Evidence map›Paper›PMID 25933181›Full record

ReviewHuman vaccines & immunotherapeutics2015

Clinically feasible approaches to potentiating cancer cell-based immunotherapies.

V I Seledtsov, A G Goncharov, G V Seledtsova

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Human vaccines & immunotherapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

48 citing papers in PubMed, 90 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Cellular therapies in rheumatic and musculoskeletal diseases.Journal of translational autoimmunity · 2025
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. New insights into mechanisms and interventions of locoregional therapies for hepatocellular carcinoma.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2024
    Article
  12. Review
  13. Research progress on mitochondria regulating tumor immunity.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2024
    Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. 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

3 authors at 2 institutions in 2 countries.

V I Seledtsova lmmanuel Kant Baltic Federal University ; Kaliningrad , Russia.
A G Goncharov
G V Seledtsova
Immanuel Kant Baltic Federal University · RUInstitute of Immunology · HR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The immune system exerts both tumor-destructive and tumor-protective functions. Mature dendritic cells (DCs), classically activated macrophages (M1), granulocytes, B lymphocytes, aβ and ɣδ T lymphocytes, natural killer T (NKT) cells, and natural killer (NK) cells may be implicated in antitumor immunoprotection. Conversely, tolerogenic DCs, alternatively activated macrophages (M2), myeloid-derived suppressor cells (MDSCs), and regulatory T (Tregs) and B cells (Bregs) are capable of suppressing antitumor immune responses. Anti-cancer vaccination is a useful strategy to elicit antitumor immune responses, while overcoming immunosuppressive mechanisms. Whole tumor cells or lysates derived thereof hold more promise as cancer vaccines than individual tumor-associated antigens (TAAs), because vaccinal cells can elicit immune responses to multiple TAAs. Cancer cell-based vaccines can be autologous, allogeneic or xenogeneic. Clinical use of xenogeneic vaccines is advantageous in that they can be most effective in breaking the preexisting immune tolerance to TAAs. To potentiate immunotherapy, vaccinations can be combined with other modalities that target different immune pathways. These modalities include 1) genetic or chemical modification of cell-based vaccines; 2) cross-priming TAAs to T cells by engaging dendritic cells; 3) T-cell adoptive therapy; 4) stimulation of cytotoxic inflammation by non-specific immunomodulators, toll-like receptor (TLR) agonists, cytokines, chemokines or hormones; 5) reduction of immunosuppression and/or stimulation of antitumor effector cells using antibodies, small molecules; and 6) various cytoreductive modalities. The authors envisage that combined immunotherapeutic strategies will allow for substantial improvements in clinical outcomes in the near future.

Indexed as

Antigens, NeoplasmCancer VaccinesDendritic CellsHumansImmunotherapyAntigens, NeoplasmCancer VaccinesAb, antibodiesADCC, antibody-dependent cell cytotoxicityantitumor immunoprotectionAPC, antigen-presenting cellBCG, Bacillus Calmette-GuérinBreg, regulatory B cellcancer cell-based vaccinesCAR, chimeric antigen receptorcombined immunotherapyCOX, cyclooxygenaseCTA, cancer/testis antigenCTLA-4, cytotoxic T lymphocyte antigen-4CTL, cytotoxic T lymphocyteDC, dendritic cellDTH, delayed-type hypersensitivityGITR, glucocorticoid-induced tumor necrosis factor receptorGM-CSF, granulocyte-macrophage colony stimulating factorHIFU, high-intensity focused ultrasoundIDO, indoleamine-2, 3-dioxygenaseIFN, interferonIL, interleukinimmunosuppressionLAK, lymphokine-activated killerM1, classically activated macrophageM2, alternatively activated macrophage, MDSC, myeloid-derived suppressor cellMHC, major histocompatibility complexM, macrophageNK, natural killer (cell)PD-1, programmed death-1PGE2, prostaglandin E2reactive oxygen speciesRFA, radiofrequency ablationRNS, reactive nitrogen speciesROSTAA, tumor-associated antigenTGF, transforming growth factorTh, T-helper cellTLR, toll-like receptorTNF, tumor necrosis factorTreg, regulatory T cellVEGF, vascular endothelial growth factor

Identifiers

PMID25933181
PMCPMC4514272
OpenAlexW1839029088

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.