Evidence map›Paper›PMID 24741617›Full record

ReviewJournal of immunology research2014

Immune escape mechanisms in colorectal cancer pathogenesis and liver metastasis.

Massimo Pancione, Guido Giordano, Andrea Remo, Antonio Febbraro, Lina Sabatino, Erminia Manfrin, Michele Ceccarelli, Vittorio Colantuoni

Open access · goldAbstract readReview
In one paragraph

Review in Journal of immunology research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

81 citing papers in PubMed, 124 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Colorectal Cancer Cell's Weapon: RNF32 Engages SPP1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Colorectal clear cell carcinoma: a literature review.Journal of medical case reports · 2025
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. Article

21 more citing papers are in PubMed but not listed here.

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

8 authors at 3 institutions in 1 country.

Massimo PancioneDepartment of Sciences and Technologies, University of Sannio, 82100 Benevento, Italy.ORCID 0000-0001-6589-5560
Guido GiordanoMedical Oncology Unit, Fatebenefratelli Hospital, 82100 Benevento, Italy.ORCID 0000-0002-9310-1075
Andrea RemoDepartment of Pathology "Mater Salutis" Hospital, 37045 Legnago (VR), Italy.
Antonio FebbraroMedical Oncology Unit, Fatebenefratelli Hospital, 82100 Benevento, Italy.
Lina SabatinoDepartment of Sciences and Technologies, University of Sannio, 82100 Benevento, Italy.
Erminia ManfrinDepartment of Surgery and Oncology, University of Verona, 37129 Verona, Italy.
Michele CeccarelliDepartment of Sciences and Technologies, University of Sannio, 82100 Benevento, Italy ; Bioinformatics Lab, BIOGEM scrl, 83031 Ariano Irpino (AV), Italy.
Vittorio ColantuoniDepartment of Sciences and Technologies, University of Sannio, 82100 Benevento, Italy.
University of Sannio · ITFatebenefratelli Hospital · ITUniversity of Verona · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Over the past decade, growing evidence indicates that the tumor microenvironment (TME) contributes with genomic/epigenomic aberrations of malignant cells to enhance cancer cells survival, invasion, and dissemination. Many factors, produced or de novo synthesized by immune, stromal, or malignant cells, acting in a paracrine and autocrine fashion, remodel TME and the adaptive immune response culminating in metastasis. Taking into account the recent accomplishments in the field of immune oncology and using metastatic colorectal cancer (mCRC) as a model, we propose that the evasion of the immune surveillance and metastatic spread can be achieved through a number of mechanisms that include (a) intrinsic plasticity and adaptability of immune and malignant cells to paracrine and autocrine stimuli or genotoxic stresses; (b) alteration of positional schemes of myeloid-lineage cells, produced by factors controlling the balance between tumour-suppressing and tumour-promoting activities; (c) acquisition by cancer cells of aberrant immune-phenotypic traits (NT5E/CD73, CD68, and CD163) that enhance the interactions among TME components through the production of immune-suppressive mediators. These properties may represent the driving force of metastatic progression and thus clinically exploitable for cancer prevention and therapy. In this review we summarize results and suggest new hypotheses that favour the growing impact of tumor-infiltrating immune cells on tumour progression, metastasis, and therapy resistance.

Indexed as

Tumor EscapeAntineoplastic AgentsAutocrine CommunicationCell Transformation, NeoplasticColonColorectal NeoplasmsDNA DamageDrug Resistance, NeoplasmHumansImmunologic SurveillanceLiverLiver NeoplasmsParacrine CommunicationTumor MicroenvironmentAntineoplastic Agents

Identifiers

PMID24741617
PMCPMC3987978
OpenAlexW2020406481

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.