Evidence map›Paper›PMID 28119805›Full record

ReviewActa pharmaceutica Sinica. B2017

How to unleash mitochondrial apoptotic blockades to kill cancers?

Jing Deng

Abstract readReview
In one paragraph

Review in Acta pharmaceutica Sinica. B, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing 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

29 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. [Isobavachalcone induces cell death through multiple pathways in human breast cancer MCF-7 cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022
    Article
  13. Article
  14. Aging conundrum: A perspective for ovarian aging.Frontiers in endocrinology · 2022
    Review
  15. Article
  16. Review
  17. Article
  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

1 author.

Jing DengDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apoptosis, especially the intrinsic mitochondrial cell death pathway, is regulated by the BCL-2 family of proteins. Defects in apoptotic machinery are one of the main mechanisms that cells employ to evade cell death and become cancerous. Targeting the apoptotic defects, either by direct inhibition of BCL-2 family proteins or through modulation of regulatory pathways, can restore cell sensitivity to cell death. This review will focus on the aspects of BCL-2 family proteins, their interactions with kinase pathways, and how novel targeted agents can help overcome the apoptotic blockades. Furthermore, functional assays, such as BH3 profiling, may help in predicting responses to chemotherapies and aid in the selection of combination therapies by determining the mitochondrial threshold for initiating cell death.

Indexed as

ApoptosisASH, American Society of HematologyATAP, amphipathic tail-anchoring peptideBAD, BCL-2-associated death promoter proteinBAK, BCL-2 homologous antagonist killerBAX, BCL-2-associated X proteinBCL-2, B-cell lymphoma 2BCL-2 familyBCL-w (BCL2L2), BCL-2-like protein 2BCL-xL, B-cell lymphoma X longBCR, B-cell receptorBFL-1 (BCL2A1), BCL-2-related protein A1BH3, BCL-2 homology 3BH3 profilingBID, BH3 interacting domain death agonistBIK, BCL-2-interacting killerBIM, BCL-2-interacting mediator of cell deathBOK, BCL-2 related ovarian killerBTK, Bruton׳s tyrosine kinaseCDK, cyclin-dependent kinaseCHOP, cyclophosphamide, hydroxydaunorubicin, oncovin-vincristine and prednisoneCLL, chronic lymphocytic leukemiaCML, chronic myelogenous leukemiaCombination therapyCR, complete response;EGFR, epidermal growth factor receptorER, endoplasmic reticulumERK, extracellular signal-regulated kinaseFDA, U. S. Food and Drug AdministrationGSK-3, glycogen synthase kinase-3ITK, interleukin-2-inducible T-cell kinaseMCL, myeloid cell leukemiaMitochondrial primingMOMP, mitochondrial outer membrane permeabilizationNHL, non-Hodgkin lymphomaNIH, National Institutes of HealthNSCLC, non-small cell lung cancerPI3K, phosphatidylinositol-3-kinasePUMA, p53 up-regulated modulator of apoptosisSLL, small lymphocytic lymphomaT-ALL, T-acute lymphocytic leukemiaTargeted therapy

Identifiers

PMID28119805
PMCPMC5237704

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.