Evidence map›Paper›PMID 28066751›Full record

ReviewFrontiers in pediatrics2016

Killing Two Cells with One Stone: Pharmacologic BCL-2 Family Targeting for Cancer Cell Death and Immune Modulation.

Lindsey M Ludwig, Michele L Nassin, Abbas Hadji, James L LaBelle

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in pediatrics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

17 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Small-Molecule PROTACs for Cancer Immunotherapy.Molecules (Basel, Switzerland) · 2022
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Novel Hybrid CHC from β-carboline andFrontiers in pharmacology · 2020
    Article
  14. Article
  15. Review
  16. Article
  17. Butein Inhibited In Vitro Hexokinase-2-Mediated Tumor Glycolysis in Hepatocellular Carcinoma by Blocking Epidermal Growth Factor Receptor (EGFR).Medical science monitor : international medical journal of experimental and clinical research · 2018
    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

4 authors at 1 institution in 1 country.

Lindsey M LudwigSection of Hematology, Oncology, Stem Cell Transplantation, Department of Pediatrics, University of Chicago, Comer Children's Hospital, Chicago, IL, USA; Committee on Cancer Biology, University of Chicago, Chicago, IL, USA.
Michele L NassinSection of Hematology, Oncology, Stem Cell Transplantation, Department of Pediatrics, University of Chicago, Comer Children's Hospital , Chicago, IL , USA.
Abbas HadjiSection of Hematology, Oncology, Stem Cell Transplantation, Department of Pediatrics, University of Chicago, Comer Children's Hospital , Chicago, IL , USA.
James L LaBelleSection of Hematology, Oncology, Stem Cell Transplantation, Department of Pediatrics, University of Chicago, Comer Children's Hospital, Chicago, IL, USA; Committee on Cancer Biology, University of Chicago, Chicago, IL, USA.
Comer Children's Hospital · US

Funding

Multi-Disciplinary Training Grant in Cancer ResearchT32CA009594 · NCI · UNIVERSITY OF CHICAGO · PI KAY F MACLEOD, Scott A. Oakes · 1989 to 2026
$11.5M
6 · The paper itself

Abstract

A crucial component of regulating organismal homeostasis is maintaining proper cell number and eliminating damaged or potentially malignant cells. Apoptosis, or programed cell death, is the mechanism responsible for this equilibrium. The intrinsic apoptotic pathway is also especially important in the development and maintenance of the immune system. Apoptosis is essential for proper positive and negative selection during B- and T-cell development and for efficient contraction of expanded lymphocytes following an immune response. Tight regulation of the apoptotic pathway is critical, as excessive cell death can lead to immunodeficiency while apoptotic resistance can lead to aberrant lymphoproliferation and autoimmune disease. Dysregulation of cell death is implicated in a wide range of hematological malignancies, and targeting various components of the apoptotic machinery in these cases is an attractive chemotherapeutic strategy. A wide array of compounds has been developed with the purpose of reactivating the intrinsic apoptotic pathway. These compounds, termed BH3 mimetics are garnering considerable attention as they gain greater clinical oncologic significance. As their use expands, it will be imperative to understand the effects these compounds have on immune homeostasis. Uncovering their potential immunomodulatory activity may allow for administration of BH3 mimetics for direct tumor cell killing as well as novel therapies for a wide range of immune-based directives. This review will summarize the major proteins involved in the intrinsic apoptotic pathway and define their roles in normal immune development and disease. Clinical and preclinical BH3 mimetics are described within the context of what is currently known about their ability to affect immune function. Prospects for future antitumor immune amplification and immune modulation are then proposed.

Indexed as

apoptosisBCL-2BH3 mimeticcell deathimmune systemimmunotherapylymphocytessmall molecules

Identifiers

PMID28066751
PMCPMC5174130
OpenAlexW2563886753

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.