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Pancreatic cancer medical therapy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahad Hasan, M.D.[2] Sudarshana Datta, MD [3]

Overview

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Systemic therapy is the backbone of management for nearly all patients with pancreatic ductal adenocarcinoma (PDAC), including those with resectable disease, in whom chemotherapy is given before and/or after surgery. Universal germline testing and somatic tumor profiling are now required before therapy is selected. They identify candidates for platinum-based therapy, PARP inhibitor maintenance, tumor-agnostic targeted agents, and immunotherapy.[1][2] For fit patients (ECOG 0–1) with metastatic disease, gemcitabine plus nab-paclitaxel, (modified) FOLFIRINOX, and NALIRIFOX are NCCN category 1 preferred first-line options, and none has proven superior to the others. Poorer performance status shifts treatment toward single agents or best supportive care.[1][3] After upfront resection, 6 months of adjuvant modified FOLFIRINOX is preferred for fit patients. Neoadjuvant therapy is standard for borderline resectable disease.[4][5] In August 2026 the FDA approved daraxonrasib, an oral RAS(ON) inhibitor, for metastatic disease after at least one prior systemic therapy or in patients who are not candidates for multiagent therapy.[6]

Medical Therapy

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Molecular and Germline Testing Before Therapy

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  • Germline testing is recommended for every patient with confirmed pancreatic cancer, using a comprehensive panel that includes ATM, BRCA1, BRCA2, CDKN2A, MLH1, MSH2, MSH6, PALB2, PMS2, STK11, and TP53.[1]
  • Somatic tumor profiling is recommended for all candidates for anticancer therapy. Next-generation sequencing is preferred, with RNA sequencing to detect gene fusions. Circulating tumor DNA (liquid biopsy) is acceptable when tissue is insufficient.[1][7]
  • Actionable targets include:[1]
    • Fusions: ALK, NRG1, NTRK, ROS1, FGFR2, RET
    • Mutations: BRAF, BRCA1/2, KRAS, PALB2
    • HER2 amplification/overexpression
    • Microsatellite instability-high (MSI-H), mismatch repair deficiency (dMMR), and high tumor mutational burden (TMB-H)
  • Approximately 10–25% of patients harbor an actionable alteration.[2][7]
  • Early-onset PDAC: treatment guidelines are the same as for later-onset disease. However, germline DNA damage repair variants and actionable somatic alterations are more frequent in early-onset disease. In one cohort, patients receiving matched targeted therapy had longer overall survival (OS), which reinforces the need for sequencing in this group.[8]

Metastatic Disease

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First-Line Therapy by Performance Status

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  • No randomized trial directly compares all three category 1 regimens. Regimen choice depends on performance status, comorbidity, expected toxicity, and patient preference.[1][3]
  • Under NCCN criteria, "good performance status" means ECOG 0–1 plus adequate biliary drainage and nutritional status. All three are needed before committing to a triplet regimen.[1]
First-line systemic therapy for metastatic PDAC
Clinical scenario Recommended options
ECOG 0–1, adequate biliary drainage and nutrition Gemcitabine + nab-paclitaxel (category 1)
FOLFIRINOX or modified FOLFIRINOX (category 1)
NALIRIFOX (category 1)
Germline or somatic BRCA1/2 or PALB2 alteration FOLFIRINOX/mFOLFIRINOX or gemcitabine + cisplatin
ECOG 2 Gemcitabine + nab-paclitaxel (category 1); gemcitabine monotherapy; capecitabine; CAPEOX; FOLFIRI; FOLFOX
ECOG 3 Best supportive care; single-agent gemcitabine (category 1) for patients who wish to pursue treatment
ECOG 4 Supportive care only
Category 1 first-line multiagent regimens: dosing and pivotal evidence
Regimen Dose and schedule Major toxicities
FOLFIRINOX Oxaliplatin 85 mg/m², irinotecan 180 mg/m², leucovorin 400 mg/m², fluorouracil (5-FU) 400 mg/m² IV bolus, then 5-FU 2400 mg/m² over 46 h; every 14 days[9] Grade 3–4 neutropenia (46%), febrile neutropenia, diarrhea, neuropathy[2][3]
Modified FOLFIRINOX Omits the 5-FU bolus and reduces the irinotecan dose to limit toxicity Lower hematologic and GI toxicity than the classic regimen[1]
Gemcitabine + nab-paclitaxel Albumin-bound nab-paclitaxel 125 mg/m² + gemcitabine 1000 mg/m² IV on days 1, 8, and 15 of a 28-day cycle[10] Myelosuppression and neuropathy. Fewer GI effects than triplets but more alopecia and anemia.[10][2]
NALIRIFOX Liposomal irinotecan 50 mg/m², oxaliplatin 60 mg/m², leucovorin 400 mg/m², 5-FU 2400 mg/m² over 46 h; days 1 and 15 of a 28-day cycle[11] Different toxicity profile from FOLFIRINOX; GI toxicity is prominent[12]

