Evidence map›Paper›PMID 25941795›Full record

ReviewCancers2015

Lymphoma: immune evasion strategies.

Ranjan Upadhyay, Linda Hammerich, Paul Peng, Brian Brown, Miriam Merad, Joshua D Brody

Abstract readReview
In one paragraph

Review in Cancers, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
–field-weighted citation impact
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

30 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Immunomodulatory Drugs for the Treatment of B Cell Malignancies.International journal of molecular sciences · 2021
    Review
  14. Review
  15. Prognostic Impact of Baseline Immunologic Profile in Aggressive B-cell non-Hodgkin's Lymphomas.Mediterranean journal of hematology and infectious diseases · 2021
    Article
  16. Article
  17. Natural Killer Cell Dysfunction and Its Role in COVID-19.International journal of molecular sciences · 2020
    Review
  18. Review
  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

6 authors.

Ranjan UpadhyayDivision of Hematology and Medical Oncology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. ranjan.upadhyay@mssm.edu.
Linda HammerichDivision of Hematology and Medical Oncology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. linda.hammerich@mssm.edu.
Paul PengDivision of Hematology and Medical Oncology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. paul.peng@mssm.edu.
Brian BrownDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. brian.brown@mssm.edu.
Miriam MeradDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. miriam.merad@mssm.edu.
Joshua D BrodyDivision of Hematology and Medical Oncology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. joshua.brody@mssm.edu.

Funding

Contribution of the cutaneous APC network to melanoma progression and therapy.R01CA173861 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI MERAD, MIRIAM · 2013 to 2017
$2.1M
Harnessing Csf-2 compartmentalized role on tissue resident phagocytes to uncouple anti-tumoral from pathological immunity induced by checkpoint inhibitorsR01CA190400 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI MERAD, MIRIAM · 2015 to 2019
$1.9M
NCI NIH HHS R01 CA173861NCI NIH HHS R01 CA190400
6 · The paper itself

Abstract

While the cellular origin of lymphoma is often characterized by chromosomal translocations and other genetic aberrations, its growth and development into a malignant neoplasm is highly dependent upon its ability to escape natural host defenses. Neoplastic cells interact with a variety of non-malignant cells in the tumor milieu to create an immunosuppressive microenvironment. The resulting functional impairment and dysregulation of tumor-associated immune cells not only allows for passive growth of the malignancy but may even provide active growth signals upon which the tumor subsequently becomes dependent. In the past decade, the success of immune checkpoint blockade and adoptive cell transfer for relapsed or refractory lymphomas has validated immunotherapy as a possible treatment cornerstone. Here, we review the mechanisms by which lymphomas have been found to evade and even reprogram the immune system, including alterations in surface molecules, recruitment of immunosuppressive subpopulations, and secretion of anti-inflammatory factors. A fundamental understanding of the immune evasion strategies utilized by lymphomas may lead to better prognostic markers and guide the development of targeted interventions that are both safer and more effective than current standards of care.

Identifiers

PMID25941795
PMCPMC4491682

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.