Evidence map›Paper›PMID 20379390›Full record

ArticleJournal of biomedicine & biotechnology2010

Antigen-specific polyclonal cytotoxic T lymphocytes induced by fusions of dendritic cells and tumor cells.

Shigeo Koido, Sadamu Homma, Eiichi Hara, Yoshihisa Namiki, Toshifumi Ohkusa, Jianlin Gong, Hisao Tajiri

Open access · hybridAbstract read
In one paragraph

Article in Journal of biomedicine & biotechnology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

7 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Human IP10-scFv and DC-induced CTL synergistically inhibit the growth of glioma in a xenograft model.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
  4. Article
  5. Article
  6. Review
  7. 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

7 authors at 3 institutions in 2 countries.

Shigeo KoidoDivision of Gastroenterology and Hepatology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo 105-8461, Japan. shigeo_koido@jikei.ac.jp
Sadamu Homma
Eiichi Hara
Yoshihisa Namiki
Toshifumi Ohkusa
Jianlin Gong
Hisao Tajiri
Jikei University School of Medicine · JPBoston University · USSaitama Cancer Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of cancer vaccines is induction of tumor-specific cytotoxic T lymphocytes (CTLs) that can reduce the tumor mass. Dendritic cells (DCs) are potent antigen-presenting cells and play a central role in the initiation and regulation of primary immune responses. Thus, DCs-based vaccination represents a potentially powerful strategy for induction of antigen-specific CTLs. Fusions of DCs and whole tumor cells represent an alternative approach to deliver, process, and subsequently present a broad spectrum of antigens, including those known and unidentified, in the context of costimulatory molecules. Once DCs/tumor fusions have been infused back into patient, they migrate to secondary lymphoid organs, where the generation of antigen-specific polyclonal CTL responses occurs. We will discuss perspectives for future development of DCs/tumor fusions for CTL induction.

Indexed as

Cell FusionAnimalsClinical Trials as TopicDendritic CellsEpitopesHistocompatibility AntigensHumansLymphocyte ActivationModels, AnimalNeoplasmsT-Lymphocytes, CytotoxicT-Lymphocytes, RegulatoryEpitopesHistocompatibility Antigens

Identifiers

PMID20379390
PMCPMC2850552
OpenAlexW2062571451

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.