Evidence map›Paper›PMID 22390757›Full record

ReviewCurrent pharmaceutical design2012

Moving beyond VEGF for anti-angiogenesis strategies in gynecologic cancer.

Duangmani Thanapprapasr, Wei Hu, Anil K Sood, Robert L Coleman

Abstract readReview
In one paragraph

Review in Current pharmaceutical design, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

8 citing papers in PubMed, 24 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Eph receptors and ephrins: therapeutic opportunities.Annual review of pharmacology and toxicology · 2015
    Review
  7. Review
  8. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Duangmani ThanapprapasrDepartment of Gynecologic Oncology, University of Texas, M.D. Anderson Cancer Center, 1155 Herman Pressler Dr. CPB 6.3271, Houston, TX 77030, USA.
Wei Hu
Anil K Sood
Robert L Coleman
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
UNIVERSITY OF TEXAS MD ANDERSON SPORE IN OVARIAN CANCERP50CA083639 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BAST, ROBERT C · 1999 to 2015
$33.0M
Targeting the PI3K Signaling Pathway in Endometrial CarcinomaP50CA098258 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BODURKA, DIANE · 2003 to 2020
$32.0M
Texas Center for Cancer NanomedicineU54CA151668 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI CRISTINI, VITTORIO, FERRARI, MAURO · 2010 to 2014
$12.4M
Ovarian Cancer: Mechanisms of Neuroendocrine RegulationR01CA109298 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SOOD, ANIL K · 2005 to 2017
$4.5M
Subcellular localization of nanoparticlesRC2GM092599 · NIGMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI CHIU, WAH, DECUZZI, PAOLO · 2009 to 2010
$3.0M
Tumor metastasis: Biobehavioral mechanismsR01CA110793 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SOOD, ANIL K · 2004 to 2009
$2.1M
Nanovectors for Characterization and Destruction of Breast Tumor VasculatureR01CA128797 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI FERRARI, MAURO · 2007 to 2010
$1.7M
NCI NIH HHS CA083639NCI NIH HHS CA098258NCI NIH HHS CA109298NCI NIH HHS CA110793NCI NIH HHS CA128797NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA083639NCI NIH HHS P50 CA098258NCI NIH HHS R01 CA109298NCI NIH HHS R01 CA110793NCI NIH HHS R01 CA128797NCI NIH HHS U54 CA151668NCI NIH HHS U54CA151668NIGMS NIH HHS RC2 GM092599NIGMS NIH HHS RC2GM092599
6 · The paper itself

Abstract

Gynecologic cancer is a major burden in both developed and developing countries. Almost a half million deaths from gynecologic cancer are reported each year. Understanding the molecular biology of cancer is a principle resource leading to the identification of new potential therapeutic targets, which may be parlayed into novel therapeutic options in gynecologic cancer. Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase, which plays a pivotal role in many aspects of malignant growth including cancer cell survival, migration, invasion, angiogenesis and metastasis. Various human cancer tissues have demonstrated high expression of FAK or activated FAK, which has been correlated with survival of cancer patients. Among gynecologic cancers, reports have emerged demonstrating that FAK is involved in the pathogenesis of ovarian, endometrial, and cervical cancers. In addition, the polycomb group protein enhancer of Zeste homologue 2 (EZH2), Dll4/notch and EphA2 has also emerged as important regulators of endothelial cell biology and angiogenesis. Herein, we review the role of these new targets in tumor angiogenesis and the rationale for further clinical development.

Indexed as

Angiogenesis InhibitorsFemaleGenital Neoplasms, FemaleHumansNeovascularization, PathologicVascular Endothelial Growth Factor AAngiogenesis InhibitorsVascular Endothelial Growth Factor A

Identifiers

PMID22390757
PMCPMC3740204
OpenAlexW2139359713

What OpenQuestion holds

Textmetadata
LicenceTDM
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.