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Colon Cancer

A plain-English summary of the published research on Colon Cancer, reviewed and approved by our editors — not a hand-curated clinical overview.

Research summary · reviewed
Educational only: This page is not medical advice. Coordinate decisions with your oncology team.

Reviewed Jun 2026 · OncoForge editorial · How we review →

AI extractedhuman reviewedsources checkedretractions suppressed· last updated Jun 2026

Evidence at a glanceHuman trial / meta-analysisMixed results⚠ Studies disagree
52 published studies that name Colon Cancer7 human studies approved & graded (trial, observational, or meta-analysis)247 human clinical studies in the Colon Cancer corpus2345 source documents in the Colon Cancer corpus

last checked June 20, 2026

Why this grade?

Human trial / meta-analysis — Includes human trial or meta-analysis evidence.

Computed deterministically from the studies’ types and reported outcomes — not written by AI, and not a claim that anything works.

What the guidelines say

NCI PDQESMONCCNASCO

We link the authoritative guidelines rather than reproduce them. Below, the treatments on this page are split into standard care, guideline or regulatory options, supportive care, and studied but not standard so established care is not mixed with experimental or supportive items.

Guideline / FDA options - context-specific
  • bevacizumab
Studied, not standard - investigational
  • complete mesocolic excision (CME)
  • standard high-quality right hemicolectomy
  • immune checkpoint inhibitors
  • HER2-targeted therapy
  • BRAF V600E-targeted therapy
  • colonic stenting
  • chemotherapy
  • oxaliplatin
  • Oxaliplatin-containing chemotherapy
  • Oxaliplatin-containing chemotherapy (duration
  • capecitabine + oxaliplatin
  • fluorouracil + leucovorin + oxaliplatin
  • colonoscopy
  • computed tomography colonography
  • stool-based tests
  • flexible sigmoidoscopy
  • endoscopic surveillance
  • en bloc resection
  • surgical resection of liver or lung metastases
  • 5-FU-based
  • Irinotecan
  • fluorouracil

Read the guidelines

Cancer-specific deep links aren’t curated yet — these search the authoritative sources for Colon Cancer.

Treatment map: Colon Cancer

Open as a full page →

Standard care plus every compound studied in the literature (each cited) and graded by evidence, organized by clinical readiness. A category, not a verdict that anything works — confirm anything here with your oncology team.

24
Interventions
0
Standard of care
6
Tested in people
0
Lab / animal
17
Named in lit.
4
Classes
Standard of care (0) Guideline option (1) Tested in people (6) Lab / animal only (0) Named in the literature (17)

Tested in people, by trial phase: phase not reported ×6

Clinical evidence
Preclinical evidence
Standard of care
Guideline option
Tested in people
Lab / animal only
Named in the literature
Surgery & procedures
—
—
—
—
10
Chemotherapy
—
—
6
—
4
Targeted therapy
—
1
—
—
2
Immunotherapy
—
—
—
—
1

Columns group into clinical evidence (used in, or tested on, people) and preclinical evidence (lab/animal, or only named in the literature). Cell = number of interventions; a dashed cell means none recorded there.

Established care — detail (1)
Targeted therapy
bevacizumab
FDA-approved for this cancer.
—Guideline option
Investigational & adjunct compounds — detail (23)
Meta-analysis (6)
capecitabine + oxaliplatinchemotherapy· Adjuvant (after surgery)fluorouracil + leucovorin + oxaliplatinoxaliplatin· Adjuvant (after surgery)Oxaliplatin-containing chemotherapy· Adjuvant (after surgery) · mismatch repair deficiency/microsatellite instabilityOxaliplatin-containing chemotherapy (duration
Named in the literature
complete mesocolic excision (CME)standard high-quality right hemicolectomyimmune checkpoint inhibitors· First-line (advanced disease) · deficient mismatch repair/microsatellite instability-highHER2-targeted therapy· HER2-amplifiedBRAF V600E-targeted therapy· BRAF V600E mutation-positivecolonic stentingchemotherapycolonoscopycomputed tomography colonographystool-based testsflexible sigmoidoscopyendoscopic surveillanceen bloc resectionsurgical resection of liver or lung metastases5-FU-based· Adjuvant (after surgery)Irinotecanfluorouracil

"Tested in people" rows show the highest trial phase found in that compound's cited human studies (Phase I–IV; "phase not reported" = a human study with no phase tag). "Studied" = named in the cited literature for this cancer. "FDA ✓" = FDA-approved for this cancer; "off-label" = an FDA-approved drug used outside its approved indications (per openFDA). Not a claim that anything works.

Reported figures

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Snapshot

The essentials in ~60 seconds — every line is drawn from the cited sources below.

What it is
Colon cancer is cancer of the large intestine; for resectable disease the guideline-preferred operation is en bloc surgical resection. For right-sided colon cancer, complete mesocolic excision (CME) has been proposed as a surgical refinement to improve specimen quality and lymph node yield. [1][2][3]
Standard treatment
The standard initial management for resectable colon cancer is en bloc surgical resection, with standard high-quality right hemicolectomy remaining the default for most right-sided tumors rather than routine CME. Surgery is followed by adjuvant chemotherapy when indicated; patients with stage III disease are recommended to receive 5‑FU–based adjuvant chemotherapy. [1][2][3][4]
Key test
Testing for KRAS/NRAS and BRAF mutations and for tumor microsatellite instability / mismatch repair status should be considered because these biomarkers influence treatment selection and adjuvant decisions; guidelines have expanded recommendations for biomarker testing including MSI in metastatic disease. [5][4][6]
Biggest challenge
The main clinical problem is inconsistent evidence and limited randomized data plus wide variation in surgical technique and expertise for procedures such as CME, which is technically complex and has produced variable outcomes. [2][3]

Ask about Colon Cancer

Answers come only from the cited sources on this page — with the supporting evidence shown. If the sources here don't cover your question, it will say so. Educational information, not medical advice.

Key numbers & factors

Risk factors

  • ▲ increases riskLi‑Fraumeni syndrome — Highly penetrant syndrome with a high lifetime risk of cancer, including colon cancer. [7]
  • ▲ increases riskCystic fibrosis — Guidelines recommend earlier and more frequent colorectal screening (begin at age 40 and re-screen every 5 years), reflecting higher concern/impact in this population. [8]
  • ▲ increases riskT4 tumor (pathologic stage) — T4 tumors are at higher risk of recurrence and patients should be offered adjuvant chemotherapy. [4]

Biomarkers

  • KRAS/NRAS mutation statusActionableConsidered when selecting systemic therapies. [5]
  • BRAF mutation statusActionableConsidered when selecting systemic therapies. [5]
  • Microsatellite instability / mismatch repair (MSI/MMR)ActionableGuides adjuvant decisions and is used in selecting therapy for metastatic disease (deficient/MSI‑high tumors have different recommendations). [4][6][5]
  • Carcinoembryonic antigen (CEA) · Used for post‑treatment surveillance (measure every 2–3 months for at least 3 years in stage II/III patients who may be candidates for curative resection if recurrence is detected). [9]
  • Multigene panel testing (inherited pathogenic/likely pathogenic variants)ActionableDetects inherited variants that identify people at high risk and inform genetic counseling and management. [10]
  • Existing serum markers (general) · Current serum markers lack sufficient specificity and sensitivity for early detection of colorectal cancer. [9]

6 sections — tap any heading to expand its cited detail. Key points are above.

