Evidence map›Paper›PMID 35032175›Full record

ArticleCancer immunology, immunotherapy : CII2022

Antibody-dependent cellular phagocytosis of tropomyosin receptor kinase C (TrkC) expressing cancer cells for targeted immunotherapy.

Phei San Lai, Syed Muhammad Usama, Lik-Voon Kiew, Hong Boon Lee, Lip Yong Chung, Kevin Burgess, Chin Siang Kue

Open access · greenAbstract read
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 47% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Selective Modulation of Trk Receptors byACS chemical neuroscience · 2025
    Article
  2. 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 4 institutions in 2 countries.

Phei San LaiSchool of Graduates Studies, Management and Science University, Seksyen 13, 40100, Shah Alam, Selangor, Malaysia.
Syed Muhammad UsamaDepartment of Chemistry, Texas A & M University, Box 30012, College Station, TX, 77842, USA.
Lik-Voon KiewDepartment of Pharmacology, Faculty of Medicine, University of Malaya, 50603, Kuala Lumpur, Malaysia.
Hong Boon LeeSchool of Biosciences, Faculty of Health and Medical Sciences, Taylor's University, 47500, Subang Jaya, Selangor, Malaysia.
Lip Yong ChungDepartment of Pharmaceutical Chemistry, Faculty of Pharmacy, University of Malaya, 50603, Kuala Lumpur, Malaysia.
Kevin BurgessDepartment of Chemistry, Texas A & M University, Box 30012, College Station, TX, 77842, USA. burgess@chem.tamu.edu.
Chin Siang KueFaculty of Health and Life Sciences, Management and Science University, Seksyen 13, 40100, Shah Alam, Selangor, Malaysia. cskue@msu.edu.my.ORCID http://orcid.org/0000-0002-9793-5616
Management and Science University · MYTexas A&M University · USUniversity of Malaya · MYTaylor's University · MY

Funding

Evaluation Of Trk Probes In Models For Dry Eye DiseaseR01EY029695 · NEI · TEXAS A&M UNIVERSITY · PI BURGESS, KEVIN · 2019 to 2021
$1.7M
NEI NIH HHS R01 EY029695NIH HHS NIH R01EY029645
6 · The paper itself

Abstract

Conventional cancer therapies such as chemotherapy are non-selective and induce immune system anergy, which lead to serious side effects and tumor relapse. It is a challenge to prime the body's immune system in the cancer-bearing subject to produce cancer antigen-targeting antibodies, as most tumor-associated antigens are expressed abundantly in cancer cells and some of normal cells. This study illustrates how hapten-based pre-immunization (for anti-hapten antibodies production) combined with cancer receptor labeling with hapten antigen constructs can elicit antibody-dependent cellular phagocytosis (ADCP). Thus, the hapten antigen 2,4-dinitrophenol (DNP) was covalently combined with a cancer receptor-binding dipeptide (IYIY) to form a dipeptide-hapten construct (IYIY-DNP, MW = 1322.33) that targets the tropomyosin receptor kinase C (TrkC)-expressed on the surface of metastatic cancer cells. IYIY-DNP facilitated selective association of RAW264.7 macrophages to the TrkC expressing 4T1 cancer cells in vitro, forming cell aggregates in the presence of anti-DNP antibodies, suggesting initiation of anti-DNP antibody-dependent cancer cell recognition of macrophages by the IYIY-DNP. In in vivo, IYIY-DNP at 10 mg/kg suppressed growth of 4T1 tumors in DNP-immunized BALB/c mice by 45% (p < 0.05), when comparing the area under the tumor growth curve to that of the saline-treated DNP-immunized mice. Meanwhile, IYIY-DNP at 10 mg/kg had no effect on TrkC-negative 67NR tumor-bearing mice immunized with DNP. Tumor growth suppression activity of IYIY-DNP in DNP-immunized mice was associated with an increase in the anti-DNP IgG (7.3 × 10

Indexed as

Neoplasm Recurrence, LocalTropomyosinAnimalsAntibodiesAntibody FormationAntigensCarrier ProteinsDipeptidesHaptensImmunologic FactorsImmunotherapyMicePhagocytosisAntibodiesAntigensCarrier ProteinsDipeptidesHaptensImmunologic FactorsTropomyosinActive targetingAntibody-dependent cellular phagocytosisDinitrophenolImmunotherapyLigand-hapten conjugateTrkC

Identifiers

PMID35032175
PMCPMC10365225
OpenAlexW4206063147

What OpenQuestion holds

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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.