with advanced PDAC (both locally advanced and metastatic) at The Princess Margaret Cancer Centre (PM) in Toronto. The study uses the molecular results from individual patient tumours to guide selection of better second line treatment on a case-by-case basis. The primary objective of the initial study was to assess the feasibility of collecting tumour materials from patients with advanced PDAC and delivering results within 56 days of biopsy. Having achieved this objective, the trial has expanded to other cancer centres across Canada. Pancreatic cancer is one of the most deadly forms of cancer and outcomes have not improved in four decades. The PanCuRx initiative is providing a better understanding of the disease and actively applying new knowledge to cancer patients through clinical trials. This knowledge will help to improve quality of life and prolong survival for pancreatic cancer patients worldwide.

Type: Other
Archiver: European Genome-Phenome Archive (EGA)

16 Datasets 38 Publications

Click on a Dataset ID in the table below to learn more, and to find out who to contact about access to these data

Dataset ID	Description	Technology	Samples
EGAD00001003582	Genomics-Driven Precision Medicine for Advanced Pancreatic Cancer - Early Results from the COMPASS Trial - RNA-Seq unmapped reads	Illumina HiSeq 2500	50
EGAD00001003584	Genomics-Driven Precision Medicine for Advanced Pancreatic Cancer - Early Results from the COMPASS Trial - RNA-Seq mapped reads		-
EGAD00001003585	Genomics-Driven Precision Medicine for Advanced Pancreatic Cancer - Early Results from the COMPASS Trial - WGS mapped reads		-
EGAD00001004548	Integration of Genomic and Transcriptional Features in Pancreatic Cancer Reveals Increased Cell Cycle Progression in Metastases - RNA-Seq mapped and unmapped reads	Illumina HiSeq 2500	75
EGAD00001004551	Integration of Genomic and Transcriptional Features in Pancreatic Cancer Reveals Increased Cell Cycle Progression in Metastases - WGS mapped reads		-
EGAD00001005799	Bam and fastq files from RNA-seq of PDAC samples described in Transcription phenotypes of pancreatic cancer are driven by genomic events events during tumour evolution	Illumina HiSeq 2500 unspecified	34
EGAD00001006081	PURPOSE: To determine the impact of basal-like and classical subtypes in advanced PDAC and to explore GATA6 expression as a surrogate biomarker. EXPERIMENTAL DESIGN: Within the COMPASS trial patients proceeding to chemotherapy for advanced PDAC undergo tumour biopsy for RNA sequencing. Overall response rate (ORR) and overall survival (OS) were stratified by subtypes and according to chemotherapy received. Correlation of GATA6 with the subtypes using gene expression profiling, in situ hybridization (ISH) were explored. RESULTS: Between December 2015-May 2019, 195 patients (95%) had enough tissue for RNA sequencing; 39 (20%) were classified as basal-like and 156 (80%) as classical. RECIST response data were available for 157 patients; 29 basal-like and 128 classical where the ORR was 10% vs. 33% respectively (p=0.02). In patients with basal-like