Maintenance Therapy

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  • Patients with response or stable disease after 4–6 months of first-line therapy may take a chemotherapy holiday or move to maintenance therapy.[1]
  • Germline BRCA1/2 carriers without progression after at least 16 weeks of first-line platinum: maintenance olaparib 300 mg orally twice daily is preferred.[1][13]
    • POLO results:[13][2]
      • Progression-free survival (PFS) improved: 7.4 vs 3.8 months (HR 0.53).
      • No statistically significant OS benefit: median about 19 months in both arms.
      • Time off chemotherapy and long-term survival in a subset favored olaparib, and quality of life was preserved.
    • ASCO frames the choice between continued chemotherapy and olaparib as shared decision-making, given the absence of an OS benefit and the placebo comparator in POLO.[3]
  • Rucaparib is an option for germline or somatic BRCA1/2 or PALB2 alterations after platinum-based therapy.[1]
  • Non-platinum maintenance options include capecitabine after FOLFIRINOX or continued gemcitabine-based therapy.[1]

Second-Line and Subsequent Therapy

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  • Sequencing depends on which agents were used before and whether the interval since prior therapy is at least 6 months or shorter.[1]
  • After gemcitabine-based first-line therapy: 5-FU/leucovorin + liposomal irinotecan is category 1.[1][3]
    • NAPOLI-1 regimen: liposomal irinotecan 70 mg/m² (free-base equivalent) + leucovorin 400 mg/m² + 5-FU 2400 mg/m² over 46 h every 2 weeks.[14]
    • NAPOLI-1 outcome: OS 6.1 vs 4.2 months (HR 0.67).[14][3]
  • After fluoropyrimidine-based first-line therapy: gemcitabine + nab-paclitaxel is an option.[1]
  • Oxaliplatin-based second-line therapy: trial data conflict. OFF (CONKO-003) was positive, but mFOLFOX6 (PANCREOX) was negative and possibly harmful. Oxaliplatin should not be substituted for liposomal irinotecan after gemcitabine.[3][15][16]
  • Daraxonrasib (oral multi-selective RAS(ON) inhibitor):
    • FDA indication: adults with metastatic pancreatic adenocarcinoma after at least one prior systemic therapy, or who are not candidates for multiagent systemic therapy.[6]
    • NCCN lists it as category 1 subsequent therapy for good or intermediate performance status.[1]
    • Approval was based on the randomized phase 3 RASolute 302 trial versus second-line chemotherapy. Median OS was 13.2 vs 6.7 months.[6][17]
    • Dose: 300 mg orally once daily until progression or unacceptable toxicity.[18]
    • Common adverse reactions: rash, diarrhea, stomatitis, nausea, fatigue, vomiting, abdominal pain, edema, decreased appetite, and hemorrhage.[19]

Biomarker-Directed Targeted Therapy and Immunotherapy

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  • These agents apply to small, molecularly defined subsets. In matched patients, their activity can match or exceed chemotherapy benchmarks.[20]
  • NCCN lists them as "useful in certain circumstances," except daraxonrasib, which is category 1 subsequent therapy.[1]
Biomarker-directed agents in PDAC
Biomarker Agent(s)
RAS pathway (pan-RAS inhibition) Daraxonrasib
KRAS G12C (about 1–2%) Adagrasib, sotorasib
Germline or somatic BRCA1/2, PALB2 Olaparib (germline BRCA maintenance), rucaparib
MSI-H / dMMR (about 1–2%); TMB-high Pembrolizumab, dostarlimab; ipilimumab + nivolumab (TMB-H)
NTRK fusion Larotrectinib, entrectinib, repotrectinib
NRG1 fusion Zenocutuzumab
RET fusion Selpercatinib
BRAF V600E Dabrafenib + trametinib
HER2 (IHC 3+, or IHC 2+ with FISH+) Fam-trastuzumab deruxtecan
FGFR alterations Erdafitinib

Adjuvant Therapy (Resected Disease Without Prior Neoadjuvant Therapy)