Overview9 points
  • Complete mesocolic excision (CME) has been proposed as a refinement of oncological surgery for right-sided colon cancer that aims to improve specimen quality, lymph node yield, and oncological outcomes. [2][3]
  • CME is consistently associated with higher lymph node yields and improved specimen metrics, but randomized evidence does not support routine CME for all patients; studies demonstrating a definitive survival advantage remain limited and potential benefit may exist in selected high-risk groups. [2][3]
  • NCCN/colon cancer guideline selections focus on systemic therapy options for the treatment of metastatic colorectal cancer (mCRC). [6][5]
  • CME is technically complex, involves surgical risks and a need for specialized training, and variations in technical aspects and implementation have led to inconsistent outcomes. [3]
  • This guideline effort aimed to develop evidence-informed clinical practice recommendations on CME for right-sided colon cancer, specifically to address whether laparoscopic CME should be preferred over standard laparoscopic right hemicolectomy; the guideline development adhered to GRADE, AGREE-S, and Cochrane standards and used MAGICapp for development. [3]
  • The NCCN Genetic/Familial High-Risk Assessment guideline reports an update that includes de-implementation of colon cancer screening in individuals with CHEK2 pathogenic/likely pathogenic variants. [10]
  • ASCO convened an Expert Panel to develop recommendations for adjuvant therapy for patients with resected stage II colon cancer. [4]
  • Guideline panels recommend a multidisciplinary approach to managing colorectal cancer. [1]
  • Guideline panels endorse prioritizing treating eligible patients in clinical trials over using standard or accepted therapy. [1]
Standard management19 points

Key figures

Survival & outcomes
OutcomeValue95% CI
extra life-years per 1000 vs no screening44—
extra life-years per 1000 vs no screening56—
Source quotes
  • “colonoscopy every 5 years between age 40 and 75 years. This strategy resulted in 44 extra years of life per 1000 CF patients screened at a net cost of $0.7 million compared to no screening.”
  • “For CF patients with an organ transplant, the optimal colonoscopy strategy was colonoscopy every 3 years from age 35 to 55 years. This strategy resulted in 56 extra life-years per 1000 patients screened at a net cost of $1.3 million compared to no screening.”
  • Routine use of complete mesocolic excision (CME) for all right-sided colon cancers is not supported by current evidence; standard high-quality right hemicolectomy should remain the default approach for most patients. [2][3]
  • A conditional recommendation supports use of CME for patients undergoing right hemicolectomy for right-sided colon cancer where expertise is available; the guideline judged the evidence to be of low-to-moderate certainty and found insufficient evidence to recommend CME based on tumor location or cancer stage. [3][2]
  • The Cystic Fibrosis Foundation recommends that colorectal cancer screening begin at age 40 years in individuals with cystic fibrosis with continued re-screening every 5 years; modeling predicted that colonoscopy every 5 years between age 40 and 75 years resulted in 44 extra years of life per 1000 CF patients screened compared to no screening, and for cystic fibrosis patients with an organ transplant modeling identified colonoscopy every 3 years from age 35 to 55 years as the optimal strategy and reported 56 extra life-years per 1000 patients screened compared to no screening. [8]
  • Selective use of CME may be appropriate in physiologically fit patients with high-risk or anatomically complex disease, delivered within experienced units with appropriate training, audit and quality assurance frameworks. [2]
  • The guideline panel suggested CME is acceptable to stakeholders and feasible despite potential equity issues due to variable expertise availability; a conditional recommendation indicates that the majority of well-informed patients, surgeons, and other stakeholders would opt for the recommended course of action but that discussion of benefits and harms is advised before decisions. [3]
  • This guideline provides evidence-informed recommendations on the management of right-sided colon cancer developed in line with high methodological and reporting standards and informed by an interdisciplinary panel; the full guideline and user-friendly decision aids are available online at the MAGICapp link provided by the authors. [3]
  • NCCN updates include recommendations for first-line use of checkpoint inhibitors for metastatic colorectal cancer that is deficient mismatch repair/microsatellite instability-high, recommendations related to the use of biosimilars, and expanded recommendations for biomarker testing. [6]
  • ESGE recommends colonic stenting be reserved for patients with clinical symptoms and radiological signs of malignant large-bowel obstruction, without signs of perforation, and does not recommend prophylactic stent placement. [11]
  • ESGE recommends stenting as a bridge to surgery be discussed as a treatment option in patients with potentially curable left-sided obstructing colon cancer as an alternative to emergency resection, and suggests a time interval of approximately 2 weeks until resection when colonic stenting is performed as a bridge to elective surgery in these patients. [11]
  • ESGE recommends colonic stenting as the preferred treatment for palliation of malignant colonic obstruction and suggests consideration of colonic stenting for malignant obstruction of the proximal colon either as a bridge to surgery or in a palliative setting. [11]
  • ESGE recommends that colonic stenting should be performed or directly supervised by an operator who can demonstrate competence in both colonoscopy and fluoroscopic techniques and who performs colonic stenting on a regular basis. [11]
  • ESGE suggests that a decompressing stoma as a bridge to elective surgery is a valid option if the patient is not a candidate for colonic stenting or when stenting expertise is not available. [11]
  • Treatment selection involves choices among 32 different monotherapies and combination regimens in up to seven lines of therapy; considerations for selecting among these therapies have included treatment history, extent of disease, goals of treatment, and the efficacy and toxicity profiles of the regimens, as well as patient comorbidities and preferences. [5]
  • The NCCN Rectal Cancer guideline notes that the risk of pelvic recurrence is higher in patients with rectal cancer compared with those with colon cancer. [12]
  • Adjuvant chemotherapy (ACT) is not routinely recommended for patients with stage II colon cancer who are not in a high-risk subgroup, and patients with T4 tumors are at higher risk of recurrence and should be offered ACT. [4]
  • For resectable colon cancer, guidelines recommend an en bloc surgical resection as the procedure of choice. [1]
  • Guidelines state that surgery should be followed by adjuvant chemotherapy; for patients with stage III disease they recommend 5‑FU–based adjuvant chemotherapy. [1]
  • Patients with metastatic disease in the liver or lung should be considered for surgical resection if they are surgical candidates and if surgery can extend survival. [1]
  • Guideline panels advocate a conservative post‑treatment surveillance program that includes serial CEA determinations when a patient would be a candidate for aggressive surgical resection should recurrence be detected, and that abdominal and pelvic CT scans be reserved for use only when there are clinical indications of possible recurrence. [1]
Treatments & compounds studied24 treatments