tumours treated with modified FOLFIRINOX (mFFX) (n=22) the progression rate was 60% compared to 15% in classical PDAC (p= 0.0002). Median OS in the intention to treat population (n=195) was 9.3 months for classical vs. 5.9 months for basal-like PDAC (HR 0.47 95% CI 0.32-0.69, p=0.0001). GATA6 expression by RNAseq highly correlated with the classifier (p<0.001) and ISH predicted the subtypes with sensitivity of 89% and specificity of 83%. In a multivariable analysis, GATA6 expression was prognostic (p=0.02). In exploratory analyses, basal-like tumours, could be identified by keratin 5, were more hypoxic and enriched for a T cell inflamed gene expression signature. CONCLUSIONS: The basal-like subtype is chemoresistant and can be distinguished from classical PDAC by GATA6 expression.	Illumina HiSeq 2500 unspecified	101
EGAD00001006152	Bam files from WGS of PDAC samples described in: Transcription phenotypes of pancreatic cancer are driven by genomic events events during tumour evolution		-
EGAD00001006261	Bam and fastq files from RNA-seq of PDAC samples used in the PCSI mismatch repair study	Illumina HiSeq 2500 unspecified	4
EGAD00001006262	Bam files from WGS of PDAC samples used in the PCSI mismatch repair study		-
EGAD00001007571	Background and Aims: Homologous recombination deficiency (HRD) in pancreatic ductal adenocarcinoma (PDAC), remains poorly defined beyond germline(g) alterations in BRCA1, BRCA2 and PALB2. Methods: We interrogated whole genome sequencing (WGS) data on 391 patients including 49 carriers of pathogenic variants (PVs) in g_BRCA_ and PALB2. HRD classifiers were applied to the dataset and included: 1) the genomic instability score (GIS) used by Myriad MyChoice HRD assay; 2) substitution base signature 3 (SBS3); 3) HRDetect; and, 4) Structural Variant (SV) burden. Clinical outcomes and responses to chemotherapy were correlated with HRD status. Results: Biallelic tumour inactivation of g_BRCA_ or PALB2 was evident in 43/49 germline carriers identifying HRD-PDAC. HRDetect (score ?0.7) predicted gBRCA1/PALB2 deficiency with highest sensitivity (98%) and specificity (100%). HRD genomic tumour classifiers suggested that 7-10% of PDAC that do not harbor g_BRCA/PALB2_ have features of HRD. Of the somatic HRDetect cases, 69% were attributed to alterations in BRCA1/2, PALB2, RAD51C/D and XRCC2, and a tandem duplicator phenotype. TP53 loss was more common in BRCA1- compared to BRCA2-associated HRD-PDAC. HRD status was not prognostic in resected PDAC. However in advanced disease the GIS (p=0.02), SBS3 (p=0.03) and HRDetect score (p=0.005) were predictive of platinum response and superior survival. PVs in g_ATM_ (n=6) or g_CHEK2_ (n=2) did not result in HRD-PDAC by any of the classifiers. In four patients, BRCA2 reversion mutations associated with platinum resistance. Conclusions: Germline and parallel somatic profiling of PDAC outperforms germline testing alone in identifying HRD-PDAC. An additional 7-10% of patients without gBRCA/PALB2 mutations may benefit from DNA damage response agents.		-
