Evidence map›Paper›PMID 30390146›Full record

ReviewCancer immunology, immunotherapy : CII2018

Targeting CTCFL/BORIS for the immunotherapy of cancer.

Dmitri Loukinov

Open access · greenAbstract readReview
In one paragraph

Review in Cancer immunology, immunotherapy : CII, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. The Tumor Microenvironment and Immune Response in Breast Cancer.International journal of molecular sciences · 2024
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. CTCF and CTCFL in cancer.Current opinion in genetics & development · 2020
    Review
  17. Article
  18. Article
  19. Article
  20. Molecular cancer research : MCR · 2019
    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

1 author at 1 institution in 1 country.

Dmitri LoukinovMolecular Pathology Section, Laboratory of Immunogenetics, NIAID/NIH, Twinbrook 1, Room 1329, 5640 Fishers Lane, Rockville, MD, 20852, USA. dloukinov@niaid.nih.gov.ORCID http://orcid.org/0000-0002-4438-3424
National Institutes of Health · US

Funding

Normal and Pathologic Functions of CTCF and Its Distinct Classes of DNA-targetsZIAAI000860 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI LOBANENKOV, VICTOR · 2009 to 2025
$15.4M
Regulation of CTCF Functions and Target Sites by Cancer/Testis-specific CTCF Like BORIS FactorZIAAI001021 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI LOBANENKOV, VICTOR · 2009 to 2025
$12.7M
6 · The paper itself

Abstract

Cancer vaccines have great potential in the fight against metastatic malignancies. Current anti-tumor immunotherapy is hindered by existing tolerance to tumor-associated antigens (TAA) and tumor escape using various mechanisms, highlighting the need for improved targets for immunotherapy. The cancer-testis antigen CTCFL/BORIS was discovered 16 years ago and possesses all features necessary for an ideal TAA. Recently CTCFL/BORIS has received additional attention as a target expressed in cancer stem cells (CSC). These cells drive tumor growth recurrence, metastasis, and treatment resistance. CTCFL/BORIS silencing leads to senescence and death of CSC. Therefore, an immunotherapeutic strategy that targets CTCFL/BORIS may lead to the selective destruction of CSC and potential eradication of metastatic disease. The high immunotherapeutic potential of CTCFL/BORIS antigen was shown in a stringent 4T1 mouse model of breast cancer. Using these highly metastatic, poorly immunogenic carcinoma cells inoculated into T-helper2 prone mice, we showed that DC fed with recombinant CTCFL/BORIS as an immunogen inhibited tumor growth and reduced the number of metastases in distant organs. About 20% of CTCFL/BORIS immunized animals were tumor free. 50% of animals remained metastasis free. Those having metastasis showed at least tenfold fewer metastases compared to controls. In a rat model of breast cancer, we showed that alphavirus-based CTCFL/BORIS immunotherapy was capable of cancer elimination as we were able to cure 50% of animals. Based on the above data, we believe that translation of CTCFL/BORIS-targeting immunotherapeutic strategies to the clinic will provide new avenues for improving survival of breast cancer patients with advanced metastatic disease.

Indexed as

Biomarkers, TumorImmunotherapyMolecular Targeted TherapyAnimalsAntineoplastic Agents, ImmunologicalCCCTC-Binding FactorCell Transformation, NeoplasticDisease Models, AnimalDNA-Binding ProteinsGene Expression Regulation, NeoplasticHumansNeoplasmsNeoplastic Stem CellsRNA IsoformsSpermatogenesisAntineoplastic Agents, ImmunologicalBiomarkers, TumorCCCTC-Binding FactorCTCFL protein, humanDNA-Binding ProteinsRNA IsoformsCancer immunotherapy targetCancer stem cells (CSC)CITIM 2017CTCF functional interferenceCTCFL/BORISMouse and rat breast carcinoma models

Identifiers

PMID30390146
PMCPMC11028242
OpenAlexW2899341895

What OpenQuestion holds

Textmetadata
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.