Evidence map›Paper›PMID 30170620›Full record

ReviewJournal of translational medicine2018

Unleashing endogenous TNF-alpha as a cancer immunotherapeutic.

Steven F Josephs, Thomas E Ichim, Stephen M Prince, Santosh Kesari, Francesco M Marincola, Anton Rolando Escobedo, Amir Jafri

Open access · goldAbstract readReview
In one paragraph

Review in Journal of translational medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
144citing papers in PubMed, 2 pooled it
11.2field-weighted citation impact, top 1% 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

144 citing papers in PubMed, 2 syntheses or guidelines pooled it, 258 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. TNF-alpha: Roles in pathogenesis and therapeutics in cancer.The Journal of biological chemistry · 2026
    Review
  6. Article
  7. Article
  8. Article
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  10. Antitumor effect of alcohol extract ofFrontiers in oncology · 2026
    Article
  11. Article
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  13. Review
  14. Article
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  19. Article
  20. Article

84 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

Steven F JosephsImmunicom, Inc., San Diego, CA, USA.
Thomas E IchimImmune Advisors LLC, La Jolla, San Diego, CA, USA.
Stephen M PrinceImmunicom, Inc., San Diego, CA, USA. steve.prince@immunicom.com.
Santosh KesariJohn Wayne Cancer Institute and Pacific Neuroscience Institute, Santa Monica, CA, USA.
Francesco M MarincolaImmunicom, Inc., San Diego, CA, USA.
Anton Rolando EscobedoCHIPSA Hospital, Baja California, Mexico.
Amir JafriImmunicom, Inc., San Diego, CA, USA.
China United Network Communications Group (China) · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor necrosis factor (TNF)-alpha was originally identified in the 1970s as the serum mediator of innate immunity capable of inducing hemorrhagic necrosis in tumors. Today, a wide spectrum of biological activities have been attributed to this molecule, and clinical translation has mainly occurred not in using it to treat cancer, but rather to inhibit its effects to treat autoimmunity. Clinical trials utilizing systemic TNF-alpha administration have resulted in an unacceptable level of toxicities, which blocked its development. In contrast, localized administration of TNF-alpha in the form of isolated limb perfusion have yielded excellent results in soft tissue sarcomas. Here we describe a novel approach to leveraging the potent antineoplastic activities of TNF-alpha by enhancing activity of locally produced TNF-alpha through extracorporeal removal of soluble TNF-alpha receptors. Specifically, it is known that cancerous tissues are infiltrated with monocytes, T cells, and other cells capable of producing TNF-alpha. It is also known that tumors, as well as cells in the tumor microenvironment produce soluble TNF-alpha receptors. The authors believe that by selectively removing soluble TNF-alpha receptors local enhancement of endogenous TNF-alpha activity may provide for enhanced tumor cell death without associated systemic toxicities.

Indexed as

AnimalsAntineoplastic Agents, AlkylatingHumansImmunotherapyMiceReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IISarcomaSoft Tissue NeoplasmsTumor MicroenvironmentTumor Necrosis Factor-alphaAntineoplastic Agents, AlkylatingReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IITumor Necrosis Factor-alphaCancerExtracorporealImmuno-oncologyImmunotherapySoluble TNF-alpha receptorsTNF-alpha

Identifiers

PMID30170620
PMCPMC6119315
OpenAlexW2889474158

What Socratic 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 Socratic graph.