EGAD00001008155	Intratumoral heterogeneity is a critical frontier in understanding how the tumor microenvironment (TME) propels malignant progression. Here, we deconvolute the human pancreatic TME through large-scale integration of histology-guided regional multiOMICs with clinical data and patient-derived preclinical models. We discover subTMEs, histologically definable tissue states anchored in fibroblast plasticity, with regional relationships to tumor immunity, subtypes, differentiation, and treatment response. Reactive subTMEs rich in complex but functionally coordinated fibroblast communities were immune-hot and inhabited by aggressive tumor cell phenotypes. The matrix-rich deserted subTMEs harbored less activated fibroblasts and tumor- suppressive features yet were markedly chemoprotective and enriched upon chemotherapy. SubTMEs originated in fibroblast differentiation trajectories and transitory states were notable both in single cell transcriptomics and in situ. The intratumoral co-occurrence of subTMEs produced patient-specific phenotypic and computationally predictable heterogeneity tightly linked to malignant biology. Therefore, heterogeneity within the plentiful, notorious pancreatic TME is not random but marks fundamental tissue organizational units.	Illumina HiSeq 2500 unspecified	29
EGAD00001009409	BAM files from RNA-seq of PDAC samples used in the COMPASS hENT1 study		-
EGAD00001011129	Whole genome sequencing data for germline BRCA pancreatic cancer		1
EGAD00010001811	h5 files from 15 single cell PDAC samples described in "Transcription phenotypes of pancreatic cancer are driven by genomic events events during tumour evolution"		15
EGAD50000001834	WGS data from pancreatic cancer samples. These are part of a resected cohort from a tandem duplicator phenotype paper (Farooq et al, NPJ Precision Oncology, 2025). The dataset includes tumour and normal BAM files sequenced on Illumina HiSeq/NovaSeq and aligned against GRCh38 (n=189 tumour/normal pairs).		378

Publications	Citations
Genomics-Driven Precision Medicine for Advanced Pancreatic Cancer: Early Results from the COMPASS Trial. Aung KL, Fischer SE, Denroche RE, Jang GH, Dodd A, Creighton S, Southwood B, Liang SB, Chadwick D, Zhang A, O'Kane GM, Albaba H, Moura S, Grant RC, Miller JK, Mbabaali F, Pasternack D, Lungu IM, Bartlett JMS, Ghai S, Lemire M, Holter S, Connor AA, Moffitt RA, Yeh JJ, Timms L, Krzyzanowski PM, Dhani N, Hedley D, Notta F, Wilson JM, Moore MJ, Gallinger S, Knox JJ. Clin Cancer Res 24: 2018 1344-1354	422
Integration of Genomic and Transcriptional Features in Pancreatic Cancer Reveals Increased Cell Cycle Progression in Metastases. Connor AA, Denroche RE, Jang GH, Lemire M, Zhang A, Chan-Seng-Yue M, Wilson G, Grant RC, Merico D, Lungu I, Bartlett JMS, Chadwick D, Liang SB, Eagles J, Mbabaali F, Miller JK, Krzyzanowski P, Armstrong H, Luo X, Jorgensen LGT, Romero JM, Bavi P, Fischer SE, Serra S, Hafezi-Bakhtiari S, Caglar D, Roehrl MHA, Cleary S, Hollingsworth MA, Petersen GM, Thayer S, Law CHL, Nanji S, Golan T, Smith AL, Borgida A, Dodd A, Hedley D, Wouters BG, O'Kane GM, Wilson JM, Zogopoulos G, Notta F, Knox JJ, Gallinger S. Cancer Cell 35: 2019 267-282.e7	167