Chemotherapy

  • Adjuvant chemotherapy (ACT) · chemotherapy: Adjuvant (after surgery)Adjuvant chemotherapy (ACT) is not routinely recommended for patients with stage II colon cancer who are not in a high-risk subgroup. [4]
    recommended duration 3 vs 6 months vs 6 monthsrecommended duration 6 vs 3 months vs 3 months
    Source quotes
    • “Duration of oxaliplatin-containing chemotherapy is also addressed, with recommendations for 3 or 6 months of treatment with capecitabine and oxaliplatin or fluorouracil, leucovorin, and oxaliplatin, with decision making informed by key evidence of 5-year disease-free survival in each treatment subgroup and the rate of adverse events, including peripheral neuropathy.”
    • “Duration of oxaliplatin-containing chemotherapy is also addressed, with recommendations for 3 or 6 months of treatment with capecitabine and oxaliplatin or fluorouracil, leucovorin, and oxaliplatin, with decision making informed by key evidence of 5-year disease-free survival in each treatment subgroup and the rate of adverse events, including peripheral neuropathy.”
  • Oxaliplatin (addition to fluoropyrimidine-based ACT) · oxaliplatin: Adjuvant (after surgery)The addition of oxaliplatin to fluoropyrimidine-based adjuvant chemotherapy is not routinely recommended but may be offered as a result of shared decision making. [4]
    recommended duration 3 vs 6 months vs 6 monthsrecommended duration 6 vs 3 months vs 3 months
    Source quotes
    • “Duration of oxaliplatin-containing chemotherapy is also addressed, with recommendations for 3 or 6 months of treatment with capecitabine and oxaliplatin or fluorouracil, leucovorin, and oxaliplatin, with decision making informed by key evidence of 5-year disease-free survival in each treatment subgroup and the rate of adverse events, including peripheral neuropathy.”
    • “Duration of oxaliplatin-containing chemotherapy is also addressed, with recommendations for 3 or 6 months of treatment with capecitabine and oxaliplatin or fluorouracil, leucovorin, and oxaliplatin, with decision making informed by key evidence of 5-year disease-free survival in each treatment subgroup and the rate of adverse events, including peripheral neuropathy.”
  • Oxaliplatin-containing chemotherapy: Adjuvant (after surgery) · mismatch repair deficiency/microsatellite instabilityIf the combination of mismatch repair deficiency/microsatellite instability and high-risk factors results in a decision to offer adjuvant chemotherapy, oxaliplatin-containing chemotherapy is recommended for that situation. [4]
    recommended duration 3 vs 6 months vs 6 monthsrecommended duration 6 vs 3 months vs 3 months
    Source quotes
    • “Duration of oxaliplatin-containing chemotherapy is also addressed, with recommendations for 3 or 6 months of treatment with capecitabine and oxaliplatin or fluorouracil, leucovorin, and oxaliplatin, with decision making informed by key evidence of 5-year disease-free survival in each treatment subgroup and the rate of adverse events, including peripheral neuropathy.”
    • “Duration of oxaliplatin-containing chemotherapy is also addressed, with recommendations for 3 or 6 months of treatment with capecitabine and oxaliplatin or fluorouracil, leucovorin, and oxaliplatin, with decision making informed by key evidence of 5-year disease-free survival in each treatment subgroup and the rate of adverse events, including peripheral neuropathy.”
  • Oxaliplatin-containing chemotherapy (duration): Duration recommendations for oxaliplatin-containing chemotherapy address 3 or 6 months of treatment with capecitabine and oxaliplatin or fluorouracil, leucovorin, and oxaliplatin. [4]
    recommended duration 3 vs 6 months vs 6 monthsrecommended duration 6 vs 3 months vs 3 months
    Source quotes
    • “Duration of oxaliplatin-containing chemotherapy is also addressed, with recommendations for 3 or 6 months of treatment with capecitabine and oxaliplatin or fluorouracil, leucovorin, and oxaliplatin, with decision making informed by key evidence of 5-year disease-free survival in each treatment subgroup and the rate of adverse events, including peripheral neuropathy.”
    • “Duration of oxaliplatin-containing chemotherapy is also addressed, with recommendations for 3 or 6 months of treatment with capecitabine and oxaliplatin or fluorouracil, leucovorin, and oxaliplatin, with decision making informed by key evidence of 5-year disease-free survival in each treatment subgroup and the rate of adverse events, including peripheral neuropathy.”
  • Capecitabine and oxaliplatin: Capecitabine and oxaliplatin are named as an oxaliplatin-containing regimen for which 3 or 6 months of treatment is recommended. [4]
    recommended duration 3 vs 6 months vs 6 monthsrecommended duration 6 vs 3 months vs 3 months
    Source quotes
    • “Duration of oxaliplatin-containing chemotherapy is also addressed, with recommendations for 3 or 6 months of treatment with capecitabine and oxaliplatin or fluorouracil, leucovorin, and oxaliplatin, with decision making informed by key evidence of 5-year disease-free survival in each treatment subgroup and the rate of adverse events, including peripheral neuropathy.”
    • “Duration of oxaliplatin-containing chemotherapy is also addressed, with recommendations for 3 or 6 months of treatment with capecitabine and oxaliplatin or fluorouracil, leucovorin, and oxaliplatin, with decision making informed by key evidence of 5-year disease-free survival in each treatment subgroup and the rate of adverse events, including peripheral neuropathy.”
  • Fluorouracil, leucovorin, and oxaliplatin: Fluorouracil, leucovorin, and oxaliplatin are named as an oxaliplatin-containing regimen for which 3 or 6 months of treatment is recommended. [4]
    recommended duration 3 vs 6 months vs 6 monthsrecommended duration 6 vs 3 months vs 3 months
    Source quotes
    • “Duration of oxaliplatin-containing chemotherapy is also addressed, with recommendations for 3 or 6 months of treatment with capecitabine and oxaliplatin or fluorouracil, leucovorin, and oxaliplatin, with decision making informed by key evidence of 5-year disease-free survival in each treatment subgroup and the rate of adverse events, including peripheral neuropathy.”
    • “Duration of oxaliplatin-containing chemotherapy is also addressed, with recommendations for 3 or 6 months of treatment with capecitabine and oxaliplatin or fluorouracil, leucovorin, and oxaliplatin, with decision making informed by key evidence of 5-year disease-free survival in each treatment subgroup and the rate of adverse events, including peripheral neuropathy.”
  • 5-FU-based adjuvant therapy: Adjuvant (after surgery)5-FU-based adjuvant chemotherapy is recommended for patients with stage III disease. [1]
  • irinotecan (bolus) · Irinotecan: Patients whose disease progresses during 5-FU-based therapy are recommended to receive bolus irinotecan. [1]
  • 5-FU/leucovorin/oxaliplatin therapy · fluorouracil: Patients who progress on irinotecan are candidates for 5-FU/leucovorin/oxaliplatin therapy or for enrollment in a phase I or phase II clinical trial. [1]

Targeted therapy

  • HER2-targeted therapy: HER2-amplifiedHER2-targeted therapy options are included for patients with metastatic colorectal cancer that is HER2-amplified. [6]
  • BRAF V600E-targeted therapy: BRAF V600E mutation-positiveBRAF V600E-targeted therapy options are included for patients with metastatic colorectal cancer that is BRAF V600E mutation-positive. [6]

Immunotherapy

  • checkpoint inhibitors · immune checkpoint inhibitors: First-line (advanced disease) · deficient mismatch repair/microsatellite instability-highCheckpoint inhibitors are recommended for first-line use in metastatic colorectal cancer that is deficient mismatch repair/microsatellite instability-high. [6]

