Evidence map›Paper›PMID 23565070›Full record

ArticleLetters in drug design & discovery2011

Discovery of BRM Targeted Therapies: Novel Reactivation of an Anti-cancer Gene.

Sarah Gramling, David Reisman

Open access · greenAbstract read
In one paragraph

Article in Letters in drug design & discovery, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

  1. BRM Promoter Polymorphisms and Survival of Advanced Non-Small Cell Lung Cancer Patients in the Princess Margaret Cohort and CCTG BR.24 Trial.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
    Trial
  2. Review
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  6. SMARCA4-deficient thoracic sarcoma: a distinctive clinicopathological entity with undifferentiated rhabdoid morphology and aggressive behavior.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2017
    Article
  7. Concomitant loss of SMARCA2 and SMARCA4 expression in small cell carcinoma of the ovary, hypercalcemic type.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2016
    Article
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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.

Sarah GramlingDepartment of Medicine, Division of Hematology/Oncology, University of Florida, Gainesville Florida 32611, USA.
David Reisman
University of Florida Health · US

Funding

TRAINING IN THE CELL BIOLOGY AND IMMUNOBIOLOGY OF CANCERT32CA009126 · NCI · UNIVERSITY OF FLORIDA · PI MAY, WILLIAM STRATFORD · 1985 to 2012
$3.5M
Identifying Agents which Restored BRM expressionR01CA136683 · NCI · UNIVERSITY OF FLORIDA · PI REISMAN, DAVID N · 2010 to 2013
$877k
Reverse the Epigenetic Suppression of BRM through High Throughput ScreeningR03DA028854 · NIDA · UNIVERSITY OF FLORIDA · PI REISMAN, DAVID N · 2009 to 2009
$29k
NCI NIH HHS R01 CA136683NCI NIH HHS T32 CA009126NIDA NIH HHS R03 DA028854
6 · The paper itself

Abstract

Drug discovery in the field of oncology has been advanced mainly through the targeting of receptor tyrosine kinases. Both antibodies and small molecule inhibitors have been found to have successful applications in blocking the proliferative functions of these cell surface receptors. Based on these early successes, additional kinases within the cytoplasm have been found to promote cancer and, as such, have been recognized as feasible targets for additional modes of therapies. Unlike these oncogene targets, most tumor suppressors are irreversibly altered during cancer progression and therefore are not feasible targets for therapy. However, a subset of these genes is reversibly epigenetically suppressed. One such gene is BRM, and when it is re-expressed in cancer cells, this gene halts their growth. Moreover, as the key catalytic subunit of the SWI/SNF complex, BRM is centrally important to a host of anticancer pathways and cellular mechanisms, and its status may serve as a biomarker. Restoring its expression will both reconnect a number of growth-controlling pathways and affect cellular adhesion, DNA repair, and immune functions. For these reasons, restoring BRM expression is not only feasible, but potentially a potent form of anticancer therapy. To identify BRM-restoring compounds, we developed a cell-based luciferase assay. In this review, we discuss some of the challenges we encountered, issues related to this type of drug discovery, and our future ambitions. We hope this review will provide insight to this type of endeavor and lead to more investigations pursuing this type of drug research.

Indexed as

AnticancerBrahmaEpigenetic suppressionHigh throughput screeningSWI/SNFTumor suppressor

Identifiers

PMID23565070
PMCPMC3615482
OpenAlexW1972323865

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.