De novo compartment deconvolution and weight estimation of tumor samples using DECODER. Peng XL, Moffitt RA, Torphy RJ, Volmar KE, Yeh JJ. Nat Commun 10: 2019 4729	34
Purity Independent Subtyping of Tumors (PurIST), A Clinically Robust, Single-sample Classifier for Tumor Subtyping in Pancreatic Cancer. Rashid NU, Peng XL, Jin C, Moffitt RA, Volmar KE, Belt BA, Panni RZ, Nywening TM, Herrera SG, Moore KJ, Hennessey SG, Morrison AB, Kawalerski R, Nayyar A, Chang AE, Schmidt B, Kim HJ, Linehan DC, Yeh JJ. Clin Cancer Res 26: 2020 82-92	143
Accurate and efficient detection of gene fusions from RNA sequencing data. Uhrig S, Ellermann J, Walther T, Burkhardt P, Fröhlich M, Hutter B, Toprak UH, Neumann O, Stenzinger A, Scholl C, Fröhling S, Brors B. Genome Res 31: 2021 448-460	314
NOX4 links metabolic regulation in pancreatic cancer to endoplasmic reticulum redox vulnerability and dependence on PRDX4. Jain P, Dvorkin-Gheva A, Mollen E, Malbeteau L, Xie M, Jessa F, Dhavarasa P, Chung S, Brown KR, Jang GH, Vora P, Notta F, Moffat J, Hedley D, Boutros PC, Wouters BG, Koritzinsky M. Sci Adv 7: 2021 eabf7114	19
NOXA expression drives synthetic lethality to RUNX1 inhibition in pancreatic cancer. Doffo J, Bamopoulos SA, Köse H, Orben F, Zang C, Pons M, den Dekker AT, Brouwer RWW, Baluapuri A, Habringer S, Reichert M, Illendula A, Krämer OH, Schick M, Wolf E, van IJcken WFJ, Esposito I, Keller U, Schneider G, Wirth M. Proc Natl Acad Sci U S A 119: 2022 e2105691119	26
Ordered and deterministic cancer genome evolution after p53 loss. Baslan T, Morris JP, Zhao Z, Reyes J, Ho YJ, Tsanov KM, Bermeo J, Tian S, Zhang S, Askan G, Yavas A, Lecomte N, Erakky A, Varghese AM, Zhang A, Kendall J, Ghiban E, Chorbadjiev L, Wu J, Dimitrova N, Chadalavada K, Nanjangud GJ, Bandlamudi C, Gong Y, Donoghue MTA, Socci ND, Krasnitz A, Notta F, Leach SD, Iacobuzio-Donahue CA, Lowe SW. Nature 608: 2022 795-802	158
Integrative analysis of KRAS wildtype metastatic pancreatic ductal adenocarcinoma reveals mutation and expression-based similarities to cholangiocarcinoma. Topham JT, Tsang ES, Karasinska JM, Metcalfe A, Ali H, Kalloger SE, Csizmok V, Williamson LM, Titmuss E, Nielsen K, Negri GL, Spencer Miko SE, Jang GH, Denroche RE, Wong HL, O'Kane GM, Moore RA, Mungall AJ, Loree JM, Notta F, Wilson JM, Bathe OF, Tang PA, Goodwin R, Morin GB, Knox JJ, Gallinger S, Laskin J, Marra MA, Jones SJM, Schaeffer DF, Renouf DJ. Nat Commun 13: 2022 5941	35
XDec-CHI reveals immunosuppressive interactions in pancreatic ductal adenocarcinoma. LaPlante EL, Liu D, Petrosyan V, Yao Q, Milosavljevic A. iScience 25: 2022 105249	1
Spatial transcriptomics technology in cancer research. Yu Q, Jiang M, Wu L. Front Oncol 12: 2022 1019111	50
MACHETE identifies interferon-encompassing chromosome 9p21.3 deletions as mediators of immune evasion and metastasis. Barriga FM, Tsanov KM, Ho YJ, Sohail N, Zhang A, Baslan T, Wuest AN, Del Priore I, Meškauskaitė B, Livshits G, Alonso-Curbelo D, Simon J, Chaves-Perez A, Bar-Sagi D, Iacobuzio-Donahue CA, Notta F, Chaligne R, Sharma R, Pe'er D, Lowe SW. Nat Cancer 3: 2022 1367-1385	84