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  • All patients who recover after upfront resection and did not receive preoperative therapy should be offered 6 months of adjuvant chemotherapy, unless there is a medical or surgical contraindication.[4]
  • Modified FOLFIRINOX is preferred for fit patients (ECOG 0–1) based on PRODIGE-24/CCTG PA6:[4][21][22]
    • Primary analysis: median OS 54.4 vs 35.0 months vs gemcitabine.
    • Final 5-year analysis: 5-year OS 43.2% vs 31.4%.
  • Biomarker analysis (2026): in PRODIGE-24, the mFOLFIRINOX benefit was confined to KRAS-mutant tumors, and HRR/BRCA status was not predictive in the adjuvant setting. These findings are hypothesis-generating.[23]
Adjuvant regimens after upfront resection
Regimen Dose and schedule Comments
Modified FOLFIRINOX (preferred, ECOG 0–1) Oxaliplatin 85 mg/m², leucovorin 400 mg/m², irinotecan 150 mg/m², 5-FU 2.4 g/m² over 46 h; every 14 days × 12 cycles PRODIGE-24/CCTG PA6[21][4]
Gemcitabine + capecitabine (category 1) Gemcitabine 1000 mg/m² IV on days 1, 8, and 15, plus capecitabine 1660 mg/m²/day orally on days 1–21; 28-day cycle × 6 cycles ESPAC-4; option for patients not fit for a triplet[1][24]
Gemcitabine monotherapy or 5-FU/leucovorin — For patients unable to tolerate combination therapy[1][4]

Neoadjuvant Therapy

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  • Borderline resectable disease: neoadjuvant chemotherapy, with or without radiation therapy, followed by surgery is the standard of care. Randomized evidence shows superior OS compared with upfront surgery.[5][25]
  • Resectable disease: upfront surgery followed by adjuvant therapy remains standard. Neoadjuvant therapy is an option, particularly with high-risk features:[1][5]
    • Large tumor
    • Regional adenopathy
    • Markedly elevated CA 19-9
    • Weight loss
  • Preferred NCCN neoadjuvant regimens: gemcitabine + nab-paclitaxel or (m)FOLFIRINOX, each with or without consolidative chemoradiation. Platinum-based regimens are preferred for BRCA1/2 or PALB2 carriers.[1]
  • No neoadjuvant regimen is clearly superior:[25][26]
    • PREOPANC-2 found no OS difference between neoadjuvant FOLFIRINOX and gemcitabine-based chemoradiotherapy.
    • SWOG S1505, ESPAC-5F, and NORPACT-1 showed no regimen superiority.
    • CASSANDRA suggested PAXG was superior to mFOLFIRINOX.
  • A practical advantage of neoadjuvant sequencing is guaranteed systemic exposure. About one-third of patients undergoing upfront surgery never receive adjuvant therapy because recovery is slow.[5][25]

Locally Advanced (Unresectable, Non-Metastatic) Disease

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  • First-line systemic options are the same as for metastatic disease: gemcitabine + nab-paclitaxel, (m)FOLFIRINOX, or NALIRIFOX. This is largely extrapolated from metastatic trials.[1]
  • Chemoradiation or stereotactic body radiation therapy (SBRT) is an option in two settings:[1]
    • In selected patients after at least 4–6 cycles of induction chemotherapy
    • Upfront, for poorly controlled pain or local obstruction
  • In LAP07, adding conventional chemoradiation after gemcitabine-based induction did not improve OS. It did improve local control and delayed the need to resume therapy.[1][27]

Role of Radiation Within Medical Management

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  • Adjuvant radiation remains controversial and is under trial evaluation. It is reserved for high-risk features such as positive margins, with chemotherapy given before chemoradiation.[1]
  • Neoadjuvant radiation may increase margin-negative resection and local control. It should follow neoadjuvant chemotherapy.[1]
  • Trials conflict on whether adjuvant or neoadjuvant radiation improves OS.[1][5]

Supportive and Palliative Care

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Areas of Uncertainty and Guideline Disagreement

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  • Optimal first-line regimen: no randomized trial directly compares the three category 1 regimens. Meta-analytic data suggest similar OS, so the best regimen is unresolved.[12][5]
  • BRCA maintenance: olaparib versus continued chemotherapy is unsettled. POLO used a placebo comparator and showed no OS benefit.[13][3]
  • Neoadjuvant regimen: the optimal regimen for resectable and borderline resectable disease remains undefined, as trial results conflict.[25][26]
  • RAS inhibition: durability of KRAS G12C inhibitors is limited. Daraxonrasib is being studied in the first-line metastatic setting (RASolute 303, alone or with gemcitabine/nab-paclitaxel) and in the adjuvant setting (RASolute 304). Both are investigational uses.[16][19]

