Evidence map›Paper›PMID 32787882›Full record

ReviewJournal of hematology & oncology2020

Targeting immune checkpoints in hematological malignancies.

Basit Salik, Mark J Smyth, Kyohei Nakamura

Open access · goldAbstract readReview
In one paragraph

Review in Journal of hematology & oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 1 pooled it
9.0field-weighted citation impact, top 2% 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

86 citing papers in PubMed, 1 synthesis or guideline pooled it, 146 citations in OpenAlex.

  1. Pooled it
  2. Axicabtagene Ciloleucel in Combination with Atezolizumab in Patients with Refractory Diffuse Large B-Cell Lymphoma: The Phase 1/2 ZUMA-6 Trial.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Trial
  3. Trial
  4. Review
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  6. Article
  7. Open life sciences · 2026
    Article
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  11. Current Status of Molecularly Targeted Therapeutics in Blood Cancers.International journal of molecular sciences · 2025
    Review
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  16. Review
  17. Review
  18. Review
  19. Article
  20. Article

26 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

3 authors at 1 institution in 1 country.

Basit SalikImmunology in Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, Queensland, 4006, Australia.
Mark J SmythImmunology in Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, Queensland, 4006, Australia.ORCID 0000-0001-7098-7240
Kyohei NakamuraImmunology in Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, Queensland, 4006, Australia. kyohei.nakamura@qimrberghofer.edu.au.
QIMR Berghofer Medical Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune checkpoint blockade (ICB) therapies such as anti-programmed death 1 (PD-1) and anti-CTLA-4 (cytotoxic T lymphocyte-associated protein 4) have dramatically transformed treatment in solid tumor oncology. While immunotherapeutic approaches such as stem cell transplantation and anti-cancer monoclonal antibodies have made critical contributions to improve outcomes in hematological malignancies, clinical benefits of ICB are observed in only limited tumor types that are particularly characterized by a high infiltration of immune cells. Importantly, even patients that initially respond to ICB are unable to achieve long-term disease control using these therapies. Indeed, primary and acquired resistance mechanisms are differentially orchestrated in hematological malignancies depending on tumor types and/or genotypes, and thus, an in-depth understanding of the disease-specific immune microenvironments will be essential in improving efficacy. In addition to PD-1 and CTLA-4, various T cell immune checkpoint molecules have been characterized that regulate T cell responses in a non-redundant manner. Several lines of evidence suggest that these T cell checkpoint molecules might play unique roles in hematological malignancies, highlighting their potential as therapeutic targets. Targeting innate checkpoint molecules on natural killer cells and/or macrophages has also emerged as a rational approach against tumors that are resistant to T cell-mediated immunity. Given that various monoclonal antibodies against tumor surface proteins have been clinically approved in hematological malignancies, innate checkpoint blockade might play a key role to augment antibody-mediated cellular cytotoxicity and phagocytosis. In this review, we discuss recent advances and emerging roles of immune checkpoint blockade in hematological malignancies.

Indexed as

Antineoplastic AgentsCTLA-4 AntigenHematologic NeoplasmsHumansImmune Checkpoint InhibitorsImmunotherapy, AdoptiveKiller Cells, NaturalLeukemia, Myeloid, AcuteLymphocyte ActivationLymphomaMacrophagesMultiple MyelomaMyelodysplastic SyndromesNeoplasm ProteinsProgrammed Cell Death 1 ReceptorT-LymphocytesAntineoplastic AgentsCTLA-4 AntigenImmune Checkpoint InhibitorsNeoplasm ProteinsPDCD1 protein, humanProgrammed Cell Death 1 ReceptorHematological malignancyImmune checkpoint moleculeImmunotherapyTumor microenvironment

Identifiers

PMID32787882
PMCPMC7425174
OpenAlexW3048618543

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.