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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] Roukoz A. Karam, M.D.[3]; Saarah T. Alkhairy, M.D.; Elliot B. Tapper, M.D.

Overview

Systemic therapy for colorectal cancer (CRC) includes:

Surgical resection is the foundation of curative treatment, and radiation is used for rectal but not colon cancer; both are covered in their own microchapters. Drug selection is now biomarker-driven. Before systemic therapy for advanced disease, NCCN requires testing for:[1]

  • KRAS, NRAS, and BRAF V600E mutations
  • HER2 (ERBB2) amplification/overexpression
  • Mismatch-repair/microsatellite instability (MMR/MSI) status

Multigene panel testing is preferred because it also detects rare actionable alterations (POLE/POLD1, RET, and NTRK fusions).[1] Primary tumor sidedness determines the value of anti-EGFR therapy.[2] Pretreatment DPYD genotyping is now part of fluoropyrimidine safety.[3]

Medical Therapy

General Principles and Pretreatment Testing

Biomarker testing

  • At diagnosis of metastatic disease, order MMR/MSI, extended RAS (KRAS/NRAS), BRAF V600E, and HER2 testing as soon as possible, preferably by multigene panel. Results guide nearly every first-line decision.[1]
  • Obtain MMR/MSI status on all stage II–III tumors. It identifies stage II patients to observe and stage III patients eligible for adjuvant immunotherapy.[1]
  • Test stage II–III tumors for somatic PI3K-pathway alterations when adjuvant aspirin is being considered.[1]

DPYD pharmacogenetic testing

  • Mechanism: dihydropyrimidine dehydrogenase (DPD), encoded by DPYD, is the rate-limiting enzyme in fluorouracil (5-FU) and capecitabine catabolism.
  • Frequency and risk: about 3–8% of patients carry a deleterious DPYD variant. This causes partial DPD deficiency and a markedly increased risk of severe, occasionally fatal, toxicity.[4]
  • Actionable variants:[1]
    • DPYD*2A (c.1905+1G>A)
    • c.2846A>T
    • DPYD*13 (c.1679T>G)
    • HapB3 tagging variant c.1236G>A
  • FDA labeling for capecitabine and 5-FU (updated February 2026):[3]
    • Boxed warning: test for DPYD variants before starting therapy unless immediate treatment is required.
    • Avoid use in complete DPD deficiency (homozygous or compound heterozygous no-function variants).
    • Individualize dosing with close monitoring in partial deficiency.
  • Dosing in intermediate metabolizers (activity score 1–1.5): CPIC-aligned practice is to start at 50% of the standard dose and titrate to tolerance.[5]
  • Limits of a negative test: a negative targeted assay excludes only the variants tested. Actionable European-derived variants were about 10-fold less frequent in admixed Mexican patients, so standard panels may perform poorly in Hispanic/Latino populations.[6]

Other drug-specific safety considerations

  • Irinotecan: use cautiously in Gilbert syndrome or with elevated bilirubin. UGT1A1 testing is available, but routine thresholds are not established.[1]
  • Oxaliplatin: causes cumulative, duration-dependent sensory peripheral neuropathy. In metastatic disease, strongly consider stopping oxaliplatin after 3–4 months while continuing the fluoropyrimidine with or without a biologic.[1]
  • Anti-angiogenic agents: hold for at least 28 days before elective surgery, and for at least 28 days after surgery until wound healing.

