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.
3 studies⚠ Conflicting evidenceMechanism (2)
Tracking 3 published studies of Colon Cancer: 3 reviews/other.
Reported direction across studies: 1 positive, 1 mixed, 1 inconclusive.
Findings conflict — both supportive and negative/mixed results exist (see below). Human evidence is absent so far.
These counts summarize what the studies reported; they are not a measure of whether anything works for Colon Cancer.
ReviewMechanismMixed resultsLimited evidenceTier 1 · lab
International journal of molecular sciences · Aug 2021 · review
breast cancercolon cancerprostate cancerendometrial cancerthyroid cancerbladder cancerglioblastomaadrenocortical carcinomaovarian epithelial carcinoma
This review discusses nucleobindin-2/nesfatin-1 (NUCB2/NESF-1) as a cancer-related molecule. It summarizes reports that higher expression is linked with poorer outcomes and with increased cancer cell proliferation, migration, and invasion in several cancers, while other reports suggest it may inhibit growth in some cancer cell types. The article does not present new experimental data.
Key findings
- High NUCB2/NESF-1 expression has been associated with poor outcomes in several cancers.
- Reported effects include increased cell proliferation, migration, and invasion in breast, colon, prostate, endometrial, thyroid, and bladder cancers, and glioblastoma.
- The review also notes conflicting findings where nesfatin-1 inhibited proliferation in human adrenocortical carcinoma and ovarian epithelial carcinoma cells.
- The authors propose NUCB2/NESF-1 as a prognostic and predictive marker in cancers.
Limitations: Review article; no original experimental or clinical data.; The abstract summarizes heterogeneous prior studies with conflicting findings.; No quantitative effect estimates are reported in the abstract.; No details on study quality, sample sizes, or methods of the cited studies are provided..
This is a review of a molecule reported to be associated with cancer progression and prognosis, not a primary intervention study.
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewMechanismReported positiveLimited evidenceTier 4 · clinical
Future oncology (London, England) · Dec 2014 · Review
gastric cancerglioblastoma multiformehepatocellular carcinomabladder cancerlung cancercolon cancerovarian cancerleukemiabreast cancerhead and neck cancerrhabdomyosarcomaneuroblastoma
This is a narrative review summarizing published reports about the adaptor protein CRKL in cancer. The authors report that CRKL is overexpressed in many tumor types and appears to promote aggressive or malignant behaviors, and they suggest CRKL has potential as a diagnostic/prognostic biomarker.
Key findings
- CRKL is a member of the CRK family and functions as an adaptor protein in intracellular signal transduction.
- CRKL has been reported overexpressed in a variety of cancers.
- CRKL appears to play a tumor-promotion role in multiple cancers, including those listed in the abstract.
- The review summarizes associations between CRKL and malignant tumor behaviors and potential mechanisms of action.
- The authors state CRKL has potential to be used as a biomarker for diagnosis, treatment and prognosis of certain tumors.
Limitations: This is a review article and does not present new primary experimental data.; Abstract provides no information on search strategy, inclusion criteria, or quality assessment of included studies.; Heterogeneity across many cancer types and study designs likely limits generalizability of conclusions.; The abstract does not report quantitative synthesis or effect sizes..
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed
ReviewInconclusiveLimited evidenceTier 4 · clinical
APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · Jul 2004
uveal melanomacutaneous melanomamucous membrane melanomainflammatory breast carcinomaductal breast carcinomaovarian carcinomaprostatic carcinomasynovial sarcomarhabdomyosarcomaosteosarcomapheochromocytomasoft tissue sarcomamelanoma
This review describes vasculogenic mimicry, where aggressive tumor cells form fluid-conducting channels, and distinguishes two types (tubular and patterned matrix). It reports that patterned matrix channels contain extracellular matrix proteins, connect with blood vessels, are seen in many tumor types, and suggests that tumors with such heterogeneity in microcirculation may not respond to angiogenesis-only therapies.
Key findings
- Vasculogenic mimicry is formation of fluid-conducting channels by highly invasive, genetically dysregulated tumor cells.
- Two types are described: tubular type (morphologically similar to endothelial-lined vessels) and patterned matrix type (does not resemble blood vessels).
- Patterned matrix contains matrix proteins such as laminin, heparan sulfate proteoglycan, and collagens IV and VI.
- The patterned matrix anastomoses with blood vessels and systemically injected tracers co-localize to these patterns.
- Patterned matrix vasculogenic mimicry has been identified in multiple tumor types including uveal, cutaneous and mucous membrane melanomas, inflammatory and ductal breast carcinoma, ovarian and prostatic carcinoma, and several soft tissue sarcomas.
- Because tumor microcirculation may be heterogeneous (including incorporated/co-opted vessels, angiogenic vessels, mosaic vessels, and vasculogenic mimicry), therapies that target angiogenesis alone may be ineffective against tumors containing patterned matrices.
Limitations: This is a narrative review rather than primary experimental data reported in this abstract.; No quantitative results, methods, or systematic search/meta-analysis details are provided in the abstract.; Therapeutic implications (ineffectiveness of anti-angiogenesis alone) are presented as a conceptual caution and are not tested within this paper per the abstract..
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed