Evidence map›Paper›PMID 12601523›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2003

Therapeutic vaccination with tumor cells that engage CD137.

Karl Erik Hellstrom, Ingegerd Hellstrom

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

10 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Immunotherapy targeting 4-1BB and its ligand.International journal of hematology · 2006
    Article
  9. Article
  10. Review
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

2 authors at 1 institution in 1 country.

Karl Erik HellstromPacific Northwest Research Institute, Seattle, WA 98122, USA. khellstrom@pnri.org
Ingegerd Hellstrom
Pacific Northwest Diabetes Research Institute · US

Funding

Vaccinating against IGFBP-2 to prevent ovarian cancer relapseP50CA083636 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI DRESCHER, CHARLES, URBAN, NICOLE DENISE · 1999 to 2015
$35.1M
MESOTHELIN ANTIGENS FOR DIAGNOSIS/THERAPY OF OVARIAN CAR01CA085780 · NCI · PACIFIC NORTHWEST RESEARCH INSTITUTE · PI HELLSTROM, INGEGERD E. · 2000 to 2003
$1.3M
BOLSTERING OF CELL MEDIATED IMMUNITY TO HUMAN CARCINOMAR01CA079490 · NCI · PACIFIC NORTHWEST RESEARCH INSTITUTE · PI HELLSTROM, KARL ERIK · 1999 to 2002
$1.0M
NCI NIH HHS 1 P50 CA83636NCI NIH HHS CA 79490NCI NIH HHS CA85780NCI NIH HHS P50 CA083636
6 · The paper itself

Abstract

Therapeutic cancer vaccination is based on the finding that tumors in both humans and experimental animals, such as mice, express potential immunological targets, some of which have high selectivity for cancer cells. In contrast to the successful vaccination against some infectious diseases, where most vaccines induce neutralizing antibodies that act prophylactically, the aim of therapeutic cancer vaccines is to treat established tumors (primarily micrometastases). Since most tumor-destructive immune responses are cell-mediated, therapeutic cancer vaccination needs to induce and expand such responses and also to overcome "escape" mechanisms that allow tumors to evade immunological destruction. Tumor antigens (as with other antigens) are presented by "professional" antigen-presenting cells, most notably dendritic cells (DC). Therefore DC that have been transfected or "pulsed" to present antigen provide a logical source of tumor vaccines, and some encouraging results have been obtained clinically as well as in preclinical models. An alternative and more physiological approach is to develop vaccines that deliver tumor antigen for in vivo uptake and presentation by the DC. Vaccines of the latter type include tumor cells that have been modified to produce certain lymphokines or express costimulatory molecules, as well as cDNAs, recombinant viruses, proteins, peptides and glycolipids which are often given together with an adjuvant. Several studies over the past 5 years have demonstrated dramatic therapeutic responses against established mouse tumors as a result of repeated injections of agonistic monoclonal antibodies (MAbs) to the costimulatory molecule CD137 (4-1BB). However, the clinical use of such MAbs may be problematic since they depress antibody formation, for example, to infectious agents. The alternative approach to transfect tumor cells to express the CD137 ligand (CD137L) increases their immunogenicity, but vaccination with tumor cells expressing CD137L is ineffective in several systems where injection of anti-CD137 MAb produces tumor regression. Recent findings indicate that a more effective way to engage CD137 towards tumor destruction is to transfect tumor cells to express a cell-bound form of anti-CD137 single-chain Fv fragments (scFv). Notably, tumors from melanoma K1735, growing either subcutaneously or in the lung, could be eradicated following vaccination with K1735 cells that expressed anti-CD137 scFv. This was in spite of the fact that K1735, as with many human neoplasms, expresses very low levels of MHC class I and has low immunogenicity. Similar results were subsequently obtained with other tumors of low immunogenicity, including sarcoma Ag104. We hypothesize that the concomitant expression of tumor antigen and anti-CD137 scFv effectively engages NK cells, monocytes and dendritic cells, as well as activated CD4(+) and CD8(+) T cells (all of which express CD137) so as to induce and expand a tumor-destructive Th1 response. While vaccines in the form of transfected tumor cells can be effective, at least in mouse models, the logical next step is to construct vaccines that combine genes that encode molecularly defined tumor antigens with a gene that encodes anti-CD137 scFv. Before planning any clinical trials, vaccines that engage CD137 via scFv need to be compared in demanding mouse models for efficacy and side effects with vaccines that are already being tested clinically, including transfected DC and tumor cells producing granulocyte-macrophage colony-stimulating factor.

Indexed as

Cancer VaccinesAnimalsAntigens, CDAntigens, NeoplasmCell TransplantationLungMiceNeoplasmsReceptors, Nerve Growth FactorReceptors, Tumor Necrosis FactorTumor Necrosis Factor Receptor Superfamily, Member 9Antigens, CDAntigens, NeoplasmCancer VaccinesReceptors, Nerve Growth FactorReceptors, Tumor Necrosis FactorTNFRSF9 protein, humanTnfrsf9 protein, mouseTumor Necrosis Factor Receptor Superfamily, Member 9

Identifiers

PMID12601523
OpenAlexW2096925909

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.