Adjuvant Therapy for Resected Colon Cancer

  • Irinotecan, bevacizumab, and anti-EGFR antibodies have no role in the adjuvant setting.[1]
  • Adjuvant recommendations do not differ by age. Younger patients often receive more intensive therapy without proportional survival gain and with more neuropathy.[7]
Adjuvant systemic therapy by stage (resected colon cancer)
Stage / subgroup Recommended approach Key notes
Stage 0–I Resection alone. No chemotherapy.[1] —
Stage II, average/good risk (pMMR) Observation preferred.[1][8] —
Stage II, high risk (pMMR) Consider a fluoropyrimidine (capecitabine or 5-FU/leucovorin) for 6 months.
FOLFOX is reasonable only with multiple high-risk factors.[1] 		High-risk features:[1]
• T4
• Poorly differentiated or undifferentiated histology (excluding MSI-H)
• Lymphovascular or perineural invasion
• Obstruction or perforation
• <12 nodes examined
• Close or positive margins
• High-tier tumor budding
Oxaliplatin has no proven survival benefit in stage II overall.
Stage II, dMMR/MSI-H Observe.[1][7] Favorable prognosis. No benefit from single-agent fluoropyrimidine.
Stage III, low risk (T1–3, N1), pMMR CAPEOX for 3 months (preferred), or FOLFOX for 3–6 months.[1] Supported by IDEA and SCOT.
Stage III, high risk (T4, N1–2, or any T, N2), pMMR FOLFOX for 6 months, or CAPEOX for 3–6 months.[1] 3 months of FOLFOX is inferior.
Stage III, dMMR/MSI-H mFOLFOX6 or CAPEOX plus atezolizumab (preferred).[1] ATOMIC: 3-year DFS 86.4% vs. 76.6% (HR 0.50).[1]
Stage II–III with somatic PI3K-pathway alteration (PIK3CA exon 9/20 and others, PIK3R1, PTEN) Aspirin 100–162 mg daily for 3 years after surgical recovery, unless contraindicated.[1] Given in addition to indicated chemotherapy.

Stage III: regimen and duration

  • Regimen: oxaliplatin-based doublets (FOLFOX or CAPEOX/CAPOX) are standard and superior to fluoropyrimidine alone. Adjuvant FOLFOX reduced the absolute risk of death by about 4% (MOSAIC).[7]
  • IDEA collaboration (pooled analysis of 6 phase III trials, 12,834 patients):[9]
    • Non-inferiority of 3 vs. 6 months was not confirmed overall.
    • A prespecified regimen interaction supported 3 months of CAPOX but not 3 months of FOLFOX.
  • Neurotoxicity: grade ≥3 neurotoxicity is far lower with 3 vs. 6 months (FOLFOX 3% vs. 16%; CAPEOX 3% vs. 9%).[1]
  • SCOT final analysis (largest IDEA trial, CAPOX-predominant): 3 months was non-inferior to 6 months for both DFS and OS. This supports 3-month CAPEOX for most patients.[10]
  • ASCO recommends 6 months for high-risk stage III and shared decision-making for lower-risk disease.[11]

Rectal Cancer: Neoadjuvant and Perioperative Systemic Therapy

  • All patients require pelvic MRI staging. The tumor's relationship to the mesorectal fascia/circumferential resection margin is the dominant local-recurrence risk factor.[12]
  • Radiation technique and surgery are covered in their own microchapters.
Rectal cancer: systemic therapy strategy by risk and MMR status
Clinical scenario Approach Supporting data
Stage II–III pMMR/MSS with high-risk features (T4, N2, EMVI+, threatened MRF) or low rectal tumor Total neoadjuvant therapy (TNT): all chemotherapy and chemoradiation before surgery (NCCN category 1).[13]
ASCO prefers:[14]
• Chemotherapy sequenced after radiation
• Long-course chemoradiation over short-course RT 		pCR roughly doubles with TNT:
• RAPIDO: 28.4% vs. 14.3%[15]
• PRODIGE 23: 27.5% vs. 11.7%[16]
TNTCRT (doublet long-course TNT vs. conventional chemoradiation): 3-year DFS 74.8% vs. 66.0%.[17]
Lower-risk pMMR (cT2N1, cT3N0, cT3N1; mid/upper rectum; sphincter-sparing candidate; MRF uninvolved) Neoadjuvant FOLFOX, with chemoradiation reserved for poor responders (PROSPECT). PROSPECT, FOLFOX vs. chemoradiation:[18]
• Only ~9% needed radiation
• 5-year local recurrence 1.8% vs. 1.6%
• 5-year DFS 80.8% vs. 78.6%
FOLFOX gave less diarrhea and better bowel function, but more neuropathy, nausea, and fatigue.[19]
dMMR/MSI-H locally advanced rectal cancer PD-1 checkpoint inhibitor for up to 6 months: preferred neoadjuvant/definitive therapy.
Nonoperative "watch-and-wait" management for complete responders at experienced centers.[13] 		Single-agent dostarlimab gave clinical complete response (cCR) in all initial patients, without chemoradiation or surgery.[20]
In the expanded cohort, all 49 rectal patients who completed treatment had cCR and chose nonoperative management.[21]
Assess response closely with MRI, endoscopy, digital rectal examination, and biopsy, as in the pivotal study.[20]
  • Postoperative chemotherapy: FOLFOX or CAPEOX completes perioperative therapy when it was not given entirely before surgery. Total perioperative duration generally should not exceed about 6 months.
  • SCOT rectal subgroup: 3 months of adjuvant oxaliplatin doublet was non-inferior for OS in 1,087 patients with rectal cancer.[10]