Metastatic phenotype and immunosuppressive tumour microenvironment in pancreatic ductal adenocarcinoma: Key role of the urokinase plasminogen activator (PLAU). Hosen SMZ, Uddin MN, Xu Z, Buckley BJ, Perera C, Pang TCY, Mekapogu AR, Moni MA, Notta F, Gallinger S, Pirola R, Wilson J, Ranson M, Goldstein D, Apte M. Front Immunol 13: 2022 1060957	35
Systemic inflammatory prognostic scores in advanced pancreatic adenocarcinoma. Ma LX, Wang Y, Espin-Garcia O, Allen MJ, Jang GH, Zhang A, Dodd A, Ramotar S, Hutchinson S, Tehfe M, Ramjeesingh R, Biagi J, Wilson JM, Notta F, Fischer SE, Zogopoulos G, Gallinger S, Grant RC, Khokha R, Chan N, Grünwald BT, Knox JJ, O'Kane GM. Br J Cancer 128: 2023 1916-1921	16
RBFOX2 modulates a metastatic signature of alternative splicing in pancreatic cancer. Jbara A, Lin KT, Stossel C, Siegfried Z, Shqerat H, Amar-Schwartz A, Elyada E, Mogilevsky M, Raitses-Gurevich M, Johnson JL, Yaron TM, Ovadia O, Jang GH, Danan-Gotthold M, Cantley LC, Levanon EY, Gallinger S, Krainer AR, Golan T, Karni R. Nature 617: 2023 147-153	65
Spectrum of Response to Platinum and PARP Inhibitors in Germline BRCA-Associated Pancreatic Cancer in the Clinical and Preclinical Setting. Stossel C, Raitses-Gurevich M, Atias D, Beller T, Glick Gorman Y, Halperin S, Peer E, Denroche RE, Zhang A, Notta F, Wilson JM, O'Kane GM, Haimov Talmoud E, Amison N, Schvimer M, Salpeter SJ, Bar V, Zundelevich A, Tirosh I, Tal R, Dinstag G, Kinar Y, Eliezer Y, Ben-David U, Gavert NS, Straussman R, Gallinger SJ, Berger R, Golan T. Cancer Discov 13: 2023 1826-1843	27
High-dimensional deconstruction of pancreatic cancer identifies tumor microenvironmental and developmental stemness features that predict survival. Storrs EP, Chati P, Usmani A, Sloan I, Krasnick BA, Babbra R, Harris PK, Sachs CM, Qaium F, Chatterjee D, Wetzel C, Goedegebuure SP, Hollander T, Anthony H, Ponce J, Khaliq AM, Badiyan S, Kim H, Denardo DG, Lang GD, Cosgrove ND, Kushnir VM, Early DS, Masood A, Lim KH, Hawkins WG, Ding L, Fields RC, Das KK, Chaudhuri AA. NPJ Precis Oncol 7: 2023 105	22
Clinically impactful metabolic subtypes of pancreatic ductal adenocarcinoma (PDAC). Pervin J, Asad M, Cao S, Jang GH, Feizi N, Haibe-Kains B, Karasinska JM, O'Kane GM, Gallinger S, Schaeffer DF, Renouf DJ, Zogopoulos G, Bathe OF. Front Genet 14: 2023 1282824	7
Pre-treatment inflamed tumor immune microenvironment is associated with FOLFIRINOX response in pancreatic cancer. Gao Z, Kang SW, Erstad D, Azar J, Van Buren G, Fisher W, Sun Z, Rubinstein MP, Lee HS, Camp ER. Front Oncol 13: 2023 1274783	0
RBFOX2 deregulation promotes pancreatic cancer progression and metastasis through alternative splicing. Maurin M, Ranjouri M, Megino-Luque C, Newberg JY, Du D, Martin K, Miner RE, Prater MS, Wee DKB, Centeno B, Pruett-Miller SM, Stewart P, Fleming JB, Yu X, Bravo-Cordero JJ, Guccione E, Black MA, Mann KM. Nat Commun 14: 2023 8444	27
