Evidence map›Paper›PMID 28956957›Full record

ReviewExpert opinion on therapeutic targets2017

The potential of targeting Sin3B and its associated complexes for cancer therapy.

David J Cantor, Gregory David

Open access · greenAbstract readReview
In one paragraph

Review in Expert opinion on therapeutic targets, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.4field-weighted citation impact, top 36% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. SIN3B Loss Heats up Cold Tumor Microenvironment to Boost Immunotherapy in Pancreatic Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  4. Article
  5. Article
  6. Review
  7. Review
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

2 authors at 1 institution in 1 country.

David J Cantora Department of Biochemistry and Molecular Pharmacology , New York University School of Medicine , New York , NY , USA.
Gregory Davida Department of Biochemistry and Molecular Pharmacology , New York University School of Medicine , New York , NY , USA.
New York University · US

Funding

MEDICAL SCIENTIST TRAININGT32GM007308 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI PHILIPS, MARK REID · 1985 to 2019
$23.2M
TRAINING PROGRAM IN MOLECULAR ONCOLOGY &IMMUNOLOGYT32CA009161 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI CARROLL, WILLIAM L., LEVY, DAVID E · 1985 to 2020
$13.3M
Regulation of Cellular Senescence and Oncogenic Transformation by Sin3B.R01CA148639 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI DAVID, GREGORY · 2011 to 2015
$2.0M
Role of cell cycle withdrawal in restricting pancreatic cancer progression.R21CA155736 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI DAVID, GREGORY · 2012 to 2014
$590k
(PQ1) Cellular senescence as an initiating event in malignant transformationR21CA206013 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI DAVID, GREGORY · 2017 to 2018
$373k
The role of Sin3B in normal and malignant hematopoietic stem cell functionsF30CA203047 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI CANTOR, DAVID JOHN · 2016 to 2017
$98k
NCI NIH HHS F30 CA203047NCI NIH HHS R01 CA148639NCI NIH HHS R21 CA155736NCI NIH HHS R21 CA206013NCI NIH HHS T32 CA009161NIGMS NIH HHS T32 GM007308
6 · The paper itself

Abstract

introductionSin3B serves as a scaffold for chromatin-modifying complexes that repress gene transcription to regulate distinct biological processes. Sin3B-containing complexes are critical for cell cycle withdrawal, and abrogation of Sin3B-dependent cell cycle exit impacts tumor progression. Areas covered: In this review, we discuss the biochemical characteristics of Sin3B-containing complexes and explore how these complexes regulate gene transcription. We focus on how Sin3B-containing complexes, through the association of the Rb family of proteins, repress the expression of E2F target genes during quiescence, differentiation, and senescence. Finally, we speculate on the potential benefits of the inhibition of Sin3B-containing complexes for the treatment of cancer. Expert opinion: Further identification and characterization of specific Sin3B-containing complexes provide a unique opportunity to prevent the pro-tumorigenic effects of the senescence-associated secretory phenotype, and to abrogate cancer stem cell quiescence and the associated resistance to therapy.

Indexed as

Molecular Targeted TherapyAnimalsCell CycleCell DifferentiationCellular SenescenceDisease ProgressionHumansNeoplasmsNeoplastic Stem CellsRepressor ProteinsTranscription, GeneticRepressor ProteinsSIN3B protein, humanCancer stem cellcellular senescencechromatin modifiersquiescencesenescence associated secretory phenotypeSin3B

Identifiers

PMID28956957
PMCPMC5679076
OpenAlexW2757501965

What OpenQuestion holds

Textmetadata
LicenceTDM
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.