Evidence map›Paper›PMID 36216147›Full record

ReviewCancer letters2022

CD55 in cancer: Complementing functions in a non-canonical manner.

Rashmi Bharti, Goutam Dey, Feng Lin, Justin Lathia, Ofer Reizes

Open access · greenAbstract readReview
In one paragraph

Review in Cancer letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
3.4field-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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Immune cells mediate the causal pathway linking circulating complements to cancer: A Mendelian randomization study.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Pooled it
  2. Article
  3. Immune regulation by CD55 in chronic beryllium disease.American journal of respiratory cell and molecular biology · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Complement system in cancer: friend or foe of immunotherapy.Journal for immunotherapy of cancer · 2026
    Review
  10. ROS Activated NETosis of Bone Marrow CD55Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  11. Article
  12. Article
  13. Article
  14. The complement system in intestinal inflammation and cancer.The Journal of clinical investigation · 2025
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
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

5 authors at 1 institution in 1 country.

Rashmi BhartiDepartment of Cardiovascular and Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Goutam DeyDepartment of Cardiovascular and Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Feng LinDepartment of Inflammation & Immunity, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Justin LathiaDepartment of Cardiovascular and Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA; Case Comprehensive Cancer Center, Cleveland, OH, USA.
Ofer ReizesDepartment of Cardiovascular and Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA; Case Comprehensive Cancer Center, Cleveland, OH, USA. Electronic address: reizeso@ccf.org.
Cleveland Clinic Lerner College of Medicine · US

Funding

New mechanisms by which complementýregulates the pathogenesis of experimental autoimmune uveitisR01EY032458 · NEI · CLEVELAND CLINIC LERNER COM-CWRU · PI LIN, FENG C · 2021 to 2024
$1.6M
Development of a novel antibody-drug conjugate for treating T-cell lymphoma.R41CA275639 · NCI · ABCON THERAPEUTICS, INC. · PI LIN, FENG C · 2022 to 2022
$403k
NCI NIH HHS R41 CA275639NEI NIH HHS R01 EY032458
6 · The paper itself

Abstract

CD55, or decay accelerating factor, is a membrane lipid microdomain-associated, GPI-anchored protein implicated in the shielding of cells from complement-mediated attack via accelerating decay of C3 and C5. Loss of CD55 is associated with a number of pathologies due to hyperactivation of the complement system. CD55 is also implicated in cancer progression thought to be driven via its role in cell shielding mechanisms. We now appreciate that CD55 can signal intracellularly to promote malignant transformation, cancer progression, cell survival, angiogenesis, and inhibition of apoptosis. Outside-in signaling via CD55 is mediated by signaling pathways including JNK, JAK/STAT, MAPK/NF-κB, and LCK. Moreover, CD55 is enriched in the cancer stem cell (CSC) niche of multiple tumors including breast, ovarian, cervical, and can be induced by chemotherapeutics and hypoxic environments. CSCs are implicated in tumor recurrence and chemoresistance. Here, we review the unexpected roles of CD55 in cancer including the roles of canonical and noncanonical pathways that CD55 orchestrates. We will highlight opportunities for therapeutic targeting CD55 and gaps in the field that require more in-depth mechanistic insights.

Indexed as

CD55 AntigensNeoplasm Recurrence, LocalApoptosisHumansSignal TransductionCD55 AntigensCancer stem cellCD55Complement pathwayDAFDecay accelerating factor

Identifiers

PMID36216147
PMCPMC11019835
OpenAlexW4303183303

What OpenQuestion holds

Textmetadata
LicenceTDM
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.