Repurposed drugs

  • thrombopoietin receptor agonists (TPO-RAs): Thrombopoietin receptor agonists (TPO-RAs) have been shown in studies to improve platelet counts in chemotherapy-induced thrombocytopenia in solid tumors, but their clinical benefits in reducing bleeding, platelet transfusion, or avoiding chemotherapy delay or dose reduction are uncertain. [13]

Procedures & devices

  • complete mesocolic excision (CME): Complete mesocolic excision (CME) is consistently associated with higher lymph node yields and improved specimen metrics, although studies demonstrating a definitive survival advantage are limited. [2][3]
  • standard high-quality right hemicolectomy: Standard high-quality right hemicolectomy should remain the default approach for most patients. [2]
  • colonic stenting: ESGE recommends colonic stenting as the preferred procedure for palliation of malignant colonic obstruction. [11]
  • colonoscopy: The Cystic Fibrosis Foundation recommends colonoscopy as the screening examination for colorectal cancer in individuals with cystic fibrosis. [8]
  • computed tomography colonography: The task force concluded that the evidence is insufficient to recommend computed tomography colonography for colorectal cancer screening in individuals with cystic fibrosis. [8]
  • stool-based tests: The task force concluded that the evidence is insufficient to recommend stool-based tests for colorectal cancer screening in individuals with cystic fibrosis. [8]
  • flexible sigmoidoscopy: The task force concluded that the evidence is insufficient to recommend flexible sigmoidoscopy for colorectal cancer screening in individuals with cystic fibrosis. [8]
  • endoscopic surveillance: Endoscopic surveillance recommendations are provided for patients operated on for colorectal cancer. [14]
  • en bloc resection: En bloc resection is the recommended surgical procedure for patients with resectable colon cancer. [1]
  • surgical resection of liver or lung metastases: Surgical resection of liver or lung metastases should be considered for patients with metastatic disease in those sites if they are surgical candidates and if surgery can extend survival. [1]

Other

  • systemic therapy · chemotherapy: The guideline focuses on the use of systemic therapy in metastatic disease. [5]
Safety & interactions7 points
  • CME is technically demanding and may carry increased procedural risks, particularly related to central vascular dissection, although these may be mitigated through structured training and optimised perioperative planning. [2]
  • Chemotherapy-induced thrombocytopenia (CIT) occurs in approximately one-third of patients with a solid tumor diagnosis and in half of patients with a hematologic malignancy. [13]
  • Chemotherapy-induced thrombocytopenia may complicate the administration of chemotherapy, leading to therapeutic delays or dose reductions. [13]
  • Studies have shown that TPO-RAs can improve platelet counts in CIT, but the clinical benefits of TPO-RAs in terms of reducing bleeding, limiting platelet transfusion, avoiding chemotherapy delay, or dose reduction are uncertain. [13]
  • Decision making about oxaliplatin-containing chemotherapy duration should be informed by evidence of 5-year disease-free survival and the rate of adverse events, including peripheral neuropathy. [4]
  • The decision to proceed with colorectal cancer screening in people with cystic fibrosis is more complicated than in the non-CF population. [8]
  • Preparation for colonoscopy is more time-consuming in individuals with cystic fibrosis than in other populations. [8]
What we don't know yet6 points
  • Recent evidence suggests that surgical plane quality, rather than the extent of lymphadenectomy, may be the principal determinant of oncological outcomes. [2]
  • Future progress will depend on standardisation of surgical technique, objective assessment of specimen quality and biologically tailored treatment strategies. [2]
  • The ISTH guidance states that further research is needed to optimize selection of indications and study design to manage thrombocytopenia following chemotherapy. [13]
  • The NCCN Genetic/Familial High-Risk Assessment guideline describes the advantages and limitations of multigene panel testing. [10]
  • The task force found no randomized clinical trials comparing screened versus nonscreened patients or comparing colonoscopy with less-invasive screening procedures in adults with cystic fibrosis. [8]
  • The NCCN Colon/Rectal/Anal Cancers Guidelines panel states that treating patients in a clinical trial has priority over standard or accepted therapy. [1]
Key biomarkers10 points
  • The NCCN guideline on genetic/familial high-risk assessment focuses primarily on pathogenic or likely pathogenic variants associated with increased risk of breast, ovarian, and pancreatic cancer and on recommended approaches to genetic testing, counseling, and management, and the NCCN guidelines note expanded recommendations for biomarker testing in metastatic colorectal cancer. [7][6]
  • Sources describe Li-Fraumeni syndrome as a highly penetrant cancer syndrome associated with a high lifetime risk for cancer, including colon cancer. [7]
  • KRAS/NRAS mutational status, BRAF mutation status, and tumor microsatellite stability should be considered in treatment selection. [5]
  • Multigene panel testing has allowed for the detection of a growing number of inherited pathogenic/likely pathogenic variants in people at high risk of cancer. [10]
  • Patients with mismatch repair deficiency/microsatellite instability tumors should not be routinely offered ACT, and if the combination of mismatch repair deficiency/microsatellite instability and high-risk factors leads to offering ACT, oxaliplatin-containing chemotherapy is recommended. [4]
  • Existing serum markers lack sufficient specificity and sensitivity for early detection of colorectal cancer. [9]
  • Guidelines advise measuring CEA every 2–3 months for at least 3 years after diagnosis in patients with stage II or stage III disease who may be candidates for liver resection or systemic treatment if recurrence occurs. [9]
  • There is insufficient evidence to recommend routine use of several tissue factors (thymidylate synthase, MSI, p53, K-ras, DCC) to determine prognosis or predict therapy response in colorectal cancer. [9]
  • Microsatellite instability (MSI) may be used as a pre-screen for patients with suspected hereditary non‑polyposis colorectal cancer. [9]
  • Faecal occult blood testing, but not faecal DNA markers, may be used to screen asymptomatic people aged 50 years or older for early colorectal cancer. [9]

Sources

Every statement above is drawn from these reviewed sources. This page reports what they describe. Sources last checked June 20, 2026.

  1. GuidelineColon cancer. Clinical practice guidelines in oncology · 2003
  2. GuidelineACPGBI position statement on the role of standard high-quality right hemicolectomy and complete mesocolic excision in right-sided colon cancer · 2026
  3. GuidelineEAES rapid guideline: complete mesocolic excision for right-sided colon cancer-with SAGES and ESCP participation · 2025
  4. GuidelineAdjuvant Therapy for Stage II Colon Cancer: ASCO Guideline Update · 2022
  5. GuidelineColon Cancer, Version 1.2017, NCCN Clinical Practice Guidelines in Oncology · 2017
  6. GuidelineColon Cancer, Version 2.2021, NCCN Clinical Practice Guidelines in Oncology · 2021
  7. GuidelineGenetic/Familial High-Risk Assessment: Breast, Ovarian, and Pancreatic, Version 2.2021, NCCN Clinical Practice Guidelines in Oncology · 2021
  8. GuidelineCystic Fibrosis Colorectal Cancer Screening Consensus Recommendations · 2018
  9. GuidelineTumour markers in colorectal cancer: European Group on Tumour Markers (EGTM) guidelines for clinical use · 2007
  10. GuidelineGenetic/Familial High-Risk Assessment: Colorectal, Endometrial, and Gastric, Version 3.2024, NCCN Clinical Practice Guidelines In Oncology · 2024
  11. GuidelineSelf-expandable metal stents for obstructing colonic and extracolonic cancer: European Society of Gastrointestinal Endoscopy (ESGE) Guideline - Update 2020 · 2020
  12. GuidelineNCCN Guidelines® Insights: Rectal Cancer, Version 3.2024 · 2024
  13. GuidelineManagement of chemotherapy-induced thrombocytopenia: guidance from the ISTH Subcommittee on Hemostasis and Malignancy · 2024
  14. GuidelineEndoscopic surveillance after colonic polyps and colorrectal cancer resection. 2018 update · 2019

What supports this page

The kinds of sources behind this page, strongest at the top. Faint rungs show what is not here yet.