Cytidine deaminases APOBEC3C and APOBEC3D promote DNA replication stress resistance in pancreatic cancer cells. Ubhi T, Zaslaver O, Quaile AT, Plenker D, Cao P, Pham NA, Békési A, Jang GH, O'Kane GM, Notta F, Moffat J, Wilson JM, Gallinger S, Vértessy BG, Tuveson DA, Röst HL, Brown GW. Nat Cancer 5: 2024 895-915	13
Combination immunohistochemistry for CK5/6, p63, GATA6, and HNF4a predicts clinical outcome in treatment-naïve pancreatic ductal adenocarcinoma. Shibayama T, Hayashi A, Toki M, Kitahama K, Ho YJ, Kato K, Yamada T, Kawamoto S, Kambayashi K, Ochiai K, Gondo K, Okano N, Melchor JP, Iacobuzio-Donahue CA, Sakamoto Y, Hisamatsu T, Shibahara J. Sci Rep 14: 2024 15598	3
ROR2 Regulates Cellular Plasticity in Pancreatic Neoplasia and Adenocarcinoma. Benitz S, Steep A, Nasser MM, Preall J, Mahajan UM, McQuithey H, Loveless I, Davis ET, Wen HJ, Long DW, Metzler T, Zwernik S, Louw M, Rempinski D, Salas-Escabillas DJ, Brender SM, Song L, Huang L, Theisen BK, Zhang Z, Steele NG, Regel I, Bednar F, Crawford HC. Cancer Discov 14: 2024 2162-2182	5
The xenobiotic transporter <i>ABCC4</i>/MRP4 promotes epithelial mesenchymal transition in pancreatic cancer. Gancedo SN, Sahores A, Gómez N, Di Siervi N, May M, Yaneff A, de Sousa Serro MG, Fraunhoffer N, Dusetti N, Iovanna J, Shayo C, Davio CA, González B. Front Pharmacol 15: 2024 1432851	0
Distinct clinical outcomes and biological features of specific KRAS mutants in human pancreatic cancer. McIntyre CA, Grimont A, Park J, Meng Y, Sisso WJ, Seier K, Jang GH, Walch H, Aveson VG, Falvo DJ, Fall WB, Chan CW, Wenger A, Ecker BL, Pulvirenti A, Gelfer R, Zafra MP, Schultz N, Park W, O'Reilly EM, Houlihan SL, Alonso A, Hissong E, Church GM, Mason CE, Siolas D, Notta F, Gonen M, Dow LE, Jarnagin WR, Chandwani R. Cancer Cell 42: 2024 1614-1629.e5	30
Differential activity of MAPK signalling defines fibroblast subtypes in pancreatic cancer. Veghini L, Pasini D, Fang R, Delfino P, Filippini D, Neander C, Vicentini C, Fiorini E, Lupo F, D'Agosto SL, Carbone C, Agostini A, Piro G, Rosa D, Bevere M, Markus P, Behrens D, Luchini C, Lawlor RT, Scarpa A, Biffi G, Cheung PF, Siveke JT, Corbo V. Nat Commun 15: 2024 10534	6
Human Pancreatic Cancer Single-Cell Atlas Reveals Association of CXCL10+ Fibroblasts and Basal Subtype Tumor Cells. Loveless IM, Kemp SB, Hartway KM, Mitchell JT, Wu Y, Zwernik SD, Salas-Escabillas DJ, Brender S, George M, Makinwa Y, Stockdale T, Gartrelle K, Reddy RG, Long DW, Wombwell A, Clark JM, Levin AM, Kwon D, Huang L, Francescone R, Vendramini-Costa DB, Stanger BZ, Alessio A, Waters AM, Cui Y, Fertig EJ, Kagohara LT, Theisen B, Crawford HC, Steele NG. Clin Cancer Res 31: 2025 756-772	10
HMGA2 Expression Predicts Subtype, Survival, and Treatment Outcome in Pancreatic Ductal Adenocarcinoma. Yamamoto N, Dobersch S, Loveless I, Samraj AN, Jang GH, Haraguchi M, Kang LI, Ruzinova MB, Vij KR, Mudd JL, Walsh T, Safyan RA, Chiorean EG, Hingorani SR, Bolton NM, Li L, Fields RC, DeNardo DG, Notta F, Crawford HC, Steele NG, Kugel S. Clin Cancer Res 31: 2025 733-745	3
