Evidence map›Paper›PMID 17431617›Full record

ArticleCancer immunology, immunotherapy : CII2007

Treatment of hepatocellular carcinoma in a mouse xenograft model with an immunotoxin which is engineered to eliminate vascular leak syndrome.

Hao Wang, Shuichuan Song, Geng Kou, Bohua Li, Dapeng Zhang, Sheng Hou, Weizhu Qian, Jianxin Dai, Liang Tian, Jian Zhao and 1 more

Open access · greenAbstract read
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

15 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. CD3e-immunotoxin spares CD62LFrontiers in immunology · 2022
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Interactions BetweenFrontiers in oncology · 2018
    Article
  9. Review
  10. Article
  11. Disorders of Vascular Permeability.Annual review of pathology · 2016
    Review
  12. Review
  13. Article
  14. Article
  15. 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

11 authors at 2 institutions in 1 country.

Hao WangInternational Joint Cancer Institute, Second Military Medical University, Shanghai, PR China.
Shuichuan Song
Geng Kou
Bohua Li
Dapeng Zhang
Sheng Hou
Weizhu Qian
Jianxin Dai
Liang Tian
Jian Zhao
Yajun Guo
Second Military Medical University · CNShanghai Cell Therapy Research Institute · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular leak syndrome (VLS) is the major dose-limiting toxicity of immunotoxin and interleukin-2 therapy. It has been evidenced that VLS-inducing molecules share a three-amino acid consensus motif, (x)D(y), which may be responsible for initiating VLS. Here we have constructed a recombinant immunotoxin (SMFv-PE38KDEL) by genetically fusing PE38KDEL to a single-chain antibody derived from SM5-1 monoclonal antibody, which has a high specificity for melanoma, hepatocellular carcinoma and breast cancer. In order to eliminate VLS induced by this PE38KDEL-based immunotoxin, a panel of mutants were generated by changing amino acid residues adjacent to its three (x)D(y) motifs in the three-dimensional structure. One of the SMFv-PE38KDEL mutants, denoted as mut1, displayed a similar protein synthesis inhibitory in a reticulocyte lysate translation assay compared to the wild-type SMFv-PE38KDEL (wt). The in vitro cytotoxicity assay indicated that mut1 specifically killed SM5-1 binding protein-positive tumor cells, although its cytotoxicity was slightly less than wt. In contrast, mut1 was shown to be much weaker in inducing VLS in mice than wt. The LD(50) values of wt and mut1 in mice were investigated with the result that the LD(50) of mut1 was about tenfold higher than that of wt. The in vivo antitumor activity of wt and mut1 were also compared in tumor-bearing nude mice. Both wt and mut1 were effective in inhibiting the tumor growth but mut1 showed improved therapeutic efficacy. These studies suggest mut1 may be a novel PE-based immunotoxin with much less toxicity for clinical use.

Indexed as

Genetic TherapyAnimalsAntibodies, MonoclonalAntineoplastic AgentsCapillary Leak SyndromeCarcinoma, HepatocellularDisease Models, AnimalGenetic EngineeringImmunotoxinsLiver Neoplasms, ExperimentalMiceMice, NudeModels, MolecularRecombinant ProteinsTransplantation, HeterologousAntibodies, MonoclonalAntineoplastic AgentsImmunotoxinsRecombinant Proteins

Identifiers

PMID17431617
PMCPMC11030707
OpenAlexW1969459392

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.