Research Radartracking 72 published studies · 21 human · 14 clinical trials · 14 cancer pages · updated Jun 2026Open the Research Map →

Bladder Cancer

Auto-discovered from research; not yet curated.

Auto-added · review pending
Educational only: This page is not medical advice. Coordinate decisions with your oncology team.

OncoForge editorial · How we review →

AI extractedhuman reviewedsources checkedretractions suppressed

Evidence at a glanceInsufficient evidenceMixed results⚠ Studies disagree
2 published studies that name Bladder Cancer0 human studies (trial, observational, or meta-analysis)747 source documents in the Bladder Cancer corpus
Why this grade?

Insufficient evidence — No primary experimental studies yet.

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

Living document — last change June 9, 2026: New cancer type added.

Overview

Bladder Cancer is tracked here from the published studies that mention it. This page shows the research evidence collected so far — it is not a curated clinical overview.

What supports this page

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

Guideline
32
Meta-analysis
146
Systematic review
27
Randomized trial
0
Clinical trial
1
Observational
3
Case report
10
Review
528
Preclinical
0
Other
0

Evidence on specific compounds

How the published studies grade individual drugs, supplements, and other agents in Bladder Cancer — each rated by how strong the evidence is, not a recommendation.

What recent studies report in Bladder Cancer

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

2 studies⚠ Conflicting evidenceMechanism (2)

Tracking 2 published studies of Bladder Cancer: 2 reviews/other.

Reported direction across studies: 1 positive, 1 mixed.

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 Bladder Cancer.

ReviewMechanismMixed resultsLimited evidenceTier 1 · lab

Nucleobindin-2/Nesfatin-1-A New Cancer Related Molecule?

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

The role of CT10 regulation of kinase-like in cancer

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

Browse all studies mentioning Bladder Cancer →

Clinical trials in Bladder Cancer

Loading current trials from ClinicalTrials.gov… Search ClinicalTrials.gov →

Heading to an appointment? Get a printable one-page summary — studied compounds, open trials, interactions, and questions to ask.
Bring this to your appointment →