Clinical Pearls and Common Pitfalls

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  • Order germline and somatic testing, including an RNA fusion panel, at diagnosis. Results change first-line choice (platinum for BRCA/PALB2 carriers) and open targeted and immunotherapy options. Skipping profiling can miss rare but highly actionable NTRK, NRG1, or RET fusions or MSI-H disease.[1][28]
  • Platinum response is a clinical surrogate for HRD and PARP inhibitor sensitivity.[1][15]
  • Avoid full-dose classic FOLFIRINOX in patients with marginal performance status, poor biliary drainage, or malnutrition. Modified FOLFIRINOX is the practical default triplet.[1][3]
  • NALIRIFOX has not been shown superior to FOLFIRINOX. It was compared only with gemcitabine/nab-paclitaxel.[1][12]
  • Maintenance olaparib offers PFS and time-off-chemotherapy benefit, not proven OS benefit.[13][3]
  • After gemcitabine-based therapy, liposomal irinotecan/5-FU/leucovorin is the evidence-based second-line regimen. Do not substitute mFOLFOX6, which was negative in PANCREOX.[3][16]

References

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  1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 1.19 1.20 1.21 1.22 1.23 1.24 1.25 1.26 1.27 1.28 1.29 1.30 1.31 National Comprehensive Cancer Network. NCCN Clinical Practice Guidelines in Oncology: Pancreatic Adenocarcinoma. Version 4.2026. Updated September 11, 2026. https://www.nccn.org/guidelines
  2. ↑ 2.0 2.1 2.2 2.3 2.4 May MS, Park W, O'Reilly EM (2026). "Treating Pancreatic Ductal Adenocarcinoma: The Targeted Revolution is Here". Drugs. 86 (4): 507–532. doi:10.1007/s40265-026-02295-0.
  3. ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 Sohal D, Kennedy EB, Cinar P, Conroy T, Copur MS, Crane CH, Garrido-Laguna I, Lau MW, Johnson T, Krishnamurthi S, Moravek C, O'Reilly EM, Philip PA, Pant S, Shah MA, Sahai V, Uronis HE, Zaidi N, Laheru D (2020). "Metastatic Pancreatic Cancer: ASCO Guideline Update". J Clin Oncol. 38 (27): 3217–3230. doi:10.1200/JCO.20.01364. Vancouver style error: initials (help)
  4. ↑ 4.0 4.1 4.2 4.3 4.4 Khorana AA, McKernin SE, Berlin J, Hong TS, Maitra A, Moravek C, Mumber M, Schulick R, Zeh HJ, Katz M (2019). "Potentially Curable Pancreatic Adenocarcinoma: ASCO Clinical Practice Guideline Update". J Clin Oncol. 37 (23): 2082–2088. doi:10.1200/JCO.19.00946. Vancouver style error: initials (help)
  5. ↑ 5.0 5.1 5.2 5.3 5.4 5.5 Stoop TF, Javed AA, Oba A, Groot Koerkamp B, Seufferlein T, Wilmink JW, Besselink MG (2025). "Pancreatic cancer". Lancet. 405 (10485): 1182–1202. doi:10.1016/S0140-6736(25)00261-2.
  6. ↑ 6.0 6.1 6.2 U.S. Food and Drug Administration. FDA approves daraxonrasib for metastatic pancreatic adenocarcinoma. August 26, 2026. https://www.fda.gov/drugs/resources-information-approved-drugs/fda-approves-daraxonrasib-metastatic-pancreatic-adenocarcinoma
  7. ↑ 7.0 7.1 Zhen DB, Safyan RA, Konick EQ, Nguyen R, Prichard CC, Chiorean EG (2023). "The role of molecular testing in pancreatic cancer". Therap Adv Gastroenterol. 16: 17562848231171456. doi:10.1177/17562848231171456.
  8. ↑ Castet F, Fabregat-Franco C, Castillo G, et al. (2023). "Clinical and genomic characterisation of early-onset pancreatic cancer". Eur J Cancer. 194: 113338. doi:10.1016/j.ejca.2023.113338.