Metastatic Colorectal Cancer

First-line therapy is selected by MMR/MSI status, extended RAS/BRAF status, HER2 status, and primary tumor sidedness.[22]

Chemotherapy backbone (pMMR/MSS)

  • Options are FOLFOX, CAPEOX, or FOLFIRI doublets, or triplet FOLFOXIRI in fit patients.
  • Intensity is tailored to performance status and goals, such as conversion to resectability.[1]
  • FOLFOXIRI plus bevacizumab is a preferred induction regimen for initially unresectable, right-sided or RAS/BRAF-mutant, liver-limited disease (CAIRO5).[23]

Biomarker-directed therapy

Metastatic CRC: biomarker-directed systemic therapy
Molecular subgroup Preferred therapy Key evidence and notes
dMMR/MSI-H (~4–5% of mCRC) First line: immunotherapy.
• Pembrolizumab, or
• Nivolumab + ipilimumab 		KEYNOTE-177: pembrolizumab PFS 16.5 vs. 8.2 months with chemotherapy.[24]
CheckMate 8HW: nivolumab + ipilimumab gave longer PFS than chemotherapy (24-month PFS 72% vs. 14%).[25] It also gave longer PFS than nivolumab alone.[26]
About 25% show intrinsic resistance to immunotherapy, less often with dual PD-1/CTLA-4 blockade (12% vs. 31%).[27]
RAS/BRAF mutations do not preclude benefit.
RAS/BRAF wild-type, left-sided, pMMR Chemotherapy doublet + anti-EGFR antibody (cetuximab or panitumumab).[2] OS with cetuximab, left vs. right: 37.5 vs. 16.4 months.[28][2]
NCCN lists bevacizumab as a parallel option.[1]
RAS/BRAF wild-type right-sided, or RAS-mutant, pMMR Chemotherapy + bevacizumab (preferred anti-VEGF).[1] Right-sided tumors do not benefit from first-line anti-EGFR therapy.[2]
Bevacizumab can be used regardless of sidedness or RAS status and may be continued across lines.[1]
BRAF V600E (~8–10%; aggressive; mostly right-sided) First line: encorafenib + cetuximab + mFOLFOX6 (preferred), or encorafenib + cetuximab + FOLFIRI.
Previously treated: encorafenib + cetuximab or panitumumab (BEACON).[2] 		BREAKWATER: median OS 30.3 vs. 15.1 months (HR 0.49), with significant PFS improvement.[29]
BREAKWATER Cohort 3 showed similar benefit with FOLFIRI.[30]
Ensure an encorafenib-containing regimen is given in at least one line.
HER2-amplified, RAS/BRAF wild-type Trastuzumab + pertuzumab, or trastuzumab + tucatinib.
Fam-trastuzumab deruxtecan-nxki for HER2 IHC 3+.[1] 		Anti-EGFR therapy is ineffective.
Monitor for interstitial lung disease with trastuzumab deruxtecan.[1]
KRAS G12C Adagrasib + cetuximab, or sotorasib + panitumumab[1] Used after prior fluoropyrimidine, oxaliplatin, and irinotecan.[1]
Tumor-agnostic alterations • MSI-H/TMB-high: pembrolizumab or dostarlimab
• NTRK fusion: larotrectinib, entrectinib, or repotrectinib
• RET fusion: selpercatinib