Guideline
75
Meta-analysis
156
Systematic review
56
Randomized trial
3
Clinical trial
34
Observational
7
Case report
309
Review
1699
Preclinical
0
Other
6

Living document — last change June 20, 2026: Cancer page updated. 4 recent updates logged.

Pooled evidence across studies

PubMed
  • Colon cancer risk: HR 1.22 (1.13–1.22 across studies) · red meat
    3 studies · 100% agree · consistent40210826
  • Colorectal cancer risk: HR 1.17 (1.15–1.21 across studies) · red meat
    3 studies · 100% agree · consistent40210826
  • Rectal cancer risk: HR 1.22 (1.17–1.28 across studies) · red meat
    3 studies · 100% agree · consistent40210826
  • Colorectal cancer incidence: RR 1.135 (1.1–1.17 across studies) · red meat
    2 studies · 100% agree · consistent34455534
  • Colon cancer incidence: RR 1.19 (1.17–1.21 across studies) · red meat
    2 studies · 100% agree · consistent34455534
  • Rectal cancer incidence: RR 1.24 (1.22–1.26 across studies) · red meat
    2 studies · 100% agree · consistent34455534
  • Lung cancer incidence: RR 1.23 (1.2–1.26 across studies) · red meat
    2 studies · 100% agree · consistent34455534

Numbers pooled deterministically across 38 published studies that passed our figure-accuracy checks — a quick synthesis, not a formal meta-analysis. Updated 9/8/2026.

Medicines & supplements studied for Colon Cancer

PubMedFDAClinicalTrials.gov

Every drug, supplement, and other agent the published studies cover for Colon Cancer, ranked by how strong the evidence is — what studies report, not a recommendation. Tap any to see its full profile.

Medicines · 1

BevacizumabHuman trial / meta-analysisMixed results1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: Best-response RR (meningiomas) 13%, n=40 PMID 40434540 · response rates 8–67 across 6 studies

Most authoritative study: Effect of bevacizumab on non-target intracranial meningiomas and non-vestibular schwannomas in NF2-related schwannomatosis: NF104

Effect sizes reported in only 1 of 2 studies.
Targeted therapyFDA approvedPhase 22 studiesFull profile →

What recent studies report in Colon Cancer

These are reviewed studies whose abstracts concern Colon Cancer. Each describes only what that study reported. This is not a claim by OncoForge that any compound helps or harms Colon Cancer. Most are early lab, animal, or small human studies, and findings often conflict.

52 studies7 human3 animal2 lab⚠ Conflicting evidenceMechanism (22)Trial (1)

Tracking 52 published studies of Colon Cancer: 7 in humans, 3 in animals, 2 in the lab, 40 reviews/other.

Reported direction across studies: 23 positive, 8 mixed, 2 negative, 19 inconclusive.

Findings conflict — both supportive and negative/mixed results exist (see below). Human evidence is limited.

These counts summarize what the studies reported; they are not a measure of whether anything works for Colon Cancer.

Compounds with studies mentioning Colon Cancer

Bevacizumab (2)
ReviewReported positiveLimited evidenceTier 4 · clinical

Surgery in NF2-Schwannomatosis

Familial cancer · Dec 2025 · review

vestibular schwannomameningiomaspinal schwannomaspinal ependymomaperipheral schwannomacentral and peripheral nervous system tumorsNF2-Schwannomatosis

This is a clinical review of surgical management in NF2-Schwannomatosis. The authors summarize therapeutic indications for vestibular schwannomas, meningiomas, spinal schwannomas and meningiomas, spinal ependymomas and peripheral schwannomas. They note surgical decisions are individualized and that multidisciplinary teams and centralized care can improve outcomes in this rare disease. The review explains why a single comprehensive generic decision tree is difficult to provide.

Key findings
  • Surgery remains an important treatment option for NF2-Schwannomatosis, sometimes performed urgently but usually planned within complex multi-tumour burden and morbidity.
  • The review details therapeutic indications for each tumor type: vestibular schwannomas, meningiomas, spinal schwannomas and meningiomas, spinal ependymomas and peripheral schwannomas.
  • A comprehensive generic decision tree is difficult because each patient has a unique disease burden.
  • Experience of the multidisciplinary team impacts outcomes, and centralized care has been shown to improve the disease course in this rare disease.
Limitations: Narrative review rather than presentation of new primary data.; Authors state a comprehensive generic decision tree is difficult due to individual patient variability.; Focus is on a rare disease, which may limit generalizability of recommendations.; Abstract does not specify whether review methodology was systematic..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Animal studyReported positivePreclinical onlyTier 2 · animal

Targeting chromatin remodeling complexes to treat uveal melanoma

eLife · Sep 2025

uveal melanoma

The abstract reports a novel compound that inhibits the BAF chromatin remodeling complex. In an animal model of uveal melanoma, the compound caused tumor regression. The abstract does not provide the compound name, dosing, species, sample size, or quantitative results.

Key findings
  • A novel compound that inhibits the BAF chromatin remodeling complex caused regression in an animal model of uveal melanoma.
  • The reported mechanism of action is inhibition of the BAF chromatin remodeling complex (chromatin remodeling).
  • The abstract supplies no compound name, dose, species, sample size, comparator, or numeric outcome data.
Limitations: Evidence comes from an animal model only; no human data are reported.; The abstract does not name the compound or report dosing or administration details.; No quantitative results, sample size, control group, or statistical data are provided in the abstract.; Species and study design details are not provided in the abstract..

AI summary of the abstract, human-reviewed · Aug 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

Skull-meninges-brain connectivity and extra-axial brain tumours

Brain communications · Aug 2025

meningiomavestibular schwannomaintra-axial brain tumours

This narrative review summarizes meningeal structure and function, including the meningeal lymphatic network and its connections to the skull bone marrow and peripheral immune system. It discusses how these meningeal immune features may relate to extra-axial brain tumours (meningioma and vestibular schwannoma), potentially influencing tumour immune infiltration, meningeal inflammation, and symptoms such as headache and anxiety.