  9. ↑ Conroy T, Desseigne F, Ychou M, Bouché O, Guimbaud R, Bécouarn Y, Adenis A, Raoul JL, Gourgou-Bourgade S, de la Fouchardière C, Bennouna J, Bachet JB, Khemissa-Akouz F, Péré-Vergé D, Delbaldo C, Assenat E, Chauffert B, Michel P, Montoto-Grillot C, Ducreux M (2011). "FOLFIRINOX versus gemcitabine for metastatic pancreatic cancer". N Engl J Med. 364 (19): 1817–25. doi:10.1056/NEJMoa1011923. PMID 21561347.
  10. ↑ 10.0 10.1 Von Hoff DD, Ervin T, Arena FP, Chiorean EG, Infante J, Moore M, Seay T, Tjulandin SA, Ma WW, Saleh MN, Harris M, Reni M, Dowden S, Laheru D, Bahary N, Ramanathan RK, Tabernero J, Hidalgo M, Goldstein D, Van Cutsem E, Wei X, Iglesias J, Renschler MF (2013). "Increased survival in pancreatic cancer with nab-paclitaxel plus gemcitabine". N Engl J Med. 369 (18): 1691–1703. doi:10.1056/NEJMoa1304369.
  11. ↑ Wainberg ZA, Melisi D, Macarulla T, Pazo Cid R, Chandana SR, De La Fouchardière C, Dean A, Kiss I, Lee WJ, Goetze TO, Van Cutsem E, Paulson AS, Bekaii-Saab T, Pant S, Hubner RA, Xiao Z, Chen H, Benzaghou F, O'Reilly EM (2023). "NALIRIFOX versus nab-paclitaxel and gemcitabine in treatment-naive patients with metastatic pancreatic ductal adenocarcinoma (NAPOLI 3): a randomised, open-label, phase 3 trial". Lancet. 402 (10409): 1272–1281. doi:10.1016/S0140-6736(23)01366-1. PMID 37708904 Check |pmid= value (help).
  12. ↑ 12.0 12.1 12.2 Nichetti F, Rota S, Ambrosini P, et al. (2024). "NALIRIFOX, FOLFIRINOX, and Gemcitabine With Nab-Paclitaxel as First-Line Chemotherapy for Metastatic Pancreatic Cancer: A Systematic Review and Meta-Analysis". JAMA Netw Open. 7 (1): e2350756. doi:10.1001/jamanetworkopen.2023.50756.
  13. ↑ 13.0 13.1 13.2 13.3 Kindler HL, Hammel P, Reni M, Van Cutsem E, Macarulla T, Hall MJ, Park JO, Hochhauser D, Arnold D, Oh DY, Reinacher-Schick A, Tortora G, Algül H, O'Reilly EM, Bordia S, McGuinness D, Cui K, Locker GY, Golan T (2022). "Overall Survival Results From the POLO Trial: A Phase III Study of Active Maintenance Olaparib Versus Placebo for Germline BRCA-Mutated Metastatic Pancreatic Cancer". J Clin Oncol. 40 (34): 3929–3939. doi:10.1200/JCO.21.01604.
  14. ↑ 14.0 14.1 Wang-Gillam A, Li CP, Bodoky G, Dean A, Shan YS, Jameson G, Macarulla T, Lee KH, Cunningham D, Blanc JF, Hubner RA, Chiu CF, Schwartsmann G, Siveke JT, Braiteh F, Moyo V, Belanger B, Dhindsa N, Bayever E, Von Hoff DD, Chen LT (2016). "Nanoliposomal irinotecan with fluorouracil and folinic acid in metastatic pancreatic cancer after previous gemcitabine-based therapy (NAPOLI-1): a global, randomised, open-label, phase 3 trial". Lancet. 387 (10018): 545–57. doi:10.1016/S0140-6736(15)00986-1. PMID 26615328.
  15. ↑ 15.0 15.1 Wang J, Yang J, Narang A, et al. (2024). "Consensus, debate, and prospective on pancreatic cancer treatments". J Hematol Oncol. 17 (1): 92. doi:10.1186/s13045-024-01613-x.
  16. ↑ 16.0 16.1 16.2 16.3 Roth S, Apte M, Balachandran VP, et al. (2026). "Pancreatic cancer". Nat Rev Dis Primers. 12 (1): 23. doi:10.1038/s41572-026-00699-6.
  17. ↑ American Association for Cancer Research. FDA Approves Daraxonrasib as First RAS Inhibitor for Pancreatic Cancer. August 2026. https://www.aacr.org/?p=1025799
  18. ↑ The ASCO Post. FDA Approves Daraxonrasib for Metastatic Pancreatic Adenocarcinoma. August 2026. https://www.ascopost.com/news/august-2026/fda-approves-daraxonrasib-for-metastatic-pancreatic-adenocarcinoma/