Biologic-specific rules

  • Anti-EGFR antibodies (cetuximab, panitumumab):[1][2]
    • Use only for KRAS/NRAS/BRAF wild-type, left-sided tumors.
    • Do not continue an EGFR inhibitor beyond progression.
    • Do not switch to the other EGFR antibody at progression.
  • Anti-VEGF agents:[1]

Refractory disease

Targeted-agent dosing

Selected targeted-agent dosing in mCRC
Drug Dose
Encorafenib 300 mg PO once daily[1]
Cetuximab 400 mg/m² IV loading dose, then 250 mg/m² weekly; or 500 mg/m² every 2 weeks[1]
Panitumumab 6 mg/kg IV every 14 days[1]
Fam-trastuzumab deruxtecan-nxki 5.4 mg/kg IV every 21 days[1]

Supportive and Palliative Care

  • Standard care includes:
    • Early integration of palliative care
    • Management of chemotherapy toxicity
    • Nutritional and psychosocial support
  • Quality of life deserves particular attention, given the morbidity of multimodality rectal therapy and the chronic nature of metastatic treatment.

Areas of Uncertainty and Guideline Disagreement

  • 3-month FOLFOX vs. 3-month CAPEOX: non-inferiority was shown for CAPOX, not FOLFOX. Clinicians choosing FOLFOX generally give 6 months, although absolute OS differences are modest.[9][10]
  • First-line biologic in left-sided RAS/BRAF wild-type disease:
    • ASCO favors anti-EGFR therapy.[2]
    • NCCN lists anti-EGFR and bevacizumab options in parallel.[1]
    • In CAIRO5, panitumumab gave no PFS or resection advantage over bevacizumab in left-sided, wild-type, liver-limited disease.[23]
  • Nonoperative management: durability and patient selection remain under study. Combining MRI with ctDNA may improve cCR assessment, but standardized response criteria are still evolving.[31]
  • ctDNA is prognostic but not yet validated to guide escalation or de-escalation outside trials.[1]
  • Combination vs. single-agent immunotherapy in dMMR/MSI-H mCRC: nivolumab + ipilimumab improved PFS over nivolumab alone. Whether this justifies the added CTLA-4–related toxicity for every patient remains a clinical judgment.[26]
  • DPYD policy: pretreatment testing has long been standard in much of Europe. U.S. labeling now recommends testing, but genotype-based dose guidance remains less prescriptive.[32][3]
  • pMMR/MSS disease: immune checkpoint inhibitors have limited efficacy. Combination strategies yield modest improvements without validated biomarkers.[33]

Common Pitfalls

  • Giving anti-EGFR therapy to RAS-mutant, BRAF V600E (without encorafenib), HER2-amplified, or right-sided tumors.[2][1]
  • Continuing or switching EGFR antibodies after progression.[1]
  • Giving full-dose fluoropyrimidine without DPYD testing.[3]
  • Using irinotecan, bevacizumab, or anti-EGFR agents as adjuvant therapy.[1]
  • Giving 3 months of FOLFOX for high-risk stage III disease.[1]
  • Omitting MMR/MSI testing, which misses immunotherapy candidates and leads to over-treatment of favorable stage II disease.[1]
  • Treating colon cancer with chemoradiation.[1]
  • Combining bevacizumab with an EGFR inhibitor.