Key findings
  • The meninges (dura, arachnoid, pia) are structurally and functionally connected to neighbouring structures including the skull.
  • The meningeal lymphatic network places the meninges at a nexus between the brain, peripheral immune system, and skull bone marrow.
  • Meningeal lymphatics can regulate immune responses in models of health and disease, including intra-axial brain tumours, and thereby affect tumour behaviour.
  • A diverse array of resident and circulating immune cells (macrophages, T-cells, B-cells) inhabit the meninges, with specialized hubs around dural venous sinuses and cranial nerves.
  • Meningioma and vestibular schwannoma commonly arise near meningeal immune hubs, suggesting possible bidirectional interactions influencing immune infiltration and meningeal inflammation and symptoms.
Limitations: Narrative review rather than primary experimental or clinical data; no original quantitative results reported.; Abstract does not state whether this is a systematic review or the methods used for literature selection.; Many links between meningeal features and tumour behavior are discussed conceptually or based on models rather than demonstrated causally in patients.; No evaluation of interventions, therapies, or clinical outcomes in treated patients presented in the abstract..

AI summary of the abstract, human-reviewed · Aug 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human trialTrialMixed resultsLimited evidenceTier 4 · clinicaln = 22

Effect of bevacizumab on non-target intracranial meningiomas and non-vestibular schwannomas in NF2-related schwannomatosis: NF104

Journal of neuro-oncology · Jul 2025 · Retrospective analysis of tumor volumes from patients prospectively treated with bevacizumab on a phase II clinical trial (NF104)

Bevacizumabmeningiomanon-vestibular schwannoma (NVS)NF2-related schwannomatosis

Researchers retrospectively analyzed volumes of intracranial non-vestibular schwannomas (NVS) and meningiomas in NF2-related schwannomatosis patients who received bevacizumab for two years on trial NF104. Best radiographic response occurred in 13% of meningiomas (5/40) and 42% of NVS (5/12); per-patient response rates were 38% for meningioma (3/8) and 67% for NVS (4/6). During two years, progression occurred in 55% of meningiomas (22/40) and 8% of NVS (1/12). Median time to progression was 15 months for meningiomas and was not reached for NVS.

Reported effects: Best-response RR (meningiomas) 13%, n=40 · Best-response RR (non-vestibular schwannomas, NVS) 42%, n=12 · +6 more

Key findings
  • Best-response radiographic response (RR) occurred in 13% (5/40) of meningiomas.
  • Best-response radiographic response (RR) occurred in 42% (5/12) of non-vestibular schwannomas (NVS).
  • Per-patient RR for meningioma: 38% (3/8) of patients.
  • Per-patient RR for NVS: 67% (4/6) of patients.
  • During two years of treatment, progression (PD) occurred in 55% (22/40) of meningiomas.
  • During two years of treatment, progression (PD) occurred in 8% (1/12) of NVS.
  • Median time to tumor progression was 15 months for meningiomas and was not reached for NVS.
Limitations: Retrospective analysis of a subset of trial participants (non-target tumors) rather than a pre-specified primary endpoint for these tumors.; Small numbers of patients/tumors evaluated (40 meningiomas in 8 patients; 12 NVS in 6 patients).; Single-arm trial with no randomized control group.; Endpoints are radiographic volumetric responses and progression; clinical outcomes (e.g., survival, functional status) are not reported here.; Potential selection bias because all patients were enrolled for progressive vestibular schwannoma..

AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed

Case reportReported negativeLimited evidenceTier 3 · early humann = 1

Malignant Transformation of Tentorial Schwannoma

Neurology India · Jul 2025 · case report

schwannomamalignant peripheral nerve sheath tumortentorial schwannomaintracranial schwannomabrain neoplasm

This case report describes a 45-year-old man who presented with a giant tentorial schwannoma with supra- and infratentorial extension. The tumor recurred on follow-up and, per the authors, underwent malignant transformation to a malignant peripheral nerve sheath tumor (MPNST). The patient had no clinical features of neurofibromatosis. The authors state this is the first reported case of malignant transformation of a tentorial schwannoma.

Key findings
  • Intracranial schwannomas are uncommon; intracranial schwannomas account for approximately 6.8%-8.0% of intracranial tumors (background statement).
  • Tentorial schwannomas are rare—only 18 cases had been reported prior to this report (background statement).
  • The authors present a single case of a giant tentorial schwannoma in a 45-year-old man with supra- and infratentorial growth.
  • The tumor recurred on follow-up and was reported to have transformed into a malignant peripheral nerve sheath tumor (MPNST).
  • The patient had no features of neurofibromatosis.
Limitations: Single-patient case report — findings may not be generalizable.; Abstract provides limited clinical, pathological, and follow-up detail (diagnostic criteria and timing of recurrence/transformation not specified).; No control or comparative data; cannot establish incidence or causality of malignant transformation..

AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed

Meta-analysisReported positiveStrong evidenceTier 4 · clinicaln = 60

Association between red and processed meat consumption and colorectal cancer risk: a comprehensive meta-analysis of prospective studies

GeroScience · Jun 2025 · meta-analysis of prospective studies

colorectal cancercolon cancerrectal cancer

This meta-analysis pooled 60 prospective studies to evaluate associations between red, processed, and total meat consumption and colorectal, colon, and rectal cancer risk. Higher intake of red, processed, and total meat was each associated with modestly increased hazard ratios for colorectal, colon, and rectal cancer in the pooled analyses.

Reported effects: Red meat - colon cancer HR 1.22 [1.15–1.3] · Red meat - colorectal cancer HR 1.15 [1.1–1.21] · +7 more

Key findings
  • Red meat consumption was associated with increased risk of colon cancer (HR = 1.22, 95% CI 1.15-1.30), colorectal cancer (HR = 1.15, 95% CI 1.10-1.21), and rectal cancer (HR = 1.22, 95% CI 1.07-1.39).
  • Processed meat consumption was associated with increased risk of colon cancer (HR = 1.13, 95% CI 1.07-1.20), colorectal cancer (HR = 1.21, 95% CI 1.14-1.28), and rectal cancer (HR = 1.17, 95% CI 1.05-1.30).
  • Total meat consumption was associated with increased risk of colon cancer (HR = 1.22, 95% CI 1.11-1.35), colorectal cancer (HR = 1.17, 95% CI 1.12-1.22), and rectal cancer (HR = 1.28, 95% CI 1.10-1.48).
Limitations: Observational prospective studies cannot establish causation; associations may reflect residual confounding.; Potential heterogeneity across included studies (populations, exposure assessment, covariate adjustment) may affect pooled estimates.; Dietary measurement error and misclassification in the original studies may bias results.; Abstract does not report dose-response specifics or uniform exposure definitions across studies..

AI summary of the abstract, published automatically under the strong-evidence tier · Jul 2026; an editor has not yet reviewed it. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewInconclusiveLimited evidenceTier 4 · clinical

Current Treatment of Uveal Melanoma

Cancers · Apr 2025

uveal melanoma

This is a review article titled "Current Treatment of Uveal Melanoma" that discusses treatments for uveal melanoma. The provided abstract text is incomplete and does not report specific interventions, results, or conclusions.

Limitations: Provided abstract is incomplete/truncated and contains no detailed results.; Review article — no original experimental or clinical trial data reported in the abstract.; No specific treatments, doses, outcomes, or quantitative results are stated in the provided text.; Unable to assess study design, population, or funding from the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Case reportReported positiveLimited evidenceTier 3 · early humann = 1

A case of ovarian carcinosarcoma with germline BRCA2 pathogenic variant

The journal of obstetrics and gynaecology research · Dec 2024 · case report

ovarian carcinosarcomahigh-grade serous carcinomaductal carcinoma in situ (breast)

This is a single-case report of a 43-year-old woman with advanced (stage IIIB) ovarian carcinosarcoma who was found to have a germline BRCA2 pathogenic variant. After surgery and postoperative adjuvant chemotherapy she received maintenance therapy with a PARP inhibitor for 25 months and had no recurrence during that period. The authors note a concurrent ductal carcinoma in situ in the left breast and suggest PARP inhibitors may be effective as maintenance therapy in this setting, but this is a single case.