  19. ↑ 19.0 19.1 American Gastroenterological Association. FDA approves first RAS-targeted therapy for metastatic pancreatic cancer. AGA News. August 2026. https://news.gastro.org/issues/2026/august-2026/fda-approves-first-rastargeted-therapy-for-metastatic-pancreatic-cancer/
  20. ↑ Fivaz M, Bornand A, Corro C, Koessler T, Genoud V (2025). "Actionable Mutations in Pancreatic Cancer: Where Targeted Therapies Are Making a Difference". BMJ Open Gastroenterol. 12 (1): e001925. doi:10.1136/bmjgast-2025-001925.
  21. ↑ 21.0 21.1 Conroy T, Hammel P, Hebbar M, Ben Abdelghani M, Wei AC, Raoul JL, et al. (2018). "FOLFIRINOX or Gemcitabine as Adjuvant Therapy for Pancreatic Cancer". N Engl J Med. 379 (25): 2395–2406. doi:10.1056/NEJMoa1809775. PMID 30575490.
  22. ↑ Conroy T, Castan F, Lopez A, Turpin A, Ben Abdelghani M, Wei AC, Mitry E, Biagi JJ, Evesque L, Artru P, Lecomte T, Assenat E, Bauguion L, Ychou M, Bouché O, Monard L, Lambert A, Hammel P (2022). "Five-Year Outcomes of FOLFIRINOX vs Gemcitabine as Adjuvant Therapy for Pancreatic Cancer: A Randomized Clinical Trial". JAMA Oncol. 8 (11): 1571–1578. doi:10.1001/jamaoncol.2022.3829. PMID 36048453 Check |pmid= value (help).
  23. ↑ Witz A, Conroy T, Lambert A, et al. (2026). "Impact of Tumor Genomic Profile on Adjuvant Chemotherapy Efficacy in Resected Pancreatic Adenocarcinoma: Results From the PRODIGE-24/CCTG PA6 Study". J Clin Oncol. 44 (26): 2517–2528. doi:10.1200/JCO-25-02508.
  24. ↑ Neoptolemos JP, Palmer DH, Ghaneh P, Psarelli EE, Valle JW, Halloran CM, et al. (2017). "Comparison of adjuvant gemcitabine and capecitabine with gemcitabine monotherapy in patients with resected pancreatic cancer (ESPAC-4): a multicentre, open-label, randomised, phase 3 trial". Lancet. 389 (10073): 1011–1024. doi:10.1016/S0140-6736(16)32409-6. PMID 28129987.
  25. ↑ 25.0 25.1 25.2 25.3 Janssen QP, van Dam JL, van Bekkum ML, et al. (2025). "Neoadjuvant FOLFIRINOX Versus Neoadjuvant Gemcitabine-Based Chemoradiotherapy in Resectable and Borderline Resectable Pancreatic Cancer (PREOPANC-2): A Multicentre, Open-Label, Phase 3 Randomised Trial". Lancet Oncol. 26 (10): 1346–1356. doi:10.1016/S1470-2045(25)00363-8.
  26. ↑ 26.0 26.1 Reni M, Macchini M, Orsi G, et al. (2026). "Preoperative mFOLFIRINOX Versus PAXG for Stage I-III Resectable and Borderline Resectable Pancreatic Ductal Adenocarcinoma (PACT-21 CASSANDRA): Results of the First Randomisation Analysis of a Randomised, Open-Label, 2 × 2 Factorial Phase 3 Trial". Lancet. 406 (10522): 2945–2956. doi:10.1016/S0140-6736(25)01685-X.
  27. ↑ Hammel P, Huguet F, van Laethem JL, Goldstein D, Glimelius B, Artru P, Borbath I, Bouché O, Shannon J, André T, Mineur L, Chibaudel B, Bonnetain F, Louvet C (2016). "Effect of Chemoradiotherapy vs Chemotherapy on Survival in Patients With Locally Advanced Pancreatic Cancer Controlled After 4 Months of Gemcitabine With or Without Erlotinib: The LAP07 Randomized Clinical Trial". JAMA. 315 (17): 1844–53. doi:10.1001/jama.2016.4324. PMID 27139057.
  28. ↑ Reddy NK, Subbiah V (2024). "Redefining Pancreatic Cancer Management With Tumor-Agnostic Precision Medicine". Carcinogenesis. 45 (11): 836–844. doi:10.1093/carcin/bgae066.


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