References

  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 1.32 1.33 1.34 1.35 1.36 1.37 1.38 1.39 1.40 1.41 1.42 National Comprehensive Cancer Network. NCCN Clinical Practice Guidelines in Oncology: Colon Cancer. Version 2.2026. https://www.nccn.org/guidelines/category_1
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 Morris VK, Kennedy EB, Baxter NN; et al. (2023). "Treatment of Metastatic Colorectal Cancer: ASCO Guideline". J Clin Oncol. 41 (3): 678–700. doi:10.1200/JCO.22.01690. PMID 36252154 Check |pmid= value (help).
  3. ↑ 3.0 3.1 3.2 3.3 U.S. Food and Drug Administration. Safety labeling update for capecitabine and fluorouracil (5-FU) on risks associated with dihydropyrimidine dehydrogenase (DPD) deficiency. February 5, 2026. https://www.fda.gov/drugs/resources-information-approved-drugs/safety-labeling-update-capecitabine-and-fluorouracil-5-fu-risks-associated-dihydropyrimidine
  4. ↑ Henricks LM, Lunenburg CATC, de Man FM; et al. (2018). "DPYD genotype-guided dose individualisation of fluoropyrimidine therapy in patients with cancer: a prospective safety analysis". Lancet Oncol. 19 (11): 1459–1467. doi:10.1016/S1470-2045(18)30686-7. PMID 30348537.
  5. ↑ Pratt VM, Cavallari LH, Fulmer ML; et al. (2024). "DPYD Genotyping Recommendations: A Joint Consensus Recommendation of the Association for Molecular Pathology, American College of Medical Genetics and Genomics, Clinical Pharmacogenetics Implementation Consortium, College of American Pathologists, Dutch Pharmacogenetics Working Group of the Royal Dutch Pharmacists Association, European Society for Pharmacogenomics and Personalized Therapy, Pharmacogenomics Knowledgebase, and Pharmacogene Variation Consortium". J Mol Diagn. 26 (10): 851–863. doi:10.1016/j.jmoldx.2024.05.015. PMID 39032821 Check |pmid= value (help).
  6. ↑ Gonzalez-Covarrubias V, Morales-Alfaro A, Bonilla-Jimenez O, Rodríguez-Dorantes M, Frías-Jimenez E, Soto-Perez-de-Celis E (2026). "Characterization of DPYD pharmacogenetic variation in Mexican patients with gastrointestinal malignancies". Cancer Chemother Pharmacol.
  7. ↑ 7.0 7.1 7.2 Eng C, Jácome AA, Agarwal R; et al. (2022). "A comprehensive framework for early-onset colorectal cancer research". Lancet Oncol. 23 (3): e116–e128. doi:10.1016/S1470-2045(21)00588-X. PMID 35090673 Check |pmid= value (help).
  8. ↑ Baxter NN, Kennedy EB, Bergsland E; et al. (2022). "Adjuvant Therapy for Stage II Colon Cancer: ASCO Guideline Update". J Clin Oncol. 40 (8): 892–910. doi:10.1200/JCO.21.02538. PMID 34936379 Check |pmid= value (help).
  9. ↑ 9.0 9.1 André T, Meyerhardt J, Iveson T; et al. (2020). "Effect of duration of adjuvant chemotherapy for patients with stage III colon cancer (IDEA collaboration): final results from a prospective, pooled analysis of six randomised, phase 3 trials". Lancet Oncol. 21 (12): 1620–1629. doi:10.1016/S1470-2045(20)30527-1. PMID 33271092 Check |pmid= value (help).