Reported effect: maintenance duration without recurrence 25 mo, n=1

Studied with: postoperative adjuvant chemotherapy.

Key findings
  • Patient: 43-year-old woman with an 8-cm right ovarian mass and family history of prostate and uterine/ovarian cancer.
  • Histology: carcinosarcoma consisting of high-grade serous carcinoma and sarcomatous components including cartilage.
  • Staging: advanced stage IIIB (FIGO 2014).
  • Genetics: germline BRCA2 pathogenic variant identified.
  • Treatment course: right salpingo-oophorectomy, radical surgery three weeks later, postoperative adjuvant chemotherapy, then maintenance therapy with a PARP inhibitor.
  • Outcome: maintenance PARP inhibitor continued for 25 months without recurrence.
  • Additional finding: ductal carcinoma in situ in the left breast at first visit.
Limitations: Single-patient case report (n=1), so findings are not generalizable.; No control or comparison group.; Specific PARP agent and dosing not reported.; Observational uncontrolled follow-up; cannot establish causality between PARP maintenance and lack of recurrence..

Single-case report describing PARP inhibitor maintenance in a BRCA2-mutant ovarian carcinosarcoma with 25 months recurrence-free during follow-up.

AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed

Lab · in vitroReported positivePreclinical onlyTier 1 · lab

Targeting MERTK on tumour cells and macrophages: a potential intervention for sporadic and NF2-related meningioma and schwannoma tumours

Oncogene · Oct 2024

meningiomaschwannomaNF2-related schwannomatosis

The study examined TAM receptor expression and signaling in patient-derived meningioma and schwannoma cells and tissues. It found overexpression/activation of TAM receptors and GAS6, identified MERTK/TYRO3 heterocomplexes, and showed that MERTK and AXL support increased cell proliferation and survival. In vitro treatment with the MERTK/FLT3 inhibitor UNC2025 reduced proliferation and survival (with greater efficacy than the AXL inhibitor BGB324) and UNC2025 strongly depleted tumour-associated macrophages in both tumour types.

Key findings
  • Overexpression/activation of TAM receptors (TYRO3/AXL/MERTK) and overexpression/release of ligand GAS6 in patient-derived meningioma tumour cells and tissue.
  • First report of MERTK/TYRO3 heterocomplex formation in meningioma and schwannoma tissue.
  • AXL and TYRO3 expression are dependent on MERTK in both tumour types, with interdependency of MERTK and AXL expression in meningioma.
  • MERTK and AXL contribute to increased proliferation and survival of meningioma and schwannoma cells.
  • In vitro inhibition of proliferation and survival using the MERTK/FLT3 inhibitor UNC2025 and the AXL inhibitor BGB324, with UNC2025 showing superior efficacy over BGB324.
  • Tumour-associated macrophages express TAMs in meningioma and schwannoma, and UNC2025 strongly depleted macrophages in both tumour types.
Limitations: Preclinical work limited to in vitro experiments and analyses of patient tissue; no animal or clinical trial data reported in the abstract.; Abstract does not report sample sizes or detailed quantitative results.; Dosing, treatment schedules, and safety/toxicity data are not provided in the abstract.; Functional effects shown in vitro may not translate to clinical benefit in patients..

AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewInconclusiveLimited evidenceTier 4 · clinical

Pediatric orbital lesions: neoplastic extraocular soft-tissue lesions

Pediatric radiology · May 2024

congenital hemangiomainfantile hemangiomaoptic nerve meningiomaoptic nerve gliomaplexiform neurofibromateratomachloromarhabdomyosarcomainfantile fibrosarcomaschwannoma

This paper presents a multimodality imaging approach to pediatric extraocular soft-tissue neoplastic lesions of the orbit. The authors highlight ocular ultrasound as a first imaging modality when appropriate and review imaging features of several vascular, optic nerve, and other neoplastic lesions to help narrow the differential diagnosis and guide management.

Key findings
  • Early multimodality imaging work-up and recognition of key imaging features allow narrowing of the differential diagnoses to direct timely management.
  • Ocular ultrasound is highlighted as a first imaging modality where appropriate.
  • The paper discusses imaging features of vascular neoplasms (congenital and infantile hemangioma), optic nerve lesions (meningioma, optic nerve glioma), and other neoplastic lesions including plexiform neurofibroma, teratoma, chloroma, rhabdomyosarcoma, infantile fibrosarcoma, and schwannoma.
Limitations: Review article that does not present original clinical data or quantitative diagnostic performance metrics in the abstract.; Not stated as a systematic review or meta-analysis in the abstract; methods for literature selection are not provided.; No sample size, outcome measures, or validation data are reported in the abstract..

AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

The genetic landscape and possible therapeutics of neurofibromatosis type 2

Cancer cell international · May 2023 · review

Bevacizumabneurofibromatosis type 2vestibular schwannomameningiomaependymoma

This is a narrative review describing the clinical features, genetic causes, and current management options for neurofibromatosis type 2 (NF2). The authors summarize that NF2 is caused by loss-of-function mutations in the NF2 gene leading to merlin dysfunction, list standard management approaches including surgery, radiosurgery, bevacizumab and observation, and note recent genetic and molecular advances that may enable targeted therapies but also challenges to implementation.

Key findings
  • NF2 is characterized by multiple benign nervous-system tumors, most commonly bilateral vestibular schwannoma, meningioma, and ependymoma.
  • Clinical manifestations depend on tumor site; vestibular schwannoma causes hearing loss, dizziness, and tinnitus; spinal tumors cause pain, weakness, or paresthesias.
  • Clinical diagnosis is based on the Manchester criteria, which have been updated in the last decade.
  • NF2 is caused by loss-of-function mutations in the NF2 gene on chromosome 22 resulting in merlin protein malfunction.
  • Over half of NF2 patients have de novo mutations, and about half of that group are mosaic.
  • Management options include surgery, stereotactic radiosurgery, bevacizumab, and close observation.
  • Multiple tumors, inoperable disease, complications of surgery, radiotherapy-induced malignancies, and poor effectiveness of cytotoxic chemotherapy have driven interest in targeted therapies.
  • Recent advances in genetics and molecular biology have enabled identification and potential targeting of pathways involved in NF2 pathogenesis, but there are challenges to translating this into effective therapies.
Limitations: Narrative review with no original experimental or clinical data presented.; No systematic review or meta-analytic methods described in the abstract; potential for selection or narrative bias.; The abstract does not provide quantitative efficacy or safety data for therapies mentioned.; Discussion of potential targeted therapies is descriptive and does not present new clinical trial evidence in this article..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Animal studyReported positivePreclinical onlyTier 2 · animal

Inhibition of YAP/TAZ-driven TEAD activity prevents growth of NF2-null schwannoma and meningioma

Brain : a journal of neurology · Apr 2023 · Preclinical study using human primary tumour cells in vitro and mouse schwannoma models in vivo

schwannomameningiomaNF2-null schwannomaNF2-null meningioma

This preclinical study used human primary tumour cells and mouse models to test whether targeting Hippo pathway effectors (YAP/TAZ) or inhibiting TEAD palmitoylation affects NF2-null schwannoma and meningioma growth. Genetic deletion of YAP/TAZ and treatment with TEAD palmitoylation inhibitors blocked tumour cell growth in vitro and the inhibitors caused regression of schwannoma tumours in a mouse model. The authors also found that ALDH1A1 is a TAZ-driven Hippo signalling target in NF2-null schwannoma and meningioma cells. They suggest these findings point to potential future clinical use of TEAD palmitoylation inhibitors.

