ReviewOncoTargets and therapy2014
Angiogenesis and antiangiogenic agents in cervical cancer.
Review in OncoTargets and therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled 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.
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.
Who cites it
35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 82 citations in OpenAlex.
- Efficacy and Safety of Apatinib for the Treatment of Advanced or Recurrent Cervical Cancer: A Single-Arm Meta-Analysis Among Chinese Patients.Frontiers in pharmacology · 2022Pooled it
- Vascular endothelial growth factor (VEGF) targeting therapy for persistent, recurrent, or metastatic cervical cancer.The Cochrane database of systematic reviews · 2021Pooled it
- Raman Spectroscopy of Cell-Free Cervicovaginal Lavage for HPV Lesion Diagnosis: A Pilot Study.International journal of molecular sciences · 2025Article
- Surgical Advancements, Immunotherapy, Targeted and Conventional Therapies, Biopsy, Colposcopy, and Pap Smear Integration in the Management of Cervical Cancer.Current medicinal chemistry · 2025Review
- Pharmacotherapy for cervical cancer: current standard of care and new perspectives.Expert opinion on pharmacotherapy · 2024Review
- Small molecule inhibitors of the VEGF and tyrosine kinase for the treatment of cervical cancer.Medical oncology (Northwood, London, England) · 2024Review
- Potential inhibitors of VEGFR1, VEGFR2, and VEGFR3 developed through Deep Learning for the treatment of Cervical Cancer.Scientific reports · 2024Article
- New insights for gynecological cancer therapies: from molecular mechanisms and clinical evidence to future directions.Cancer metastasis reviews · 2023Review
- LKB1/STK11 Tumor Suppressor Reduces Angiogenesis by Directly Interacting with VEGFR2 in Tumorigenesis.Biomolecules & therapeutics · 2023Article
- Associations of human papillomavirus genotypes and cervical vascular abnormality in a cohort of women underwent colposcopy, a retrospective study of 6716 patients.Frontiers in oncology · 2023Article
- Article
- Encapsulation, Release, and Cytotoxicity of Doxorubicin Loaded in Liposomes, Micelles, and Metal-Organic Frameworks: A Review.Pharmaceutics · 2022Review
- Placental vascularization in middle and late gestation in the pig.Reproduction & fertility · 2022Article
- The Changing Landscape of Systemic Treatment for Cervical Cancer: Rationale for Inhibition of the TGF-β and PD-L1 Pathways.Frontiers in oncology · 2022Review
- Understanding the Role and Clinical Applications of Exosomes in Gynecologic Malignancies: A Review of the Current Literature.Cancers · 2021Review
- Exosomes from cervical cancer cells facilitate pro-angiogenic endothelial reconditioning through transfer of Hedgehog-GLI signaling components.Cancer cell international · 2021Article
- Therapeutic Potential of Natural Products in Treatment of Cervical Cancer: A Review.Nutrients · 2021Review
- MDM2/X Inhibitors as Radiosensitizers for Glioblastoma Targeted Therapy.Frontiers in oncology · 2021Review
- Intratumoral Injection of a Human Papillomavirus Therapeutic Vaccine-Induced Strong Anti-TC-1-Grafted Tumor Activity in Mice.Cancer management and research · 2021Article
- Induction of systemic immune responses and reversion of immunosuppression in the tumor microenvironment by a therapeutic vaccine for cervical cancer.Cancer immunology, immunotherapy : CII · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Standard treatment of cervical cancer (CC) consists of surgery in the early stages and of chemoradiation in locally advanced disease. Metastatic CC has a poor prognosis and is usually treated with palliative platinum-based chemotherapy. Current chemotherapeutic regimens are associated with significant adverse effects and only limited activity, making identification of active and tolerable novel targeted agents a high priority. Angiogenesis is a complex process that plays a crucial role in the development of many types of cancer. The dominant role of angiogenesis in CC seems to be directly related to human papillomavirus-related inhibition of p53 and stabilization of hypoxia-inducible factor-1α. Both of these mechanisms are able to increase expression of vascular endothelial growth factor (VEGF). Activation of VEGF promotes endothelial cell proliferation and migration, favoring formation of new blood vessels and increasing permeability of existing blood vessels. Since bevacizumab, a recombinant humanized monoclonal antibody binding to all isoforms of VEGF, has been demonstrated to significantly improve survival in gynecologic cancer, some recent clinical research has explored the possibility of using novel therapies directed toward inhibition of angiogenesis in CC too. Here we review the main results from studies concerning the use of antiangiogenic drugs that are being investigated for the treatment of CC.
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Registered trials
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.