  10. ↑ 10.0 10.1 10.2 Iveson T, Saunders MP, Kelly C; et al. (2026). "Three Versus 6 Months of Adjuvant Oxaliplatin-Fluoropyrimidine Chemotherapy for Colorectal Cancer: Final Results of SCOT—An International, Randomized, Phase III, Noninferiority Trial". J Clin Oncol. 44 (7): 534–539. doi:10.1200/JCO-25-00621. PMID 41512219 Check |pmid= value (help).
  11. ↑ Lieu C, Kennedy EB, Bergsland E; et al. (2019). "Duration of Oxaliplatin-Containing Adjuvant Therapy for Stage III Colon Cancer: ASCO Clinical Practice Guideline". J Clin Oncol. 37 (16): 1436–1447. doi:10.1200/JCO.19.00281. PMID 30986117.
  12. ↑ Wo JY, Ashman JB, Bhadkamkar NA; et al. (2025). "Radiation Therapy for Rectal Cancer: An ASTRO Clinical Practice Guideline Focused Update". Pract Radiat Oncol. doi:10.1016/j.prro.2024.11.003. PMID 39603501 Check |pmid= value (help).
  13. ↑ 13.0 13.1 National Comprehensive Cancer Network. NCCN Clinical Practice Guidelines in Oncology: Rectal Cancer. Version 2.2026. https://www.nccn.org/guidelines/category_1
  14. ↑ Scott AJ, Kennedy EB, Berlin J; et al. (2024). "Management of Locally Advanced Rectal Cancer: ASCO Guideline". J Clin Oncol. 42 (28): 3355–3375. doi:10.1200/JCO.24.01160. PMID 39116386 Check |pmid= value (help).
  15. ↑ Bahadoer RR, Dijkstra EA, van Etten B; et al. (2021). "Short-course radiotherapy followed by chemotherapy before total mesorectal excision (TME) versus preoperative chemoradiotherapy, TME, and optional adjuvant chemotherapy in locally advanced rectal cancer (RAPIDO): a randomised, open-label, phase 3 trial". Lancet Oncol. 22 (1): 29–42. doi:10.1016/S1470-2045(20)30555-6. PMID 33301740 Check |pmid= value (help).
  16. ↑ Conroy T, Bosset JF, Etienne PL; et al. (2021). "Neoadjuvant chemotherapy with FOLFIRINOX and preoperative chemoradiotherapy for patients with locally advanced rectal cancer (UNICANCER-PRODIGE 23): a multicentre, randomised, open-label, phase 3 trial". Lancet Oncol. 22 (5): 702–715.
  17. ↑ Wang X, Tang Y, Lu J; et al. (2026). "Total Neoadjuvant Therapy With Long-Course Radiotherapy Versus Chemoradiotherapy in High-Risk Locally Advanced Rectal Cancer (TNTCRT): A Multicenter, Randomized, Phase III Trial". J Clin Oncol. ClinicalTrials.gov NCT03177382.
  18. ↑ Schrag D, Shi Q, Weiser MR; et al. (2023). "Preoperative Treatment of Locally Advanced Rectal Cancer". N Engl J Med. 389 (4): 322–334. doi:10.1056/NEJMoa2303269. PMID 37272534 Check |pmid= value (help).
  19. ↑ Basch E, Dueck AC, Mitchell SA; et al. (2023). "Patient-Reported Outcomes During and After Treatment for Locally Advanced Rectal Cancer in the PROSPECT Trial (Alliance N1048)". J Clin Oncol. 41 (21): 3724–3734. PMID 37270691 Check |pmid= value (help).
  20. ↑ 20.0 20.1 Cercek A, Lumish M, Sinopoli J; et al. (2022). "PD-1 Blockade in Mismatch Repair-Deficient, Locally Advanced Rectal Cancer". N Engl J Med. 386 (25): 2363–2376. doi:10.1056/NEJMoa2201445. PMID 35660797 Check |pmid= value (help).
  21. ↑ Cercek A, Foote MB, Rousseau B; et al. (2025). "Nonoperative Management of Mismatch Repair-Deficient Tumors". N Engl J Med. 392 (23): 2297–2308. doi:10.1056/NEJMoa2404512. PMID 40293177 Check |pmid= value (help).
