Evidence map›Paper›PMID 18551250›Full record

ReviewPharmaceutical research2008

Inhibition of tumor angiogenesis by tumstatin: insights into signaling mechanisms and implications in cancer regression.

Akulapalli Sudhakar, Chandra S Boosani

RetractedOpen access · hybridAbstract readReviewRetracted Publication
In one paragraph

Review in Pharmaceutical research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.5field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Cdc42 is involved in NC1 peptide-regulated BTB dynamics through actin and microtubule cytoskeletal reorganization.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  6. Review
  7. Regulation of spermatogenesis by a local functional axis in the testis: role of the basement membrane-derived noncollagenous 1 domain peptide.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Novel aspects of corneal angiogenic and lymphangiogenic privilege.Progress in retinal and eye research · 2010
    Review
  19. History of Cancer, Ancient and Modern Treatment Methods.Journal of cancer science & therapy · 2009
    Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Akulapalli SudhakarCell Signaling and Tumor Angiogenesis Laboratory, Department of Genetics, Boys Town National Research Hospital, Omaha, NE 68131, USA. akulapallis@boystown.org
Chandra S Boosani
Boys Town · USBoys Town National Research Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Growing tumors develop additional new blood vessels to meet the demand for adequate nutrients and oxygen, a process called angiogenesis. Cancer is a highly complex disease promoted by excess angiogenesis; interfering with this process poses for an attractive approach for controlling tumor growth. This hypothesis led to the identification of endogenous angiogenesis inhibitors generated from type IV collagen, a major component of vascular basement membrane (VBM). Type IV collagen and the angiogenesis inhibitors derived from it are involved in complex roles, than just the molecular construction of basement membranes. Protease degradation of collagens in VBM occurs in various physiological and pathological conditions and produces several peptides. Some of these peptides are occupied in the regulation of functions conflicting from those of their original integral molecules. Tumstatin (alpha3(IV)NC1), a proteolytic C-terminal non-collagenous (NC1) domain from type IV collagen alpha3 chain has been highlighted recently because of its potential role in anti-angiogenesis, however its biological actions are not limited to these processes. alpha3(IV)NC1 inhibits proliferation by promoting endothelial cell apoptosis and suppresses diverse tumor angiogenesis, thus making it a potential candidate for future cancer therapy. The present review surveys the physiological functions of type IV collagen and discovery of alpha3(IV)NC1 as an antiangiogenic protein with a comprehensive overview of the knowledge gained by us towards understanding its signaling mechanisms.

Indexed as

Angiogenesis InhibitorsAnimalsAutoantigensCollagen Type IVHumansIntegrin alpha3beta1Integrin alphaVbeta3NeoplasmsNeovascularization, PathologicSignal TransductionAngiogenesis InhibitorsAutoantigensCollagen Type IVIntegrin alpha3beta1Integrin alphaVbeta3type IV collagen alpha3 chain

Identifiers

PMID18551250
PMCPMC7275098
OpenAlexW1971287424

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.