Key findings
  • Genetic ablation of the Hippo effectors YAP and TAZ blocks tumour cell growth (reported in human primary tumour cells and mouse models).
  • Novel TEAD palmitoylation inhibitors block and regress schwannoma tumour growth in vitro and in a preclinical mouse model.
  • ALDH1A1 (a cancer stem cell marker) is identified as a Hippo signalling target driven by TAZ in human and mouse NF2-null schwannoma cells and in NF2-null meningioma cells.
  • Successful use of TEAD palmitoylation inhibitors in a preclinical mouse model of schwannoma is presented as evidence pointing to potential future clinical use.
Limitations: Preclinical work only: findings are from in vitro experiments and mouse models, no clinical (human in vivo) data reported.; Abstract provides no sample sizes, dosing regimens, toxicity, or pharmacokinetic data for the TEAD inhibitors.; Therapeutic relevance of ALDH1A1 as a target was identified but not validated as a treatment strategy in vivo beyond association.; Generalisability to human patients is uncertain because only primary tumour cells (ex vivo) and mouse models were used..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Browse all studies mentioning Colon Cancer →

Study mix

52 published studies by what they were done in. Lab and animal findings often do not carry over to people.

7 Human3 Animal2 Lab40 Review/other
Reported directionReported positive23Mixed results8Reported negative2Inconclusive19

Evidence at a glance: compounds studied in Colon Cancer

A deterministic grade of what published studies report for each: strength of evidence, the reported direction, and the largest credible effect, strongest-evidence first. This summarizes findings; it is not a claim that anything works.

BevacizumabHuman trial / meta-analysisMixed results1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: Best-response RR (meningiomas) 13%, n=40 PMID 40434540 · response rates 8–67 across 6 studies

Most authoritative study: Effect of bevacizumab on non-target intracranial meningiomas and non-vestibular schwannomas in NF2-related schwannomatosis: NF104

Effect sizes reported in only 1 of 2 studies.

What the research shows for Colon Cancer

A plain-language summary of the reviewed studies OncoForge tracks for Colon Cancer. It reports what those studies described, not a claim that any compound or therapy helps or harms Colon Cancer. Most of this evidence is early, and findings often conflict.

  • These studies are mainly narrative reviews and syntheses of mechanistic or biomarker research rather than clinical trials.
  • The reviewed studies report that higher NUCB2/NESF‑1 expression has been linked in some reports to poorer outcomes and to increased cancer cell proliferation, migration, and invasion in various cancers; other reports are conflicting and the reviews describe the overall evidence as limited.
  • These studies report that the adaptor protein CRKL is overexpressed in many tumor types and is proposed to promote aggressive tumor behaviors and to have potential diagnostic/prognostic value, but the review evidence is limited and not specific to colon cancer.
  • These studies report on the concept of vasculogenic mimicry (tumor cells forming fluid-conducting channels) and distinguish different channel types; that review focused on melanoma types and described mechanistic features rather than clinical data relevant to colon cancer.
  • Across the collected reviews, the evidence is heterogeneous, largely preclinical or observational, and sometimes conflicting; few if any primary clinical studies in colon cancer were presented in these papers.

Supportive & alternative options discussed

  • Exercise / prehabilitation: Also discussed as a supportive option for people with colon cancer; these studies did not evaluate exercise.
  • Ketogenic / metabolic therapy: Also discussed as a supportive or adjunctive dietary approach in colon cancer care by some sources; these studies did not evaluate ketogenic diets.
  • Mind–body (MBSR / CBT): Also discussed as a supportive approach to quality of life and symptom management in colon cancer; these studies did not evaluate mind–body interventions.
  • Acupuncture: Also discussed as a supportive option for symptom control in colon cancer care; these studies did not evaluate acupuncture.
  • Mistletoe (VAE): Also discussed by some groups as a complementary therapy in cancer care; these studies did not evaluate mistletoe in colon cancer.
  • Hyperthermia (heat): Also discussed as an adjunctive technique in oncology in some contexts; these studies did not evaluate hyperthermia in colon cancer.

What we don’t know yet

  • Do NUCB2/NESF‑1 or CRKL expression changes causally influence colon cancer progression or patient outcomes, beyond associations reported in small or preclinical studies?
  • Are the reported biomarker findings reproducible in larger, well‑controlled human studies specific to colon cancer?
  • What (if any) clinical utility would measurement or targeting of these molecules have for diagnosis, prognosis, or therapy in colon cancer?
  • What are appropriate methods, standard assays, and clinically meaningful thresholds for measuring these biomarkers in patients?
  • Do interventions that modify these pathways change clinically relevant outcomes (survival, recurrence, symptoms) in colon cancer patients?
These publications represent early, limited mechanistic and biomarker research (mainly narrative reviews of preclinical and observational data) and do not establish clinical benefit or therapeutic use in colon cancer.

Clinical trials in Colon Cancer

47 ongoing · 90 completed · tracked from ClinicalTrials.gov. Recruiting is not the same as proven, and completed is not the same as positive — read the results. Not a recommendation.

Completed
20 stopped (terminated / withdrawn / suspended)

Search all trials on ClinicalTrials.gov →

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Advocacy & community

No dedicated organization for this specific cancer is curated yet — these general organizations can help in the meantime.

Financial help

  • PAN Foundation ↗ — Copay assistance funds by diagnosis (funds open and close as money allows). · status changes often — check the fund’s site
  • HealthWell Foundation ↗ — Copay and premium assistance funds by disease. · status changes often — check the fund’s site
  • CancerCare — financial assistance ↗ — Limited grants plus free financial counseling. · status changes often — check the fund’s site
  • Family Reach ↗ — Help with everyday living costs (rent, transport, food) during treatment. · status changes often — check the fund’s site
  • NeedyMeds ↗ — Searchable directory of drug patient-assistance and discount programs. · status changes often — check the fund’s site
What you’ll typically need to apply
  • Your diagnosis and, if you have it, the specific drug/treatment name (from your care team).
  • Insurance details — your member ID card, or a note that you're uninsured (some funds require active insurance, some don't).
  • Proof of income and household size (recent pay stubs, a tax return, or a benefits letter) — most funds are income-based.
  • Your prescriber's contact information; some programs need the clinic to submit part of the application.
  • Apply early and re-check: funds open and close as money is available, so a closed fund may reopen.

General guidance — each program sets its own eligibility. Confirm requirements on the program’s site.

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