  22. ↑ Bando H, Ohtsu A, Yoshino T (2023). "Therapeutic landscape and future direction of metastatic colorectal cancer". Nat Rev Gastroenterol Hepatol. 20 (5): 306–322. doi:10.1038/s41575-022-00736-1. PMID 36670267 Check |pmid= value (help).
  23. ↑ 23.0 23.1 Bond MJG, Bolhuis K, Loosveld OJL; et al. (2023). "First-line systemic treatment strategies in patients with initially unresectable colorectal cancer liver metastases (CAIRO5): an open-label, multicentre, randomised, controlled, phase 3 study from the Dutch Colorectal Cancer Group". Lancet Oncol. 24 (7): 757–771. doi:10.1016/S1470-2045(23)00219-X. PMID 37329889 Check |pmid= value (help).
  24. ↑ André T, Shiu KK, Kim TW; et al. (2020). "Pembrolizumab in Microsatellite-Instability-High Advanced Colorectal Cancer". N Engl J Med. 383 (23): 2207–2218. doi:10.1056/NEJMoa2017699. PMID 33264544 Check |pmid= value (help).
  25. ↑ André T, Elez E, Van Cutsem E; et al. (2024). "Nivolumab plus Ipilimumab in Microsatellite-Instability-High Metastatic Colorectal Cancer". N Engl J Med. 391 (21): 2014–2026. doi:10.1056/NEJMoa2402141. PMID 39602630 Check |pmid= value (help).
  26. ↑ 26.0 26.1 André T, Elez E, Lenz HJ; et al. (2025). "Nivolumab plus ipilimumab versus nivolumab in microsatellite instability-high metastatic colorectal cancer (CheckMate 8HW): a randomised, open-label, phase 3 trial". Lancet. 405 (10476): 383–395. doi:10.1016/S0140-6736(24)02848-4. PMID 39874977 Check |pmid= value (help).
  27. ↑ Wang R, Lian J, Wang X; et al. (2023). "Intrinsic resistance and efficacy of immunotherapy in microsatellite instability-high colorectal cancer: A systematic review and meta-analysis". Biomol Biomed. 23 (2): 198–208. doi:10.17305/bjbms.2022.8286. PMID 36408953 Check |pmid= value (help).
  28. ↑ Dekker E, Tanis PJ, Vleugels JLA; et al. (2019). "Colorectal cancer". Lancet. 394 (10207): 1467–1480. doi:10.1016/S0140-6736(19)32319-0. PMID 31631858.
  29. ↑ Elez E, Yoshino T, Shen L; et al. (2025). "Encorafenib, Cetuximab, and mFOLFOX6 in BRAF-Mutated Colorectal Cancer". N Engl J Med. 392 (24): 2425–. doi:10.1056/NEJMoa2501912.
  30. ↑ Kopetz S, Tabernero J, Lonardi S; et al. (2026). "A randomised study of encorafenib, cetuximab, and FOLFIRI versus FOLFIRI with or without bevacizumab in BRAF V600E-mutant colorectal cancer: BREAKWATER Cohort 3". Ann Oncol. doi:10.1016/j.annonc.2026.04.017.
  31. ↑ Huang P, Zhao X, Fei H; et al. (2026). "Watch-and-Wait strategy for locally advanced rectal cancer after neoadjuvant chemoradiotherapy: a comprehensive review". Front Oncol. 16: 1760042. doi:10.3389/fonc.2026.1760042.
  32. ↑ Hertz DL; et al. (2023). "Response to the FDA Decision Regarding DPYD Testing Prior to Fluoropyrimidine Chemotherapy". Clin Pharmacol Ther. doi:10.1002/cpt.2978.
  33. ↑ Guven DC, Kavgaci G, Erul E; et al. (2024). "The Efficacy of Immune Checkpoint Inhibitors in Microsatellite Stable Colorectal Cancer: A Systematic Review". Oncologist. 29. doi:10.1093/oncolo/oyae013.
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