Dissecting tumor transcriptional heterogeneity from single-cell RNA-seq data by generalized binary covariance decomposition. Liu Y, Carbonetto P, Willwerscheid J, Oakes SA, Macleod KF, Stephens M. Nat Genet 57: 2025 263-273	5
Spatial tumor immune heterogeneity facilitates subtype co-existence and therapy response in pancreatic cancer. Klein L, Tu M, Krebs N, Urbach L, Grimm D, Latif MU, Penz F, Blandau A, Wu X, Samuel RD, Küffer S, Wegwitz F, Chan N, Aliar K, Vyas F, Kishore U, Hessmann E, Trumpp A, Espinet E, Papantonis A, Khokha R, Ellenrieder V, Grünwald BT, Singh SK. Nat Commun 16: 2025 335	7
Intratumor heterogeneity in KRAS signaling shapes treatment resistance. Petrenko O, Kirillov V, D'Amico S, Reich NC. iScience 28: 2025 111662	1
FGFR2 Abrogation Intercepts Pancreatic Ductal Adenocarcinoma Development. Tonelli C, Deschênes A, Gaeth VA, Jensen A, Vithlani N, Yao MA, Zhao Z, Park Y, Tuveson DA. Cancer Res 85: 2025 1960-1977	0
The tandem duplicator phenotype may be a novel targetable subgroup in pancreatic cancer. Farooq AR, Zhang AX, Chan-Seng-Yue M, Topham JT, O'Kane GM, Jang GH, Fischer S, Dodd A, Holter S, Wilson J, Grant RC, Aung KL, Zogopoulos G, Elimova E, Prince R, Jang R, Moore M, Biagi J, Tang P, Goodwin R, Bathe OF, Marra M, Laskin J, Renouf DJ, Schaeffer DF, Karasinska JM, Notta F, Gallinger S, Knox JJ, Tsang ES. NPJ Precis Oncol 9: 2025 100	1
P4HA1 mediates hypoxia-induced invasion in human pancreatic cancer organoids. Navarro-Serer B, Wissler MF, Glover BK, Lerner MG, Oza HH, Wang V, Knutsdottir H, Shojaeian F, Noller K, Baskaran SG, Hughes S, Weaver AM, Wilentz D, Olayemi O, Bader JS, Fertig EJ, Gilkes DM, Wood LD. Cancer Res Commun 5: 2025 881-895	1
Whole genome and transcriptome profiling in advanced pancreatic cancer patients on the COMPASS trial. Knox JJ, Jang GH, Grant RC, Zhang A, Ma L, Elimova E, Jang R, Moore M, Biagi J, Tehfe M, Ramjeesingh R, Tsang ES, Holter S, Ramotar S, Hutchinson S, Liang SB, Lungu IM, Moura S, Wang Y, Perera S, Chan-Seng-Yue M, Monajemzadeh M, Aung K, Prince R, Romero JM, Fuentes-Antras J, Gonzalez Conchas GA, Picardo S, Gonzalez R, Ghai S, Khalili K, Kyoung Kim T, Ng K, Bartlett J, Pugh TJ, Kalimuthu SN, Fischer SE, Wilson JM, Dodd A, Zogopoulos G, Grünwald BT, Notta F, Gallinger S, O'Kane GM. Nat Commun 16: 2025 5919	0
Targeting FGFR4 abrogates HNF1A-driven metastasis in pancreatic ductal adenocarcinoma. Crawford KJ, Humphrey KS, Cortes E, Wang J, Kumarasamy V, Wan Y, Long MD, Feigin ME, Witkiewicz AK, Mann KM, Knudsen ES, Abel EV. Mol Cancer 24: 2025 208	2
ALDH1A3 promotes aggressive basal-like pancreatic cancer through an AP-1/RUNX2 enhancer network. Zou X, Nie S, Cao J, Shi M, Schuck K, Shi Z, Zhang L, Li H, Sun Y, Fang C, Hu J, Niu Y, Yu Y, Zhang Z, Li C, Hu M, Wang L, Jiang K, Lu Z, Akkan J, Raulefs S, Kahlert C, Roth S, Herr I, Wan Y, Mihaljevic A, Qian X, Zhang Q, Wang MH, Kleeff J, Friess H, Gu Z, Michalski CW, Shen S, Kong B. Oncogene 44: 2025 3774-3786	0
A framework to mine laser microdissection-based omics data and uncover regulators of pancreatic cancer heterogeneity. Chiaro PD, Diaferia GR, Natoli G, Barozzi I. Gigascience 14: 2025 giaf101	0